Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice
IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (...
Saved in:
Published in | The Journal of immunology (1950) Vol. 187; no. 1; pp. 64 - 73 |
---|---|
Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
01.07.2011
|
Subjects | |
Online Access | Get full text |
ISSN | 0022-1767 1550-6606 1550-6606 |
DOI | 10.4049/jimmunol.1100500 |
Cover
Abstract | IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1–dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling. |
---|---|
AbstractList | IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1–dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling. IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE(2), causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4(+) T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE(2), causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4(+) T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling. IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE(2), causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4(+) T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling. IL-1 beta is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1 beta . The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1 beta , SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1 alpha , IL-1 beta , IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1 beta by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling. Interleukin (IL)-1β is a cytokine critical to several inflammatory diseases in which pathogenic T H 17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1 dependent processing and secretion of IL-1β. The acute phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship between these mediators has yet to be identified. Herein, we demonstrate that Saa3 is expressed in the lung of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE 2 , causes dendritic cell maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by dendritic cells and macrophages. CD4 + T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed dendritic cells produced IL-17 and the capacity of polyclonally-stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled ovalbumin, resulting in leukocyte influx after antigen challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1 receptor signaling. |
Author | Boyson, Jonathan E Eisenbarth, Stephanie C Flavell, Richard A Suratt, Benjamin T Foley, Kathryn L Poynter, Matthew E Martin, Rebecca Fitzgerald, Katherine A Ather, Jennifer L Ckless, Karina |
AuthorAffiliation | Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA, 06520 Department of Chemistry, SUNY Plattsburgh, Plattsburgh, NY, USA, 12901 Howard Hughes Medical Institute, Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA, 06520 Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worchester, MA, USA, 01655 Department of Surgery, University of Vermont, Burlington, VT, USA 05405 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, USA 05405 |
AuthorAffiliation_xml | – name: Department of Chemistry, SUNY Plattsburgh, Plattsburgh, NY, USA, 12901 – name: Department of Surgery, University of Vermont, Burlington, VT, USA 05405 – name: Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, USA 05405 – name: Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worchester, MA, USA, 01655 – name: Howard Hughes Medical Institute, Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA, 06520 – name: Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA, 06520 |
Author_xml | – sequence: 1 givenname: Jennifer L surname: Ather fullname: Ather, Jennifer L – sequence: 2 givenname: Karina surname: Ckless fullname: Ckless, Karina – sequence: 3 givenname: Rebecca surname: Martin fullname: Martin, Rebecca – sequence: 4 givenname: Kathryn L surname: Foley fullname: Foley, Kathryn L – sequence: 5 givenname: Benjamin T surname: Suratt fullname: Suratt, Benjamin T – sequence: 6 givenname: Jonathan E surname: Boyson fullname: Boyson, Jonathan E – sequence: 7 givenname: Katherine A surname: Fitzgerald fullname: Fitzgerald, Katherine A – sequence: 8 givenname: Richard A surname: Flavell fullname: Flavell, Richard A – sequence: 9 givenname: Stephanie C surname: Eisenbarth fullname: Eisenbarth, Stephanie C – sequence: 10 givenname: Matthew E surname: Poynter fullname: Poynter, Matthew E |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21622869$$D View this record in MEDLINE/PubMed |
BookMark | eNqFkc1v1DAQxS1URLeFOyfkG6eUceI48QUpqlpYaQsVlAsXy3acrit_FNuptP89u-puRZEQpznM7z29mXeCjkIMBqG3BM4oUP7hzno_h-jOCAFoAV6gBWlbqBgDdoQWAHVdkY51x-gk5zsAYFDTV-i4Jqyue8YX6Od3k2aPB79x0Y54wIMu9kEWk3FZG_xl9e26wcswOem9zNEbLMOIr1P0ccfcrEmHB-dMurUaD7msvcQ24CurzWv0cpIumzf7eYp-XF7cnH-uVl8_Lc-HVaVpS0rFKVXN2BlgkoLiRk0jJUCUangvQWupJtbJEbjUvBkVaWEyLe3V1G_vqTVpTtHHR9_7WXkzahNKkk7cJ-tl2ogorXi-CXYtbuODaAjhHdsZvN8bpPhrNrkIb7M2zslg4pwFB0o70lL2X7LvmoZQ1sOWfPdnqKc0h89vAXgEdIo5JzM9IQTErlxxKFfsy91K2F8SbYssNu7Osu7fwt-r1au6 |
CitedBy_id | crossref_primary_10_1016_j_jmb_2021_167183 crossref_primary_10_1128_mBio_01817_14 crossref_primary_10_1080_00207454_2017_1398153 crossref_primary_10_1111_all_14760 crossref_primary_10_1177_03946320221104554 crossref_primary_10_1371_journal_pone_0192352 crossref_primary_10_3389_fimmu_2015_00023 crossref_primary_10_1016_j_jaci_2013_12_1035 crossref_primary_10_1093_toxsci_kfx080 crossref_primary_10_1016_j_bbi_2024_10_016 crossref_primary_10_1371_journal_pone_0096703 crossref_primary_10_1038_s41590_020_0698_1 crossref_primary_10_1097_MD_0000000000038085 crossref_primary_10_1111_imr_12183 crossref_primary_10_1016_j_prp_2023_154410 crossref_primary_10_1038_mi_2013_26 crossref_primary_10_1099_mic_0_073445_0 crossref_primary_10_1016_j_toxlet_2015_04_011 crossref_primary_10_3892_ol_2019_10542 crossref_primary_10_3389_fgene_2021_668448 crossref_primary_10_1016_j_ijbiomac_2023_126537 crossref_primary_10_1177_01455613211051311 crossref_primary_10_1038_s41591_021_01332_7 crossref_primary_10_1016_j_fsi_2019_12_068 crossref_primary_10_1073_pnas_1521206112 crossref_primary_10_4049_jimmunol_1201797 crossref_primary_10_1371_journal_pone_0094934 crossref_primary_10_1111_cmi_12257 crossref_primary_10_1111_j_1939_1676_2012_00993_x crossref_primary_10_1371_journal_pone_0062372 crossref_primary_10_1016_j_resinv_2019_09_005 crossref_primary_10_1126_scitranslmed_3005681 crossref_primary_10_4168_aair_2022_14_1_40 crossref_primary_10_1074_jbc_M112_410613 crossref_primary_10_1111_imm_13644 crossref_primary_10_1183_13993003_01124_2017 crossref_primary_10_4049_jimmunol_1102349 crossref_primary_10_1080_08916934_2024_2310269 crossref_primary_10_1146_annurev_genet_120213_092421 crossref_primary_10_1161_ATVBAHA_121_316066 crossref_primary_10_1186_1743_8977_10_26 crossref_primary_10_1016_j_it_2019_06_005 crossref_primary_10_1007_s10238_024_01413_0 crossref_primary_10_1016_j_molmed_2020_06_005 crossref_primary_10_3389_fimmu_2021_786238 crossref_primary_10_1002_eji_201847811 crossref_primary_10_1016_j_freeradbiomed_2013_01_025 crossref_primary_10_1016_j_ajpath_2013_09_007 crossref_primary_10_1007_s00262_022_03268_4 crossref_primary_10_1016_j_smim_2013_09_003 crossref_primary_10_1038_s41598_018_34901_x crossref_primary_10_1016_j_jaci_2023_11_917 crossref_primary_10_1080_14728222_2023_2239495 crossref_primary_10_1371_journal_pone_0064974 crossref_primary_10_1016_j_jare_2023_01_001 crossref_primary_10_1111_all_13619 crossref_primary_10_1164_rccm_201712_2426OC crossref_primary_10_1016_j_smim_2013_09_001 crossref_primary_10_1242_dmm_012039 crossref_primary_10_1002_jcsm_12596 crossref_primary_10_1016_j_jaci_2016_08_032 crossref_primary_10_4103_0366_6999_182841 crossref_primary_10_1371_journal_pone_0065829 crossref_primary_10_1016_j_bbrep_2015_08_008 crossref_primary_10_3390_ani12060744 crossref_primary_10_1002_jmv_28000 crossref_primary_10_1016_j_reval_2013_02_181 crossref_primary_10_1002_alr_22669 crossref_primary_10_4049_jimmunol_1800671 crossref_primary_10_1186_s12989_021_00432_z crossref_primary_10_4142_jvs_2017_18_3_349 crossref_primary_10_1002_smll_201907476 crossref_primary_10_2119_molmed_2015_00109 crossref_primary_10_1164_rccm_201211_2139OC crossref_primary_10_2147_COPD_S266844 crossref_primary_10_1128_microbiolspec_MCHD_0051_2016 crossref_primary_10_1165_rcmb_2013_0047OC crossref_primary_10_1152_ajplung_00322_2020 crossref_primary_10_1371_journal_pone_0175824 crossref_primary_10_1016_j_jare_2023_01_012 crossref_primary_10_1038_s41598_018_37232_z crossref_primary_10_1016_j_cytogfr_2015_12_010 crossref_primary_10_1016_j_jaci_2016_12_963 crossref_primary_10_1113_EP087397 crossref_primary_10_1016_j_imlet_2018_10_013 crossref_primary_10_1111_imm_13295 crossref_primary_10_3390_jcm8101615 crossref_primary_10_1152_ajplung_00105_2015 crossref_primary_10_1189_jlb_3VMR0315_080R crossref_primary_10_1093_femspd_ftu027 crossref_primary_10_1080_15287394_2014_892446 crossref_primary_10_1016_j_molimm_2021_04_022 crossref_primary_10_1038_s41392_021_00679_0 crossref_primary_10_1111_j_1476_5381_2012_01984_x crossref_primary_10_1002_cti2_1323 crossref_primary_10_1111_all_14600 crossref_primary_10_4049_jimmunol_2300518 crossref_primary_10_1194_jlr_M080887 crossref_primary_10_1080_21623945_2021_1916220 crossref_primary_10_1111_cea_12206 crossref_primary_10_1007_s10620_017_4606_y crossref_primary_10_1016_j_pupt_2012_04_005 crossref_primary_10_1038_s41420_023_01455_5 crossref_primary_10_1111_imr_12540 crossref_primary_10_1189_jlb_3A0315_085R crossref_primary_10_1016_j_ijid_2021_03_025 crossref_primary_10_34133_research_0435 crossref_primary_10_1038_nm_2737 crossref_primary_10_1172_JCI59643 crossref_primary_10_4103_ejdv_ejdv_27_19 crossref_primary_10_3390_toxics9100253 crossref_primary_10_1016_j_vetmic_2016_05_013 crossref_primary_10_3389_fimmu_2023_1314123 crossref_primary_10_1016_j_virusres_2016_01_011 crossref_primary_10_1165_rcmb_2012_0423OC crossref_primary_10_1096_fj_202002017R crossref_primary_10_1111_cei_12458 crossref_primary_10_1016_j_arr_2015_02_005 crossref_primary_10_3390_ijms24032478 crossref_primary_10_1016_j_yexmp_2012_04_011 crossref_primary_10_1128_IAI_02370_14 crossref_primary_10_1016_j_intimp_2024_113081 crossref_primary_10_1093_femspd_ftv011 crossref_primary_10_3390_cells10092220 crossref_primary_10_1016_j_molmet_2022_101462 crossref_primary_10_1152_ajplung_00235_2013 crossref_primary_10_1016_j_molimm_2019_08_013 crossref_primary_10_1016_j_biopha_2018_02_079 crossref_primary_10_1371_journal_ppat_1006315 crossref_primary_10_3390_vaccines10040614 crossref_primary_10_4049_jimmunol_1203013 crossref_primary_10_4049_jimmunol_1800503 crossref_primary_10_3389_fimmu_2021_691155 crossref_primary_10_4049_jimmunol_1600035 crossref_primary_10_1016_j_imbio_2014_08_002 crossref_primary_10_1128_IAI_00316_16 crossref_primary_10_1016_j_tim_2019_07_002 crossref_primary_10_1016_j_jaci_2017_03_018 crossref_primary_10_3892_ijmm_2025_5489 crossref_primary_10_1183_13993003_00119_2019 crossref_primary_10_1189_jlb_1012543 crossref_primary_10_1038_icb_2017_2 crossref_primary_10_1136_bmjgast_2024_001497 crossref_primary_10_1016_j_imbio_2017_11_001 crossref_primary_10_1038_cmi_2015_97 crossref_primary_10_1038_srep38697 crossref_primary_10_1152_ajplung_00204_2020 crossref_primary_10_1016_j_cytogfr_2020_10_006 crossref_primary_10_1042_BCJ20180086 crossref_primary_10_1007_s00430_012_0247_0 crossref_primary_10_3390_cancers13030571 crossref_primary_10_1371_journal_pone_0074730 crossref_primary_10_1007_s00405_017_4809_z crossref_primary_10_1016_j_vetimm_2017_06_006 crossref_primary_10_1016_j_molimm_2018_12_024 crossref_primary_10_1007_s10753_016_0442_z crossref_primary_10_1093_rheumatology_kes162 crossref_primary_10_3390_pharmaceutics14030623 crossref_primary_10_4049_jimmunol_1402164 crossref_primary_10_1038_cddis_2013_327 crossref_primary_10_1074_jbc_RA118_002428 crossref_primary_10_1016_j_clim_2012_12_006 crossref_primary_10_1002_art_39217 crossref_primary_10_1016_j_imbio_2014_09_016 crossref_primary_10_1152_ajplung_00154_2013 crossref_primary_10_1002_eji_201343867 crossref_primary_10_1038_s41598_019_39846_3 crossref_primary_10_1073_pnas_1613405114 crossref_primary_10_3390_biomedicines9050535 crossref_primary_10_1016_j_envpol_2024_124127 crossref_primary_10_1155_2018_9021037 crossref_primary_10_3390_biom11121883 crossref_primary_10_3389_fcvm_2015_00025 crossref_primary_10_1155_2013_942375 crossref_primary_10_1073_pnas_1717802115 crossref_primary_10_15252_embr_202154446 crossref_primary_10_1523_JNEUROSCI_0801_19_2019 crossref_primary_10_1128_JB_00095_19 crossref_primary_10_1007_s00125_016_3970_z crossref_primary_10_1038_s41540_019_0115_2 crossref_primary_10_4049_jimmunol_1600336 |
Cites_doi | 10.1016/S1074-7613(00)80119-3 10.4049/jimmunol.159.7.3364 10.1002/eji.201040391 10.1016/j.immuni.2009.08.001 10.1016/0925-4439(94)00076-3 10.1016/j.cell.2009.09.033 10.1046/j.1365-2249.2001.01602.x 10.1186/1465-9921-7-135 10.1016/j.jaci.2008.01.008 10.1084/jem.20021340 10.1016/S1074-7613(00)80596-8 10.1146/annurev-physiol-021909-135926 10.4049/jimmunol.181.1.22 10.1126/science.7535475 10.1080/13547500902730714 10.1165/rcmb.2010-0106OC 10.1194/jlr.M900089-JLR200 10.1002/jlb.63.3.364 10.1111/j.1365-2222.2008.03069.x 10.1189/jlb.0607-408 10.3899/jrheum.080346 10.1182/blood-2008-05-155408 10.1038/ni.1935 10.1002/art.22794 10.1684/ecn.2009.0156 10.1084/jem.189.2.395 10.1016/0016-5085(91)70002-F 10.1016/j.immuni.2009.02.007 10.1016/j.intimp.2006.05.006 10.1006/bbrc.2000.2416 10.1053/rmed.2003.1507 10.1186/1465-9921-11-102 10.4049/jimmunol.181.1.721 10.1186/ar2143 10.4049/jimmunol.166.4.2801 10.1016/j.jaci.2009.02.024 10.1038/ni.1636 10.1016/j.jaci.2010.02.008 10.1182/blood-2009-08-236521 10.1073/pnas.89.17.7949 10.1002/jcla.20197 10.1002/eji.200838742 10.4049/jimmunol.177.6.4072 10.1186/1742-2094-3-5 10.1084/jem.20060285 10.2174/1381612023393864 10.4049/jimmunol.181.6.4089 10.1164/rccm.200905-0696OC 10.1084/jem.20101376 10.1111/j.1749-6632.2009.04687.x 10.1182/blood-2008-03-139923 10.1164/rccm.200904-0573OC 10.4049/jimmunol.162.7.3749 10.4049/jimmunol.1001536 10.1152/ajplung.00027.2009 10.1164/ajrccm.159.2.9805115 10.1016/S0002-9440(10)62559-X 10.1007/BF02274836 10.4049/jimmunol.0900614 10.1038/ni.1631 10.1183/09031936.02.00280902 10.4049/jimmunol.0904145 10.1046/j.1432-1327.1999.00657.x 10.1016/j.immuni.2006.02.004 10.4049/jimmunol.179.6.3680 10.1620/tjem.204.209 10.1067/mai.2001.117929 10.1084/jem.164.6.2006 |
ContentType | Journal Article |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 7T5 H94 5PM |
DOI | 10.4049/jimmunol.1100500 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic Immunology Abstracts AIDS and Cancer Research Abstracts PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic AIDS and Cancer Research Abstracts Immunology Abstracts |
DatabaseTitleList | CrossRef MEDLINE - Academic MEDLINE AIDS and Cancer Research Abstracts |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine Biology |
EISSN | 1550-6606 |
EndPage | 73 |
ExternalDocumentID | PMC3119761 21622869 10_4049_jimmunol_1100500 |
Genre | Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural |
GrantInformation_xml | – fundername: NHLBI NIH HHS grantid: T32 HL007974 – fundername: NCRR NIH HHS grantid: P20 RR15557 – fundername: NCRR NIH HHS grantid: P20 RR021905 – fundername: NCRR NIH HHS grantid: P20 RR015557 – fundername: Howard Hughes Medical Institute – fundername: NHLBI NIH HHS grantid: R01 HL089177 – fundername: NIAID NIH HHS grantid: R01 AI067897 – fundername: NIGMS NIH HHS grantid: P30 GM103532 – fundername: NHLBI NIH HHS grantid: R01 HL107291 – fundername: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID grantid: R01 AI067897-03 || AI – fundername: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID grantid: R01 AI067897-04 || AI – fundername: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID grantid: R01 AI067897-02 || AI – fundername: National Institute of Allergy and Infectious Diseases Extramural Activities : NIAID grantid: R01 AI067897-01A2 || AI |
GroupedDBID | --- -~X .55 0R~ 18M 1KJ 2WC 34G 39C 3O- 53G 5GY 5RE 5VS 5WD 79B 85S AARDX AAYXX ABCQX ABDFA ABEJV ABGNP ABJNI ABOCM ABPPZ ABXVV ACGFO ACGFS ACIWK ACNCT ACPRK ADBBV ADIPN ADNWM AENEX AETEA AFFNX AFHIN AFOSN AFRAH AGORE AHMMS AHWXS AIZAD ALMA_UNASSIGNED_HOLDINGS ARBBW BAWUL BCRHZ BTFSW CITATION D0L DIK DU5 E3Z EBS EJD F5P FRP GX1 H13 IH2 K-O KQ8 L7B OCZFY OK1 OWPYF P0W P2P PQQKQ R.V RHI ROX RZQ SJN TR2 TWZ W8F WH7 WOQ X7M XJT XSW XTH YHG CGR CUY CVF ECM EIF NPM 7X8 KOP 7T5 H94 5PM |
ID | FETCH-LOGICAL-c451t-944b3d7e06a40b9ebfd4101bb398a0ccabf67ad09ac93db150fe548bf80002c13 |
ISSN | 0022-1767 1550-6606 |
IngestDate | Thu Aug 21 14:21:35 EDT 2025 Sun Sep 28 00:23:30 EDT 2025 Sat Sep 27 23:33:51 EDT 2025 Mon Jul 21 06:06:48 EDT 2025 Tue Jul 01 05:19:35 EDT 2025 Thu Apr 24 22:56:47 EDT 2025 |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Language | English |
License | https://academic.oup.com/pages/standard-publication-reuse-rights |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c451t-944b3d7e06a40b9ebfd4101bb398a0ccabf67ad09ac93db150fe548bf80002c13 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
PMID | 21622869 |
PQID | 873314680 |
PQPubID | 23479 |
PageCount | 10 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_3119761 proquest_miscellaneous_904471546 proquest_miscellaneous_873314680 pubmed_primary_21622869 crossref_primary_10_4049_jimmunol_1100500 crossref_citationtrail_10_4049_jimmunol_1100500 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2011-07-01 |
PublicationDateYYYYMMDD | 2011-07-01 |
PublicationDate_xml | – month: 07 year: 2011 text: 2011-07-01 day: 01 |
PublicationDecade | 2010 |
PublicationPlace | England |
PublicationPlace_xml | – name: England |
PublicationTitle | The Journal of immunology (1950) |
PublicationTitleAlternate | J Immunol |
PublicationYear | 2011 |
References | He (2025032410183959700_r15) 2009; 113 Finkelman (2025032410183959700_r68) 2008; 121 Uhlar (2025032410183959700_r13) 1999; 265 Adachi (2025032410183959700_r44) 1998; 9 Laan (2025032410183959700_r34) 2002; 19 Al-Ramli (2025032410183959700_r29) 2009; 123 Gris (2025032410183959700_r5) 2010; 185 Eisenbarth (2025032410183959700_r39) 2008; 38 Masters (2025032410183959700_r2) 2010; 11 Bevelander (2025032410183959700_r58) 2007; 179 Bullens (2025032410183959700_r31) 2006; 7 Büyüköztürk (2025032410183959700_r25) 2004; 204 Aliahmadi (2025032410183959700_r66) 2009; 39 So (2025032410183959700_r9) 2007; 9 Takeuchi (2025032410183959700_r42) 1999; 11 Sheibanie (2025032410183959700_r52) 2007; 56 Sutton (2025032410183959700_r65) 2009; 31 Björkman (2025032410183959700_r16) 2008; 83 Zhang (2025032410183959700_r37) 2009; 20 Wong (2025032410183959700_r36) 2001; 125 Chen (2025032410183959700_r63) 2010; 181 Su (2025032410183959700_r18) 1999; 189 Halle (2025032410183959700_r22) 2008; 9 Molenaar (2025032410183959700_r62) 2009; 14 Ather (2025032410183959700_r47) 2011; 44 Sutton (2025032410183959700_r51) 2006; 203 Li (2025032410183959700_r11) 2010; 185 Kuida (2025032410183959700_r46) 1995; 267 Wang (2025032410183959700_r69) 2010; 207 Griffin (2025032410183959700_r6) 2006; 3 Tillie-Leblond (2025032410183959700_r28) 1999; 159 Poynter (2025032410183959700_r56) 2002; 160 Meek (2025032410183959700_r60) 1992; 89 Clutterbuck (2025032410183959700_r4) 2009; 1171 Wu (2025032410183959700_r27) 2007; 21 Rooney (2025032410183959700_r7) 1990; 10 Fujisawa (2025032410183959700_r38) 2009; 183 He (2025032410183959700_r41) 2006; 177 Hornung (2025032410183959700_r49) 2008; 9 Chung (2025032410183959700_r10) 2009; 30 Wilson (2025032410183959700_r40) 2009; 180 Bates (2025032410183959700_r57) 2009; 297 Chiba (2025032410183959700_r61) 2009; 50 Lee (2025032410183959700_r12) 2010; 115 Barczyk (2025032410183959700_r30) 2003; 97 Hastie (2025032410183959700_r32) 2010; 125 Eisenbarth (2025032410183959700_r50) 2002; 196 Cheng (2025032410183959700_r14) 2008; 181 Laan (2025032410183959700_r33) 2002; 8 Liang (2025032410183959700_r17) 2000; 270 Sutterwala (2025032410183959700_r45) 2006; 24 Khayrullina (2025032410183959700_r53) 2008; 181 Liepnieks (2025032410183959700_r21) 1995; 1270 Ozseker (2025032410183959700_r26) 2006; 6 Glaccum (2025032410183959700_r1) 1997; 159 Ivanov (2025032410183959700_r20) 2009; 139 Weber (2025032410183959700_r54) 2010; 3 Radema (2025032410183959700_r8) 1991; 100 Hodgkins (2025032410183959700_r48) 2010; 11 Daheshia (2025032410183959700_r3) 2008; 35 Struyf (2025032410183959700_r55) 1998; 63 Meek (2025032410183959700_r59) 1986; 164 Hoshino (2025032410183959700_r43) 1999; 162 Chizzolini (2025032410183959700_r64) 2008; 112 Kimura (2025032410183959700_r67) 2010; 40 Molet (2025032410183959700_r35) 2001; 108 Alcorn (2025032410183959700_r23) 2010; 72 McKinley (2025032410183959700_r24) 2008; 181 Vallon (2025032410183959700_r19) 2001; 166 |
References_xml | – volume: 11 start-page: 443 year: 1999 ident: 2025032410183959700_r42 article-title: Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components publication-title: Immunity doi: 10.1016/S1074-7613(00)80119-3 – volume: 159 start-page: 3364 year: 1997 ident: 2025032410183959700_r1 article-title: Phenotypic and functional characterization of mice that lack the type I receptor for IL-1 publication-title: J. Immunol. doi: 10.4049/jimmunol.159.7.3364 – volume: 40 start-page: 1830 year: 2010 ident: 2025032410183959700_r67 article-title: IL-6: regulator of Treg/Th17 balance publication-title: Eur. J. Immunol. doi: 10.1002/eji.201040391 – volume: 31 start-page: 331 year: 2009 ident: 2025032410183959700_r65 article-title: Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity publication-title: Immunity doi: 10.1016/j.immuni.2009.08.001 – volume: 1270 start-page: 81 year: 1995 ident: 2025032410183959700_r21 article-title: Characterization of amyloid A protein in human secondary amyloidosis: the predominant deposition of serum amyloid A1 publication-title: Biochim. Biophys. Acta doi: 10.1016/0925-4439(94)00076-3 – volume: 139 start-page: 485 year: 2009 ident: 2025032410183959700_r20 article-title: Induction of intestinal Th17 cells by segmented filamentous bacteria publication-title: Cell doi: 10.1016/j.cell.2009.09.033 – volume: 125 start-page: 177 year: 2001 ident: 2025032410183959700_r36 article-title: Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN-gamma, IL-4, IL-10 and IL-13) in patients with allergic asthma publication-title: Clin. Exp. Immunol. doi: 10.1046/j.1365-2249.2001.01602.x – volume: 7 start-page: 135 year: 2006 ident: 2025032410183959700_r31 article-title: IL-17 mRNA in sputum of asthmatic patients: linking T cell driven inflammation and granulocytic influx? publication-title: Respir. Res. doi: 10.1186/1465-9921-7-135 – volume: 121 start-page: 603 year: 2008 ident: 2025032410183959700_r68 article-title: Usefulness and optimization of mouse models of allergic airway disease publication-title: J. Allergy Clin. Immunol. doi: 10.1016/j.jaci.2008.01.008 – volume: 196 start-page: 1645 year: 2002 ident: 2025032410183959700_r50 article-title: Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T helper cell type 2 responses to inhaled antigen publication-title: J. Exp. Med. doi: 10.1084/jem.20021340 – volume: 9 start-page: 143 year: 1998 ident: 2025032410183959700_r44 article-title: Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function publication-title: Immunity doi: 10.1016/S1074-7613(00)80596-8 – volume: 72 start-page: 495 year: 2010 ident: 2025032410183959700_r23 article-title: TH17 cells in asthma and COPD publication-title: Annu. Rev. Physiol. doi: 10.1146/annurev-physiol-021909-135926 – volume: 181 start-page: 22 year: 2008 ident: 2025032410183959700_r14 article-title: Cutting edge: TLR2 is a functional receptor for acute-phase serum amyloid A publication-title: J. Immunol. doi: 10.4049/jimmunol.181.1.22 – volume: 267 start-page: 2000 year: 1995 ident: 2025032410183959700_r46 article-title: Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme publication-title: Science doi: 10.1126/science.7535475 – volume: 14 start-page: 26 year: 2009 ident: 2025032410183959700_r62 article-title: The acute-phase protein serum amyloid A3 is expressed in the bovine mammary gland and plays a role in host defence publication-title: Biomarkers doi: 10.1080/13547500902730714 – volume: 44 start-page: 631 year: 2011 ident: 2025032410183959700_r47 article-title: Airway epithelial NF-κB activation promotes allergic sensitization to an innocuous inhaled antigen publication-title: Am. J. Respir. Cell Mol. Biol. doi: 10.1165/rcmb.2010-0106OC – volume: 50 start-page: 1353 year: 2009 ident: 2025032410183959700_r61 article-title: Serum amyloid A3 does not contribute to circulating SAA levels publication-title: J. Lipid Res. doi: 10.1194/jlr.M900089-JLR200 – volume: 63 start-page: 364 year: 1998 ident: 2025032410183959700_r55 article-title: Synergistic induction of MCP-1 and -2 by IL-1beta and interferons in fibroblasts and epithelial cells publication-title: J. Leukoc. Biol. doi: 10.1002/jlb.63.3.364 – volume: 38 start-page: 1572 year: 2008 ident: 2025032410183959700_r39 article-title: Use and limitations of alum-based models of allergy publication-title: Clin. Exp. Allergy doi: 10.1111/j.1365-2222.2008.03069.x – volume: 83 start-page: 245 year: 2008 ident: 2025032410183959700_r16 article-title: Serum amyloid A mediates human neutrophil production of reactive oxygen species through a receptor independent of formyl peptide receptor like-1 publication-title: J. Leukoc. Biol. doi: 10.1189/jlb.0607-408 – volume: 35 start-page: 2306 year: 2008 ident: 2025032410183959700_r3 article-title: The interleukin 1beta pathway in the pathogenesis of osteoarthritis publication-title: J. Rheumatol. doi: 10.3899/jrheum.080346 – volume: 112 start-page: 3696 year: 2008 ident: 2025032410183959700_r64 article-title: Prostaglandin E2 synergistically with interleukin-23 favors human Th17 expansion publication-title: Blood doi: 10.1182/blood-2008-05-155408 – volume: 11 start-page: 897 year: 2010 ident: 2025032410183959700_r2 article-title: Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes publication-title: Nat. Immunol. doi: 10.1038/ni.1935 – volume: 56 start-page: 2608 year: 2007 ident: 2025032410183959700_r52 article-title: Prostaglandin E2 exacerbates collagen-induced arthritis in mice through the inflammatory interleukin-23/interleukin-17 axis publication-title: Arthritis Rheum. doi: 10.1002/art.22794 – volume: 20 start-page: 148 year: 2009 ident: 2025032410183959700_r37 article-title: Long-term exposure to IL-1beta enhances Toll-IL-1 receptor-mediated inflammatory signaling in murine airway hyperresponsiveness publication-title: Eur. Cytokine Netw. doi: 10.1684/ecn.2009.0156 – volume: 189 start-page: 395 year: 1999 ident: 2025032410183959700_r18 article-title: A seven-transmembrane, G protein-coupled receptor, FPRL1, mediates the chemotactic activity of serum amyloid A for human phagocytic cells publication-title: J. Exp. Med. doi: 10.1084/jem.189.2.395 – volume: 100 start-page: 1180 year: 1991 ident: 2025032410183959700_r8 article-title: Interleukin 1 beta is expressed predominantly by enterocytes in experimental colitis publication-title: Gastroenterology doi: 10.1016/0016-5085(91)70002-F – volume: 30 start-page: 576 year: 2009 ident: 2025032410183959700_r10 article-title: Critical regulation of early Th17 cell differentiation by interleukin-1 signaling publication-title: Immunity doi: 10.1016/j.immuni.2009.02.007 – volume: 6 start-page: 1569 year: 2006 ident: 2025032410183959700_r26 article-title: Serum amyloid A (SAA) in induced sputum of asthmatics: a new look to an old marker publication-title: Int. Immunopharmacol. doi: 10.1016/j.intimp.2006.05.006 – volume: 270 start-page: 331 year: 2000 ident: 2025032410183959700_r17 article-title: Serum amyloid A is a chemotactic agonist at FPR2, a low-affinity N-formylpeptide receptor on mouse neutrophils publication-title: Biochem. Biophys. Res. Commun. doi: 10.1006/bbrc.2000.2416 – volume: 97 start-page: 726 year: 2003 ident: 2025032410183959700_r30 article-title: Interleukin-17 in sputum correlates with airway hyperresponsiveness to methacholine publication-title: Respir. Med. doi: 10.1053/rmed.2003.1507 – volume: 11 start-page: 102 year: 2010 ident: 2025032410183959700_r48 article-title: NO2 inhalation induces maturation of pulmonary CD11c+ cells that promote antigenspecific CD4+ T cell polarization publication-title: Respir. Res. doi: 10.1186/1465-9921-11-102 – volume: 181 start-page: 721 year: 2008 ident: 2025032410183959700_r53 article-title: In vitro differentiation of dendritic cells in the presence of prostaglandin E2 alters the IL-12/IL-23 balance and promotes differentiation of Th17 cells publication-title: J. Immunol. doi: 10.4049/jimmunol.181.1.721 – volume: 9 start-page: R28 year: 2007 ident: 2025032410183959700_r9 article-title: A pilot study of IL-1 inhibition by anakinra in acute gout publication-title: Arthritis Res. Ther. doi: 10.1186/ar2143 – volume: 166 start-page: 2801 year: 2001 ident: 2025032410183959700_r19 article-title: Serum amyloid A (apoSAA) expression is up-regulated in rheumatoid arthritis and induces transcription of matrix metalloproteinases publication-title: J. Immunol. doi: 10.4049/jimmunol.166.4.2801 – volume: 123 start-page: 1185 year: 2009 ident: 2025032410183959700_r29 article-title: T(H)17-associated cytokines (IL-17A and IL-17F) in severe asthma publication-title: J. Allergy Clin. Immunol. doi: 10.1016/j.jaci.2009.02.024 – volume: 9 start-page: 857 year: 2008 ident: 2025032410183959700_r22 article-title: The NALP3 inflammasome is involved in the innate immune response to amyloid-beta publication-title: Nat. Immunol. doi: 10.1038/ni.1636 – volume: 125 start-page: 1028 year: 2010 ident: 2025032410183959700_r32 article-title: Analyses of asthma severity phenotypes and inflammatory proteins in subjects stratified by sputum granulocytes publication-title: J. Allergy Clin. Immunol. doi: 10.1016/j.jaci.2010.02.008 – volume: 115 start-page: 530 year: 2010 ident: 2025032410183959700_r12 article-title: Regulating human Th17 cells via differential expression of IL-1 receptor publication-title: Blood doi: 10.1182/blood-2009-08-236521 – volume: 89 start-page: 7949 year: 1992 ident: 2025032410183959700_r60 article-title: Murine serum amyloid A3 is a high density apolipoprotein and is secreted by macrophages publication-title: Proc. Natl. Acad. Sci. USA doi: 10.1073/pnas.89.17.7949 – volume: 21 start-page: 367 year: 2007 ident: 2025032410183959700_r27 article-title: A panel of multiple markers associated with chronic systemic inflammation and the risk of atherogenesis is detectable in asthma and chronic obstructive pulmonary disease publication-title: J. Clin. Lab. Anal. doi: 10.1002/jcla.20197 – volume: 39 start-page: 1221 year: 2009 ident: 2025032410183959700_r66 article-title: TLR2-activated human langerhans cells promote Th17 polarization via IL-1beta, TGF-beta and IL-23 publication-title: Eur. J. Immunol. doi: 10.1002/eji.200838742 – volume: 177 start-page: 4072 year: 2006 ident: 2025032410183959700_r41 article-title: Serum amyloid A is an endogenous ligand that differentially induces IL-12 and IL-23 publication-title: J. Immunol. doi: 10.4049/jimmunol.177.6.4072 – volume: 3 start-page: 5 year: 2006 ident: 2025032410183959700_r6 article-title: Interleukin-1 mediates Alzheimer and Lewy body pathologies publication-title: J. Neuroinflammation doi: 10.1186/1742-2094-3-5 – volume: 203 start-page: 1685 year: 2006 ident: 2025032410183959700_r51 article-title: A crucial role for interleukin (IL)-1 in the induction of IL-17-producing T cells that mediate autoimmune encephalomyelitis publication-title: J. Exp. Med. doi: 10.1084/jem.20060285 – volume: 8 start-page: 1855 year: 2002 ident: 2025032410183959700_r33 article-title: IL-17 as a potential target for modulating airway neutrophilia publication-title: Curr. Pharm. Des. doi: 10.2174/1381612023393864 – volume: 3 start-page: cm1 year: 2010 ident: 2025032410183959700_r54 article-title: Interleukin-1 (IL-1) pathway publication-title: Sci. Signal. – volume: 181 start-page: 4089 year: 2008 ident: 2025032410183959700_r24 article-title: TH17 cells mediate steroid-resistant airway inflammation and airway hyperresponsiveness in mice publication-title: J. Immunol. doi: 10.4049/jimmunol.181.6.4089 – volume: 181 start-page: 360 year: 2010 ident: 2025032410183959700_r63 article-title: Serum amyloid A regulates granulomatous inflammation in sarcoidosis through Toll-like receptor-2 publication-title: Am. J. Respir. Crit. Care Med. doi: 10.1164/rccm.200905-0696OC – volume: 207 start-page: 2479 year: 2010 ident: 2025032410183959700_r69 article-title: A novel subset of CD4(+) T(H)2 memory/effector cells that produce inflammatory IL-17 cytokine and promote the exacerbation of chronic allergic asthma publication-title: J. Exp. Med. doi: 10.1084/jem.20101376 – volume: 1171 start-page: 428 year: 2009 ident: 2025032410183959700_r4 article-title: Interleukin-1beta-induced extracellular matrix degradation and glycosaminoglycan release is inhibited by curcumin in an explant model of cartilage inflammation publication-title: Ann. N. Y. Acad. Sci. doi: 10.1111/j.1749-6632.2009.04687.x – volume: 113 start-page: 429 year: 2009 ident: 2025032410183959700_r15 article-title: Serum amyloid A induces G-CSF expression and neutrophilia via Toll-like receptor 2 publication-title: Blood doi: 10.1182/blood-2008-03-139923 – volume: 180 start-page: 720 year: 2009 ident: 2025032410183959700_r40 article-title: Allergic sensitization through the airway primes Th17-dependent neutrophilia and airway hyperresponsiveness publication-title: Am. J. Respir. Crit. Care Med. doi: 10.1164/rccm.200904-0573OC – volume: 162 start-page: 3749 year: 1999 ident: 2025032410183959700_r43 article-title: Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product publication-title: J. Immunol. doi: 10.4049/jimmunol.162.7.3749 – volume: 185 start-page: 4148 year: 2010 ident: 2025032410183959700_r11 article-title: IL-1β-mediated signals preferentially drive conversion of regulatory T cells but not conventional T cells into IL-17-producing cells publication-title: J. Immunol. doi: 10.4049/jimmunol.1001536 – volume: 297 start-page: L401 year: 2009 ident: 2025032410183959700_r57 article-title: Animal models of asthma publication-title: Am. J. Physiol. Lung Cell. Mol. Physiol. doi: 10.1152/ajplung.00027.2009 – volume: 159 start-page: 487 year: 1999 ident: 2025032410183959700_r28 article-title: Balance between proinflammatory cytokines and their inhibitors in bronchial lavage from patients with status asthmaticus publication-title: Am. J. Respir. Crit. Care Med. doi: 10.1164/ajrccm.159.2.9805115 – volume: 160 start-page: 1325 year: 2002 ident: 2025032410183959700_r56 article-title: Rapid activation of nuclear factor-kappaB in airway epithelium in a murine model of allergic airway inflammation publication-title: Am. J. Pathol. doi: 10.1016/S0002-9440(10)62559-X – volume: 10 start-page: 217 year: 1990 ident: 2025032410183959700_r7 article-title: Interleukin 1 beta in synovial fluid is related to local disease activity in rheumatoid arthritis publication-title: Rheumatol. Int. doi: 10.1007/BF02274836 – volume: 183 start-page: 6236 year: 2009 ident: 2025032410183959700_r38 article-title: Regulation of airway MUC5AC expression by IL-1beta and IL-17A; the NF-kappaB paradigm publication-title: J. Immunol. doi: 10.4049/jimmunol.0900614 – volume: 9 start-page: 847 year: 2008 ident: 2025032410183959700_r49 article-title: Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization publication-title: Nat. Immunol. doi: 10.1038/ni.1631 – volume: 19 start-page: 534 year: 2002 ident: 2025032410183959700_r34 article-title: Free, soluble interleukin-17 protein during severe inflammation in human airways publication-title: Eur. Respir. J. doi: 10.1183/09031936.02.00280902 – volume: 185 start-page: 974 year: 2010 ident: 2025032410183959700_r5 article-title: NLRP3 plays a critical role in the development of experimental autoimmune encephalomyelitis by mediating Th1 and Th17 responses publication-title: J. Immunol. doi: 10.4049/jimmunol.0904145 – volume: 265 start-page: 501 year: 1999 ident: 2025032410183959700_r13 article-title: Serum amyloid A, the major vertebrate acute-phase reactant publication-title: Eur. J. Biochem. doi: 10.1046/j.1432-1327.1999.00657.x – volume: 24 start-page: 317 year: 2006 ident: 2025032410183959700_r45 article-title: Critical role for NALP3/CIAS1/Cryopyrin in innate and adaptive immunity through its regulation of caspase-1 publication-title: Immunity doi: 10.1016/j.immuni.2006.02.004 – volume: 179 start-page: 3680 year: 2007 ident: 2025032410183959700_r58 article-title: Nitrogen dioxide promotes allergic sensitization to inhaled antigen publication-title: J. Immunol. doi: 10.4049/jimmunol.179.6.3680 – volume: 204 start-page: 209 year: 2004 ident: 2025032410183959700_r25 article-title: Acute phase reactants in allergic airway disease publication-title: Tohoku J. Exp. Med. doi: 10.1620/tjem.204.209 – volume: 108 start-page: 430 year: 2001 ident: 2025032410183959700_r35 article-title: IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines publication-title: J. Allergy Clin. Immunol. doi: 10.1067/mai.2001.117929 – volume: 164 start-page: 2006 year: 1986 ident: 2025032410183959700_r59 article-title: Amyloid A gene family expression in different mouse tissues publication-title: J. Exp. Med. doi: 10.1084/jem.164.6.2006 |
SSID | ssj0006024 |
Score | 2.475555 |
Snippet | IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by... IL-1 beta is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by... Interleukin (IL)-1β is a cytokine critical to several inflammatory diseases in which pathogenic T H 17 responses are implicated. Activation of the NLRP3... |
SourceID | pubmedcentral proquest pubmed crossref |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
StartPage | 64 |
SubjectTerms | Allergens - genetics Allergens - physiology Animals Carrier Proteins - genetics Carrier Proteins - metabolism Cell Polarity - genetics Cell Polarity - immunology Cells, Cultured Dendritic Cells - immunology Dendritic Cells - metabolism Dendritic Cells - pathology Disease Models, Animal Epitopes, T-Lymphocyte - genetics Epitopes, T-Lymphocyte - immunology Inflammasomes - deficiency Inflammasomes - genetics Inflammasomes - metabolism Interleukin 1 Receptor Antagonist Protein - administration & dosage Interleukin-1alpha - antagonists & inhibitors Interleukin-1alpha - physiology Interleukin-1beta - metabolism Interleukin-1beta - physiology Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic NLR Family, Pyrin Domain-Containing 3 Protein Respiratory Hypersensitivity - immunology Respiratory Hypersensitivity - metabolism Respiratory Hypersensitivity - pathology Respiratory Mucosa - immunology Respiratory Mucosa - metabolism Respiratory Mucosa - pathology Serum Amyloid A Protein - physiology Signal Transduction - genetics Signal Transduction - immunology Spleen - immunology Spleen - metabolism Spleen - pathology Th17 Cells - immunology Th17 Cells - metabolism Th17 Cells - pathology Toll-Like Receptor 2 - deficiency Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - physiology |
Title | Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice |
URI | https://www.ncbi.nlm.nih.gov/pubmed/21622869 https://www.proquest.com/docview/873314680 https://www.proquest.com/docview/904471546 https://pubmed.ncbi.nlm.nih.gov/PMC3119761 |
Volume | 187 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
journalDatabaseRights | – providerCode: PRVAFT databaseName: Open Access Digital Library customDbUrl: eissn: 1550-6606 dateEnd: 99991231 omitProxy: true ssIdentifier: ssj0006024 issn: 0022-1767 databaseCode: KQ8 dateStart: 19980101 isFulltext: true titleUrlDefault: http://grweb.coalliance.org/oadl/oadl.html providerName: Colorado Alliance of Research Libraries – providerCode: PRVBFR databaseName: Free Medical Journals customDbUrl: eissn: 1550-6606 dateEnd: 20241001 omitProxy: true ssIdentifier: ssj0006024 issn: 0022-1767 databaseCode: DIK dateStart: 19980101 isFulltext: true titleUrlDefault: http://www.freemedicaljournals.com providerName: Flying Publisher – providerCode: PRVFQY databaseName: GFMER Free Medical Journals customDbUrl: eissn: 1550-6606 dateEnd: 20241001 omitProxy: true ssIdentifier: ssj0006024 issn: 0022-1767 databaseCode: GX1 dateStart: 19160101 isFulltext: true titleUrlDefault: http://www.gfmer.ch/Medical_journals/Free_medical.php providerName: Geneva Foundation for Medical Education and Research |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLbKEIgXBOPWcZEfAAlNYUns2MljNW1M0A6EWqniJYodR61Y010yofHrOSd2krZD4_ISVakbp_4-H_scnwshrzFJt2JKeUmktceziHkJNyGmEGUB1wwWXQwUHh2Lown_OI2mvd6P1eiSSr3XP38bV_I_qMI9wBWjZP8B2fahcAM-A75wBYTh-lcYw0RH-_oClO55DlN8oOtiZZi1AV0Xh1-_MBAABYC-yC6WizY0AOCBNuNZIHcHGAoI0g9wqmaLDM0fI-cO1-xZu-gxm2ACI0ps5qY39fmYv2pNqBwHGq-Z3da4vP_9xNgK7Z9APy_b5aBLZOCg7hZGZ09Hj4_zq9I9Ku9srrIxUXQhA4G0dTc6sSuv8csKUZvW3C3HttDJpqDnoNigoHd_GYMZ_Mj3u0WtOcg__pweTobDdHwwHb89PfOw3Bgey7vaK7fI7VAKgaUvPkw73yDhh7xJM4_vbc-3sdO9zS7X9zPXlJRNX9uVzcv4Abnv0KMDS6GHpGfKbXLH1iG92iZ3R87D4hH5VnOKOk7RAW05RQFaWnOKrnKKAqdowymKnKINp6jlFJ2XFDn1mEwOD8b7R56rv-FpHgUVTFquWC6NLzLuq8SoIucgwZViSZz5wAdVCJnlfpLphOUKVIvCgAKsihjXWR2wJ2SrXJbmGaE6TqJIAoeCgvE81jHHVIPSRIwXOleyT_aaUUy1S06PNVJOUlBScdzTZtxTN-598q79xalNzHJDW9oAk4L0xCOxrDTLy4s0xpKlXMQ3NEl8Dhu4iIs-eWqhbPsLAxGGsUj6RK6B3DbA3O3r35TzWZ3DneHxvQh2_tztc3Kvm1MvyFZ1fmlewka4Uq9q0v4CE8q2gQ |
linkProvider | Geneva Foundation for Medical Education and Research |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Serum+Amyloid+A+Activates+the+NLRP3+Inflammasome+and+Promotes+Th17+Allergic+Asthma+in+Mice&rft.jtitle=The+Journal+of+immunology+%281950%29&rft.au=Ather%2C+Jennifer+L&rft.au=Ckless%2C+Karina&rft.au=Martin%2C+Rebecca&rft.au=Foley%2C+Kathryn+L&rft.date=2011-07-01&rft.issn=0022-1767&rft.volume=187&rft.issue=1&rft.spage=64&rft.epage=73&rft_id=info:doi/10.4049%2Fjimmunol.1100500&rft.externalDBID=NO_FULL_TEXT |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0022-1767&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0022-1767&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0022-1767&client=summon |