CXCL16/CXCR6 Axis Drives Microglia/Macrophages Phenotype in Physiological Conditions and Plays a Crucial Role in Glioma
Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-...
Saved in:
| Published in | Frontiers in immunology Vol. 9; p. 2750 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Media S.A
27.11.2018
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1664-3224 1664-3224 |
| DOI | 10.3389/fimmu.2018.02750 |
Cover
| Abstract | Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-inflammatory microglia dampen immune response and promote a brain microenvironment that foster tumor growth and invasion. The chemokine CXCL16 is expressed in the brain, where it is neuroprotective against brain ischemia, and it has been found to be over-expressed in glioblastoma (GBM). Considering that CXCL16 specific receptor CXCR6 is diffusely expressed in the brain including in microglia cells, we wanted to investigate the role of CXCL16 in the modulation of microglia cell activity and phenotype, and in the progression of glioma. Here we report that CXCL16 drives microglia polarization toward an anti-inflammatory phenotype, also restraining microglia polarization toward an inflammatory phenotype upon LPS and IFNγ stimulation. In the context of glioma, we demonstrate that CXCL16 released by tumor cells is determinant in promoting glioma associated microglia/macrophages (GAMs) modulation toward an anti-inflammatory/pro-tumor phenotype, and that
mice, orthotopically implanted into the brain with GL261 glioma cells,survive longer compared to wild-type mice. We also describe that CXCL16/CXCR6 signaling acts directly on mouse glioma cells, as well as human primary GBM cells, promoting tumor cell growth, migration and invasion. All together these data suggest that CXCL16 signaling could represent a good target to modulate microglia phenotype in order to restrain inflammation or to limit glioma progression. |
|---|---|
| AbstractList | Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-inflammatory microglia dampen immune response and promote a brain microenvironment that foster tumor growth and invasion. The chemokine CXCL16 is expressed in the brain, where it is neuroprotective against brain ischemia, and it has been found to be over-expressed in glioblastoma (GBM). Considering that CXCL16 specific receptor CXCR6 is diffusely expressed in the brain including in microglia cells, we wanted to investigate the role of CXCL16 in the modulation of microglia cell activity and phenotype, and in the progression of glioma. Here we report that CXCL16 drives microglia polarization toward an anti-inflammatory phenotype, also restraining microglia polarization toward an inflammatory phenotype upon LPS and IFNγ stimulation. In the context of glioma, we demonstrate that CXCL16 released by tumor cells is determinant in promoting glioma associated microglia/macrophages (GAMs) modulation toward an anti-inflammatory/pro-tumor phenotype, and that
mice, orthotopically implanted into the brain with GL261 glioma cells,survive longer compared to wild-type mice. We also describe that CXCL16/CXCR6 signaling acts directly on mouse glioma cells, as well as human primary GBM cells, promoting tumor cell growth, migration and invasion. All together these data suggest that CXCL16 signaling could represent a good target to modulate microglia phenotype in order to restrain inflammation or to limit glioma progression. Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-inflammatory microglia dampen immune response and promote a brain microenvironment that foster tumor growth and invasion. The chemokine CXCL16 is expressed in the brain, where it is neuroprotective against brain ischemia, and it has been found to be over-expressed in glioblastoma (GBM). Considering that CXCL16 specific receptor CXCR6 is diffusely expressed in the brain including in microglia cells, we wanted to investigate the role of CXCL16 in the modulation of microglia cell activity and phenotype, and in the progression of glioma. Here we report that CXCL16 drives microglia polarization toward an anti-inflammatory phenotype, also restraining microglia polarization toward an inflammatory phenotype upon LPS and IFNγ stimulation. In the context of glioma, we demonstrate that CXCL16 released by tumor cells is determinant in promoting glioma associated microglia/macrophages (GAMs) modulation toward an anti-inflammatory/pro-tumor phenotype, and that cxcr6ko mice, orthotopically implanted into the brain with GL261 glioma cells,survive longer compared to wild-type mice. We also describe that CXCL16/CXCR6 signaling acts directly on mouse glioma cells, as well as human primary GBM cells, promoting tumor cell growth, migration and invasion. All together these data suggest that CXCL16 signaling could represent a good target to modulate microglia phenotype in order to restrain inflammation or to limit glioma progression. Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-inflammatory microglia dampen immune response and promote a brain microenvironment that foster tumor growth and invasion. The chemokine CXCL16 is expressed in the brain, where it is neuroprotective against brain ischemia, and it has been found to be over-expressed in glioblastoma (GBM). Considering that CXCL16 specific receptor CXCR6 is diffusely expressed in the brain including in microglia cells, we wanted to investigate the role of CXCL16 in the modulation of microglia cell activity and phenotype, and in the progression of glioma. Here we report that CXCL16 drives microglia polarization toward an anti-inflammatory phenotype, also restraining microglia polarization toward an inflammatory phenotype upon LPS and IFNγ stimulation. In the context of glioma, we demonstrate that CXCL16 released by tumor cells is determinant in promoting glioma associated microglia/macrophages (GAMs) modulation toward an anti-inflammatory/pro-tumor phenotype, and that cxcr6ko mice, orthotopically implanted into the brain with GL261 glioma cells,survive longer compared to wild-type mice. We also describe that CXCL16/CXCR6 signaling acts directly on mouse glioma cells, as well as human primary GBM cells, promoting tumor cell growth, migration and invasion. All together these data suggest that CXCL16 signaling could represent a good target to modulate microglia phenotype in order to restrain inflammation or to limit glioma progression. Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-inflammatory microglia dampen immune response and promote a brain microenvironment that foster tumor growth and invasion. The chemokine CXCL16 is expressed in the brain, where it is neuroprotective against brain ischemia, and it has been found to be over-expressed in glioblastoma (GBM). Considering that CXCL16 specific receptor CXCR6 is diffusely expressed in the brain including in microglia cells, we wanted to investigate the role of CXCL16 in the modulation of microglia cell activity and phenotype, and in the progression of glioma. Here we report that CXCL16 drives microglia polarization toward an anti-inflammatory phenotype, also restraining microglia polarization toward an inflammatory phenotype upon LPS and IFNγ stimulation. In the context of glioma, we demonstrate that CXCL16 released by tumor cells is determinant in promoting glioma associated microglia/macrophages (GAMs) modulation toward an anti-inflammatory/pro-tumor phenotype, and that cxcr6ko mice, orthotopically implanted into the brain with GL261 glioma cells,survive longer compared to wild-type mice. We also describe that CXCL16/CXCR6 signaling acts directly on mouse glioma cells, as well as human primary GBM cells, promoting tumor cell growth, migration and invasion. All together these data suggest that CXCL16 signaling could represent a good target to modulate microglia phenotype in order to restrain inflammation or to limit glioma progression.Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or detrimental for brain homeostasis. Anti-inflammatory microglia release soluble factors that might promote brain repair; however, in glioma, anti-inflammatory microglia dampen immune response and promote a brain microenvironment that foster tumor growth and invasion. The chemokine CXCL16 is expressed in the brain, where it is neuroprotective against brain ischemia, and it has been found to be over-expressed in glioblastoma (GBM). Considering that CXCL16 specific receptor CXCR6 is diffusely expressed in the brain including in microglia cells, we wanted to investigate the role of CXCL16 in the modulation of microglia cell activity and phenotype, and in the progression of glioma. Here we report that CXCL16 drives microglia polarization toward an anti-inflammatory phenotype, also restraining microglia polarization toward an inflammatory phenotype upon LPS and IFNγ stimulation. In the context of glioma, we demonstrate that CXCL16 released by tumor cells is determinant in promoting glioma associated microglia/macrophages (GAMs) modulation toward an anti-inflammatory/pro-tumor phenotype, and that cxcr6ko mice, orthotopically implanted into the brain with GL261 glioma cells,survive longer compared to wild-type mice. We also describe that CXCL16/CXCR6 signaling acts directly on mouse glioma cells, as well as human primary GBM cells, promoting tumor cell growth, migration and invasion. All together these data suggest that CXCL16 signaling could represent a good target to modulate microglia phenotype in order to restrain inflammation or to limit glioma progression. |
| Author | Lepore, Francesca D'Alessandro, Giuseppina Santoro, Antonio Limatola, Cristina Esposito, Vincenzo Antonangeli, Fabrizio Trettel, Flavia |
| AuthorAffiliation | 4 Department of Neurology and Psychiatry, Sapienza University , Rome , Italy 3 Department of Molecular Medicine, Sapienza University, Laboratory affiliated to Istituto Pasteur Italia–Fondazione Cenci Bolognetti Rome , Italy 2 IRCCS Neuromed , Pozzilli , Italy 5 Department of Physiology and Pharmacology, Sapienza University, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti Rome , Italy 1 Department of Physiology and Pharmacology, Sapienza University , Rome , Italy |
| AuthorAffiliation_xml | – name: 4 Department of Neurology and Psychiatry, Sapienza University , Rome , Italy – name: 1 Department of Physiology and Pharmacology, Sapienza University , Rome , Italy – name: 2 IRCCS Neuromed , Pozzilli , Italy – name: 3 Department of Molecular Medicine, Sapienza University, Laboratory affiliated to Istituto Pasteur Italia–Fondazione Cenci Bolognetti Rome , Italy – name: 5 Department of Physiology and Pharmacology, Sapienza University, Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti Rome , Italy |
| Author_xml | – sequence: 1 givenname: Francesca surname: Lepore fullname: Lepore, Francesca – sequence: 2 givenname: Giuseppina surname: D'Alessandro fullname: D'Alessandro, Giuseppina – sequence: 3 givenname: Fabrizio surname: Antonangeli fullname: Antonangeli, Fabrizio – sequence: 4 givenname: Antonio surname: Santoro fullname: Santoro, Antonio – sequence: 5 givenname: Vincenzo surname: Esposito fullname: Esposito, Vincenzo – sequence: 6 givenname: Cristina surname: Limatola fullname: Limatola, Cristina – sequence: 7 givenname: Flavia surname: Trettel fullname: Trettel, Flavia |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30542347$$D View this record in MEDLINE/PubMed |
| BookMark | eNp1Uk1v1DAQjVARLaV3TihHLrvrr9jJBakKtFTaiqoCiZs160yyrhx7iZPC_vt6d0vVIuHLjGfeezPSvLfZkQ8es-w9JXPOy2rR2r6f5ozQck6YKsir7IRKKWacMXH0LD_OzmK8I-mJinNevMmOOSkE40KdZL_rn_WSykUKtzI__2Nj_nmw9xjza2uG0DkLi2tI2WYNXarerNGHcbvB3Pr02UYbXOisAZfXwTd2tMHHHHyT3zjYpiyvh8nY1L4Nbk-6dDb08C573YKLePYYT7MfF1--119ny2-XV_X5cmaEZGPan0pgqmGsXAESLsAoJQEEU2xVUigKrKipKgWtAdkaQ7DCFRLJK9JyUfLT7Oqg2wS405vB9jBsdQCr94UwdBqG0RqHWhlFKlEwCS0KiW2FwijalJIWkkmKSevTQWszrXpsDPpxAPdC9GXH27Xuwr2WTClV8CTw8VFgCL8mjKPubTToHHgMU9SMFkVFZMlYgn54PutpyN_LJQA5ANJtYhywfYJQonf-0Ht_6J0_9N4fiSL_oRg7wu5iaVvr_k98ANm1wFU |
| CitedBy_id | crossref_primary_10_1016_j_compbiomed_2024_109197 crossref_primary_10_3390_cancers13122983 crossref_primary_10_3390_ijms22116126 crossref_primary_10_3389_fimmu_2021_628966 crossref_primary_10_3389_fimmu_2023_1128244 crossref_primary_10_1002_cam4_4248 crossref_primary_10_3389_fgene_2022_787141 crossref_primary_10_1038_s41598_024_78751_2 crossref_primary_10_1080_21655979_2021_2008638 crossref_primary_10_1016_j_neuroscience_2019_07_035 crossref_primary_10_1038_s41419_023_05555_z crossref_primary_10_3390_pharmaceutics14061189 crossref_primary_10_1016_j_canlet_2024_217185 crossref_primary_10_3390_cancers14051319 crossref_primary_10_1016_j_critrevonc_2025_104649 crossref_primary_10_1007_s00221_024_06875_y crossref_primary_10_1017_erm_2021_7 crossref_primary_10_1136_svn_2018_000196 crossref_primary_10_32604_or_2023_027972 crossref_primary_10_1038_s41467_024_49908_4 crossref_primary_10_1186_s12974_023_02695_z crossref_primary_10_3389_fonc_2023_1236268 crossref_primary_10_1126_sciadv_aaz4125 crossref_primary_10_1631_jzus_B2400192 crossref_primary_10_1128_mSystems_00189_20 crossref_primary_10_1128_iai_00309_24 crossref_primary_10_1186_s12974_024_03248_8 crossref_primary_10_3390_brainsci10120987 crossref_primary_10_3390_cancers13174255 crossref_primary_10_3390_cells10082066 crossref_primary_10_1016_j_brainresbull_2020_09_010 crossref_primary_10_3390_cancers16020308 crossref_primary_10_1186_s12974_020_01744_1 crossref_primary_10_1177_1721727X221133708 crossref_primary_10_3390_brainsci11040466 crossref_primary_10_3389_fncel_2019_00553 crossref_primary_10_3390_brainsci13081152 crossref_primary_10_1124_pharmrev_120_000025 crossref_primary_10_3390_cancers16203459 crossref_primary_10_2174_0115680096265849231031101449 crossref_primary_10_1093_brain_awac222 crossref_primary_10_1186_s40246_021_00314_7 crossref_primary_10_3389_fphar_2021_748993 crossref_primary_10_2147_JIR_S461795 crossref_primary_10_3390_ijms22073490 crossref_primary_10_1016_j_pneurobio_2020_101970 crossref_primary_10_1038_s12276_021_00660_5 crossref_primary_10_1016_j_critrevonc_2022_103641 crossref_primary_10_3390_pharmaceutics13040520 crossref_primary_10_1186_s12920_024_01991_8 crossref_primary_10_3390_cancers13010019 crossref_primary_10_3390_ijms22115775 crossref_primary_10_3389_fimmu_2019_00379 crossref_primary_10_18632_aging_203103 crossref_primary_10_3389_fneur_2022_921705 crossref_primary_10_1093_neuonc_noab023 crossref_primary_10_1002_art_42297 crossref_primary_10_3389_fonc_2020_584766 crossref_primary_10_3390_cancers11030279 crossref_primary_10_3389_fimmu_2023_1331287 crossref_primary_10_3390_ijms21103704 crossref_primary_10_1158_2326_6066_CIR_24_0084 crossref_primary_10_1111_cns_13944 crossref_primary_10_1007_s12031_024_02295_3 crossref_primary_10_3389_fonc_2023_1109037 crossref_primary_10_1007_s13258_021_01172_2 crossref_primary_10_1016_j_heliyon_2024_e41601 crossref_primary_10_1016_j_ygeno_2021_07_001 crossref_primary_10_3389_fneur_2021_620948 crossref_primary_10_1186_s13073_022_01111_0 crossref_primary_10_3390_ijms23052509 crossref_primary_10_1093_noajnl_vdac157 crossref_primary_10_1002_glia_24490 crossref_primary_10_1111_imm_13264 crossref_primary_10_3389_fimmu_2022_974996 |
| Cites_doi | 10.1186/s12964-016-0149-7 10.3389/fncel.2014.00154. 10.1016/j.yexcr.2011.10.012 10.1038/onc.2016.55 10.1038/nn1997 10.1093/neuonc/nos116 10.1016/j.bbcan.2014.03.002 10.3389/fncel.2014.00144 10.1038/nrneurol.2014.207 10.1158/0008-5472.CAN-05-0470 10.1006/frne.2001.0214 10.1038/nrn2255 10.1038/srep34633 10.1098/rsob.130181 10.18632/oncotarget.1426 10.1038/ncomms7623 10.3389/fnmol.2017.00261 10.1097/00019052-200102000-00014 10.7554/eLife.33415. 10.1093/neuonc/nop013 10.1016/j.pneurobio.2007.11.003 10.1016/j.pneurobio.2013.02.001 10.3390/ph6121475 10.1038/nprot.2008.73 10.1016/j.pneurobio.2016.01.005 10.1016/j.jneuroim.2013.04.006 10.1152/physrev.00011.2010 10.3389/fncel.2014.00193 10.1038/labinvest.2017.19 10.1111/j.1471-4159.2005.03123.x 10.1523/JNEUROSCI.4046-11.2012. 10.1038/npp.2010.26 10.1002/glia.22510 10.1016/j.jneuroim.2010.05.019 10.1523/JNEUROSCI.3588-08.2008 10.1016/j.cytogfr.2009.11.007 10.1038/sj.onc.1207616 10.1038/nrc1256 10.3389/fncel.2015.00132 10.1152/ajpcell.00344.2009 10.1002/glia.22714 10.1038/cddis.2016.73 10.4049/jimmunol.165.6.3284 10.1371/journal.pone.0023902 10.1371/journal.pone.0073426 |
| ContentType | Journal Article |
| Copyright | Copyright © 2018 Lepore, D'Alessandro, Antonangeli, Santoro, Esposito, Limatola and Trettel. 2018 Lepore, D'Alessandro, Antonangeli, Santoro, Esposito, Limatola and Trettel |
| Copyright_xml | – notice: Copyright © 2018 Lepore, D'Alessandro, Antonangeli, Santoro, Esposito, Limatola and Trettel. 2018 Lepore, D'Alessandro, Antonangeli, Santoro, Esposito, Limatola and Trettel |
| DBID | AAYXX CITATION NPM 7X8 5PM DOA |
| DOI | 10.3389/fimmu.2018.02750 |
| DatabaseName | CrossRef PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef PubMed MEDLINE - Academic |
| DatabaseTitleList | PubMed MEDLINE - Academic |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Open Access Full Text url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 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 |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| EISSN | 1664-3224 |
| ExternalDocumentID | oai_doaj_org_article_7c7094526afe46ef9e4c71d86156261e PMC6277753 30542347 10_3389_fimmu_2018_02750 |
| Genre | Journal Article |
| GroupedDBID | 53G 5VS 9T4 AAFWJ AAKDD AAYXX ACGFO ACGFS ACXDI ADBBV ADRAZ AENEX AFPKN ALMA_UNASSIGNED_HOLDINGS AOIJS BAWUL BCNDV CITATION DIK EBS EMOBN GROUPED_DOAJ GX1 HYE KQ8 M48 M~E OK1 PGMZT RNS RPM IPNFZ NPM RIG 7X8 5PM |
| ID | FETCH-LOGICAL-c462t-3216a27d228bae034ac776aa4272b81a55e91c997afca6fcc0e9ebe06390f3483 |
| IEDL.DBID | M48 |
| ISSN | 1664-3224 |
| IngestDate | Wed Aug 27 01:32:21 EDT 2025 Thu Aug 21 18:31:07 EDT 2025 Fri Sep 05 06:46:54 EDT 2025 Thu Apr 03 06:57:19 EDT 2025 Thu Apr 24 23:01:07 EDT 2025 Tue Jul 01 01:35:38 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Keywords | glioma CXCR6 tumor microenvironment neuroinflammation microglia CXCL16 |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c462t-3216a27d228bae034ac776aa4272b81a55e91c997afca6fcc0e9ebe06390f3483 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This article was submitted to Cytokines and Soluble Mediators in Immunity, a section of the journal Frontiers in Immunology Reviewed by: Paola Bezzi, Université de Lausanne, Switzerland; Peter A. Ward, University of Michigan, United States These authors have contributed equally to this work Edited by: Brian A. Zabel, Palo Alto Veterans Institute for Research, United States |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.3389/fimmu.2018.02750 |
| PMID | 30542347 |
| PQID | 2155906822 |
| PQPubID | 23479 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_7c7094526afe46ef9e4c71d86156261e pubmedcentral_primary_oai_pubmedcentral_nih_gov_6277753 proquest_miscellaneous_2155906822 pubmed_primary_30542347 crossref_primary_10_3389_fimmu_2018_02750 crossref_citationtrail_10_3389_fimmu_2018_02750 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2018-11-27 |
| PublicationDateYYYYMMDD | 2018-11-27 |
| PublicationDate_xml | – month: 11 year: 2018 text: 2018-11-27 day: 27 |
| PublicationDecade | 2010 |
| PublicationPlace | Switzerland |
| PublicationPlace_xml | – name: Switzerland |
| PublicationTitle | Frontiers in immunology |
| PublicationTitleAlternate | Front Immunol |
| PublicationYear | 2018 |
| Publisher | Frontiers Media S.A |
| Publisher_xml | – name: Frontiers Media S.A |
| References | Gabrusiewicz (B32) 2011; 6 Hu (B37) 2015; 11 Li (B5) 2008; 84 Grimaldi (B29) 2016; 7 Rosito (B12) 2014; 8 Hattermann (B21) 2013; 260 Ludwig (B40) 2005; 93 Sarvaiya (B15) 2013; 12 Hattermann (B22) 2016; 14 Cheon (B31) 2017; 10 Di (B13) 2016; 6 Jan (B44) 2010; 12 Ma (B38) 2017; 157 Miller (B9) 2008; 28 Rostène (B4) 2007; 8 Rosito (B11) 2012; 32 Mukaida (B16) 2012; 318 Li (B2) 2012; 14 Garofalo (B43) 2017; 6 Neubrand (B27) 2014; 62 Ulasov (B35) 2014; 1846 Réaux-Le (B6) 2013; 104 Williams (B7) 2014; 8 Ellert-Miklaszewska (B39) 2013; 61 Sciumè (B19) 2010; 224 Wurth (B20) 2014; 8 Lakka (B41) 2004; 23 Trettel (B8) 2015; 9 Bajetto (B3) 2001; 22 Sarkar (B42) 2006; 66 Sheridan (B10) 2013; 3 Unutmaz (B23) 2000; 165 Pollard (B34) 2004; 4 Ellert-Miklaszweska (B45) 2016; 35 Garofalo (B24) 2015; 6 Mantovani (B17) 2010; 21 Gieryng (B18) 2017; 97 Lauro (B26) 2010; 35 Iadecola (B30) 2001; 14 Schmittgen (B28) 2008; 3 Ramirez (B14) 2013; 12 Kettenmann (B33) 2011; 91 Sciaccaluga (B36) 2013; 8 Hanisch (B1) 2007; 10 Sciaccaluga (B25) 2010; 299 |
| References_xml | – volume: 14 start-page: 26 year: 2016 ident: B22 article-title: “Inverse signaling” of the transmembrane chemokine CXCL16 contributes to proliferative and anti-apoptotic effects in cultured human meningioma cells publication-title: Cell Commun Signal. doi: 10.1186/s12964-016-0149-7 – volume: 8 start-page: 154 year: 2014 ident: B7 article-title: Chemokines in the balance: maintenance ofhomeostasis and protection at CNS barriers publication-title: Front Cell Neurosci. doi: 10.3389/fncel.2014.00154. – volume: 318 start-page: 95 year: 2012 ident: B16 article-title: Chemokines in tumor development and progression publication-title: Exp Cell Res doi: 10.1016/j.yexcr.2011.10.012 – volume: 35 start-page: 6366 year: 2016 ident: B45 article-title: Tumour-processed osteopontin and lactadherin drive the protumorigenic reprogramming of microglia and glioma progression publication-title: Oncogene doi: 10.1038/onc.2016.55 – volume: 10 start-page: 1387 year: 2007 ident: B1 article-title: Microglia: active sensor and versatile effector cells in the normal and pathologic brain publication-title: Nat Neurosci. doi: 10.1038/nn1997 – volume: 14 start-page: 958 year: 2012 ident: B2 article-title: The molecular profile of microglia under the influence of glioma publication-title: Neuro Oncol. doi: 10.1093/neuonc/nos116 – volume: 1846 start-page: 113 year: 2014 ident: B35 article-title: The emerging role of MMP14 in brain tumorigenesis and future therapeutics publication-title: Biochim Biophys Acta doi: 10.1016/j.bbcan.2014.03.002 – volume: 8 start-page: 144 year: 2014 ident: B20 article-title: CXCL12 modulation and CXCR7 activity in human glioblatoma stem-like cells and regulation of the tumor microenvironment publication-title: Front Cell Neurosci doi: 10.3389/fncel.2014.00144 – volume: 11 start-page: 56 year: 2015 ident: B37 article-title: Microglial and macrophage polarization-new prospects for brain repair publication-title: Nat Rev Neurol doi: 10.1038/nrneurol.2014.207 – volume: 66 start-page: 11771 year: 2006 ident: B42 article-title: Tenascin-C stimulates glioma cell invasion through matrix metalloproteinase-12 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-05-0470 – volume: 22 start-page: 214 year: 2001 ident: B3 article-title: Chemokines and their receptors in the central nervous system publication-title: Front Neuroendocrinol doi: 10.1006/frne.2001.0214 – volume: 8 start-page: 895 year: 2007 ident: B4 article-title: Chemokines: a new class of neuromodulator? publication-title: Nat Rev Neurosci doi: 10.1038/nrn2255 – volume: 6 start-page: 34633 year: 2016 ident: B13 article-title: The chemokine CXCL16 modulates neurotransmitter release in hippocampal CA1 area publication-title: Sci Rep doi: 10.1038/srep34633 – volume: 3 start-page: 13018 year: 2013 ident: B10 article-title: Neuron-glia crosstalk in health and disease: fractalkine and CX3CR1 take centre stage publication-title: Open Biol doi: 10.1098/rsob.130181 – volume: 12 start-page: 2171 year: 2013 ident: B15 article-title: Chemokines in tumor progression and metastasis publication-title: Oncotarget doi: 10.18632/oncotarget.1426 – volume: 6 start-page: 6623 year: 2015 ident: B24 article-title: Enriched environment reduces glioma growth through immune and non-immune mechanisms in mice publication-title: Nat Commun doi: 10.1038/ncomms7623 – volume: 10 start-page: 261 year: 2017 ident: B31 article-title: Regulation of microglia and macrophage polarization via apoptosis Signal-Regulating Kinase1 silencing after Ischemic/Hypoxic injury publication-title: Front Mol Neurosci. doi: 10.3389/fnmol.2017.00261 – volume: 14 start-page: 89 year: 2001 ident: B30 article-title: Cerebral ischemia and inflammation publication-title: Curr Opin Neurol doi: 10.1097/00019052-200102000-00014 – volume: 6 start-page: e33415 year: 2017 ident: B43 article-title: Environmental stimuli shape microglial plasticity in glioma publication-title: Elife doi: 10.7554/eLife.33415. – volume: 12 start-page: 58 year: 2010 ident: B44 article-title: Osteopontin regulates human glioma cell invasiveness and tumor growth in mice publication-title: Neuro Oncol doi: 10.1093/neuonc/nop013 – volume: 84 start-page: 116 year: 2008 ident: B5 article-title: Multiple roles of chemokine CXCL12 in the central nervous system: a migration from immunology to neurobiology publication-title: Prog Neurobiol doi: 10.1016/j.pneurobio.2007.11.003 – volume: 104 start-page: 67 year: 2013 ident: B6 article-title: Current status of chemokines in the adult CNS publication-title: Prog Neurobiol doi: 10.1016/j.pneurobio.2013.02.001 – volume: 12 start-page: 1475 year: 2013 ident: B14 article-title: Glioblastoma multiforme therapy and mechanismis of resistance publication-title: Pharmaceuticals doi: 10.3390/ph6121475 – volume: 3 start-page: 1101 year: 2008 ident: B28 article-title: Analyzing real-time PCR data by the comparative C(T) method publication-title: Nat Protoc doi: 10.1038/nprot.2008.73 – volume: 157 start-page: 247 year: 2017 ident: B38 article-title: The biphasic function of microglia in ischemic stroke publication-title: Prog Neurobiol doi: 10.1016/j.pneurobio.2016.01.005 – volume: 260 start-page: 47 year: 2013 ident: B21 article-title: The CXCL16-CXCR6 chemokine axis in glial tumors publication-title: J Neuroimmunol doi: 10.1016/j.jneuroim.2013.04.006 – volume: 91 start-page: 461 year: 2011 ident: B33 article-title: Physiology of microglia publication-title: Physiol Rev doi: 10.1152/physrev.00011.2010 – volume: 8 start-page: 193 year: 2014 ident: B12 article-title: Transmembrane chemokines CX3CL1 and CXCL16 drive interplay between neurons, microglia and astrocytes to counteract pMCAO and excitotoxic neuronal death publication-title: Front Cell Neurosci doi: 10.3389/fncel.2014.00193 – volume: 97 start-page: 498 year: 2017 ident: B18 article-title: Immune microenvironment of gliomas publication-title: Lab Invest doi: 10.1038/labinvest.2017.19 – volume: 93 start-page: 1293 year: 2005 ident: B40 article-title: Enhanced expression and shedding of the transmembrane chemokine CXCL16 by reactive astrocytes and glioma cells publication-title: J Neurochem doi: 10.1111/j.1471-4159.2005.03123.x – volume: 32 start-page: 3154 year: 2012 ident: B11 article-title: CXCL16 orchestrates adenosine A3 receptor and MCP1/CCL2 activity to protect neurons from excitotoxic cell death in the CNS publication-title: J Neurosci doi: 10.1523/JNEUROSCI.4046-11.2012. – volume: 35 start-page: 1550 year: 2010 ident: B26 article-title: Adenosine A1 receptors and microglial cells mediate CX3CL1-induced protection of hippocampal neurons against Glu-induced death publication-title: Neuropsychopharmacology doi: 10.1038/npp.2010.26 – volume: 61 start-page: 1178 year: 2013 ident: B39 article-title: Molecular definition of the pro-tumorigenic phenotype of glioma-activated microglia publication-title: Glia doi: 10.1002/glia.22510 – volume: 224 start-page: 8 year: 2010 ident: B19 article-title: Chemokines and glioma: invasion and more publication-title: J Neuroimmunol doi: 10.1016/j.jneuroim.2010.05.019 – volume: 28 start-page: 11792 year: 2008 ident: B9 article-title: Chemokine action in the nervous system publication-title: J Neurosci. doi: 10.1523/JNEUROSCI.3588-08.2008 – volume: 21 start-page: 27 year: 2010 ident: B17 article-title: The chemokines system in cancer biology and therapy publication-title: Cytokine Growth Factor Rev doi: 10.1016/j.cytogfr.2009.11.007 – volume: 23 start-page: 4681 year: 2004 ident: B41 article-title: Inhibition of cathepsin B and MMP-9 gene expression in glioblastoma cell line via RNA interference reduces tumor cell invasion, tumor growth and angiogenesis publication-title: Oncogene doi: 10.1038/sj.onc.1207616 – volume: 4 start-page: 71 year: 2004 ident: B34 article-title: Tumour-educated macrophages promote tumour progression and metastasis publication-title: Nat Rev Cancer doi: 10.1038/nrc1256 – volume: 9 start-page: 132 year: 2015 ident: B8 article-title: Chemokines and chemokine receptors in brain homeostasis publication-title: Front Cell Neurosci. doi: 10.3389/fncel.2015.00132 – volume: 299 start-page: 175 year: 2010 ident: B25 article-title: CXCL12-induced glioblastoma cell migration requires intermediate conductance CA2+-activated K+ channel activity publication-title: Am J Physiol Cell Physiol doi: 10.1152/ajpcell.00344.2009 – volume: 62 start-page: 1932 year: 2014 ident: B27 article-title: Mesenchymal stem cells induce the ramification of microglia via the small RhoGTPases Cdc42 and Rac1 publication-title: Glia doi: 10.1002/glia.22714 – volume: 7 start-page: e2174 year: 2016 ident: B29 article-title: KCa3 publication-title: Cell Death Dis doi: 10.1038/cddis.2016.73 – volume: 165 start-page: 3284 year: 2000 ident: B23 article-title: The primate lentiviral receptor Bonzo/STRL33 is coordinately regulated with CCR5 and its expression pattern is conserved between human and mouse publication-title: J Immunol doi: 10.4049/jimmunol.165.6.3284 – volume: 6 start-page: e23902 year: 2011 ident: B32 article-title: Characteristics of the alternative phenotype of microglia/macrophages and its modulation in experimental gliomas publication-title: PLoS ONE doi: 10.1371/journal.pone.0023902 – volume: 8 start-page: e73426 year: 2013 ident: B36 article-title: Functional cross talk between CXCR4 and PDGFR on glioblastoma cells is essential for migration publication-title: PLoS ONE doi: 10.1371/journal.pone.0073426 |
| SSID | ssj0000493335 |
| Score | 2.4831774 |
| Snippet | Microglia are patrolling cells that sense changes in the brain microenvironment and respond acquiring distinct phenotypes that can be either beneficial or... |
| SourceID | doaj pubmedcentral proquest pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | 2750 |
| SubjectTerms | CXCL16 CXCR6 glioma Immunology microglia neuroinflammation tumor microenvironment |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBYlEOilNH26L1TopQfXtiRL9jFxmobSLSE0sDch69F18dolu0uaf58Ze3fZLaW99GRjS1joG42-0YxnCHnnU-7K2vHYGeFj4cFgrWUQMZNceMfKLAxVFCZf5fmV-DzNpzulvjAmbEwPPE5coqwCCyRn0gQvpA-lF1ZlroCdGLh45lH7pmW6Y0z9GHkv5zwf_ZJghZVJaObzFYZyFR_QU5fu7UNDuv4_cczfQyV39p6zh-TBmjTS43GwR-Se7x6Rw7GM5O1jclNNqy-ZTOByKenxr2ZBT68xnSydYLjd97YxycRgra4ZaI8FvZj5rsezV9p0dAgB3WhAWvXowkZRpKZz9KI1t3BHK5AAEFR62bdDp09t08_NE3J19vFbdR6vCyrEVki2jDnLpGHKMVbUBlASxioljRFMsbrITJ77MrNlqUywRgZrU18CyMhi0sBFwZ-Sg67v_HNCg0NjMbc-57XwuSuMs6GQwvlCGUAmIslmerVdZxvHohetBqsDAdEDIBoB0QMgEXm_7fFzzLTxl7YniNi2HebIHh6A5Oi15Oh_SU5E3m7w1rCm0FFiOt-vFpqhrzaVwJ0i8mzEf_sp0I_AQIWKiNqTjL2x7L_pmtmQt1sypcA6fPE_Bv-S3MfpwL8imXpFDpbXK_8a6NGyfjOshDtLUQ45 priority: 102 providerName: Directory of Open Access Journals |
| Title | CXCL16/CXCR6 Axis Drives Microglia/Macrophages Phenotype in Physiological Conditions and Plays a Crucial Role in Glioma |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/30542347 https://www.proquest.com/docview/2155906822 https://pubmed.ncbi.nlm.nih.gov/PMC6277753 https://doaj.org/article/7c7094526afe46ef9e4c71d86156261e |
| Volume | 9 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Lb9QwELZQERIXxJvwqIzEhUO6G8exkwNCJdBWiEVVxUp7ixw_uqmySbsP0f33zDjZhUUrxCWJEjtOPGP7-zKTGULe2WFsstLEoVHchtwCYS2F4yETMbeGZZHzWRRG38XZmH-dJJPfv0f3HbjYS-0wn9R4Xh_d3qw_woD_gIwT1tuBq2azFXpppUdohAMCf9dbi9CRrwf7Vx0WjmOfcTMSgoegybyzW-69yc465cP578Ogf7tS_rE2nTwkD3pQSY87LXhE7tjmMbnXpZlcPyE_80n-LRID2F0IenxbLejnOYabpSN0x7usKzUYKczlNYXZZUHPp7Zp8dssrRrqXUQ3MyTNWzRxo6pS1Rh6Xqs1HNEcNAQUmV60ta90WlftTD0l45MvP_KzsE-4EGou2BK6JBKKScNYWiqQIldaSqEUZ5KVaaSSxGaRzjKpnFbCaT20GSgBopyhi3kaPyMHTdvYF4Q6g2Qy0TaJS24TkyqjXSq4salUgLkCMth0b6H7aOSYFKMugJWgQAovkAIFUniBBOT9tsZ1F4njH2U_ocS25TCGtj_Rzi-LfkgWUkvgtgkTylkurMss1zIyKWA8YHmRDcjbjbwLGHNoSFGNbVeLgqEtdygAWwXkeSf_bVMwfwJC5TIgckczdp5l90pTTX1cb8GkBPb48j_afUXu49viT5FMviYHy_nKvgF0tCwP_VcF2J5OokM_AH4B9HcPqQ |
| linkProvider | Scholars Portal |
| 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=CXCL16%2FCXCR6+Axis+Drives+Microglia%2FMacrophages+Phenotype+in+Physiological+Conditions+and+Plays+a+Crucial+Role+in+Glioma&rft.jtitle=Frontiers+in+immunology&rft.au=Lepore%2C+Francesca&rft.au=D%27Alessandro%2C+Giuseppina&rft.au=Antonangeli%2C+Fabrizio&rft.au=Santoro%2C+Antonio&rft.date=2018-11-27&rft.issn=1664-3224&rft.eissn=1664-3224&rft.volume=9&rft.spage=2750&rft_id=info:doi/10.3389%2Ffimmu.2018.02750&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1664-3224&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1664-3224&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1664-3224&client=summon |