Human Eosinophils Express a Distinct Gene Expression Program in Response to IL-3 Compared with Common β-Chain Cytokines IL-5 and GM-CSF

Despite recent advances in asthma management with anti–IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a common β subunit receptor with both IL-5 and GM-CSF but, through α-subunit–specific properties, uniquely influences eosinophil biology and may s...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 203; no. 2; pp. 329 - 337
Main Authors Nelson, Ryan K, Brickner, Howard, Panwar, Bharat, Ramírez-Suástegui, Ciro, Herrera-de la Mata, Sara, Liu, Neiman, Diaz, Damaris, Alexander, Laura E Crotty, Ay, Ferhat, Vijayanand, Pandurangan, Seumois, Grégory, Akuthota, Praveen
Format Journal Article
LanguageEnglish
Published United States 15.07.2019
Subjects
Online AccessGet full text
ISSN0022-1767
1550-6606
1550-6606
DOI10.4049/jimmunol.1801668

Cover

Abstract Despite recent advances in asthma management with anti–IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a common β subunit receptor with both IL-5 and GM-CSF but, through α-subunit–specific properties, uniquely influences eosinophil biology and may serve as a potential therapeutic target. We aimed to globally characterize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinophils and identify differences in gene expression using advanced statistical modeling. Human eosinophils were isolated from the peripheral blood of healthy volunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h. RNA was then extracted and bulk sequencing performed. DESeq analysis identified differentially expressed genes and weighted gene coexpression network analysis independently defined modules of genes that are highly coexpressed. GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downregulated 553 genes, producing a proinflammatory and survival phenotype that was predominantly mediated through TWEAK signaling. IL-3 stimulation yielded the most numbers of differentially expressed genes that were also highly coexpressed (n = 119). These genes were enriched in pathways involving JAK/STAT signaling. GM-CSF and IL-5 stimulation demonstrated redundancy in eosinophil gene expression. In conclusion, IL-3 produces a distinct eosinophil gene expression program among the β-chain receptor cytokines. IL-3–upregulated genes may provide a foundation for research into therapeutics for patients with eosinophilic asthma who do not respond to anti–IL-5 therapies.
AbstractList Despite recent advances in asthma management with anti–IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a common β subunit receptor with both IL-5 and GM-CSF but, through α-subunit–specific properties, uniquely influences eosinophil biology and may serve as a potential therapeutic target. We aimed to globally characterize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinophils and identify differences in gene expression using advanced statistical modeling. Human eosinophils were isolated from the peripheral blood of healthy volunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h. RNA was then extracted and bulk sequencing performed. DESeq analysis identified differentially expressed genes and weighted gene coexpression network analysis independently defined modules of genes that are highly coexpressed. GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downregulated 553 genes, producing a proinflammatory and survival phenotype that was predominantly mediated through TWEAK signaling. IL-3 stimulation yielded the most numbers of differentially expressed genes that were also highly coexpressed (n = 119). These genes were enriched in pathways involving JAK/STAT signaling. GM-CSF and IL-5 stimulation demonstrated redundancy in eosinophil gene expression. In conclusion, IL-3 produces a distinct eosinophil gene expression program among the β-chain receptor cytokines. IL-3–upregulated genes may provide a foundation for research into therapeutics for patients with eosinophilic asthma who do not respond to anti–IL-5 therapies.
Despite recent advances in asthma management with anti-IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a common β subunit receptor with both IL-5 and GM-CSF but, through α-subunit-specific properties, uniquely influences eosinophil biology and may serve as a potential therapeutic target. We aimed to globally characterize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinophils and identify differences in gene expression using advanced statistical modeling. Human eosinophils were isolated from the peripheral blood of healthy volunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h. RNA was then extracted and bulk sequencing performed. DESeq analysis identified differentially expressed genes and weighted gene coexpression network analysis independently defined modules of genes that are highly coexpressed. GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downregulated 553 genes, producing a proinflammatory and survival phenotype that was predominantly mediated through TWEAK signaling. IL-3 stimulation yielded the most numbers of differentially expressed genes that were also highly coexpressed (n = 119). These genes were enriched in pathways involving JAK/STAT signaling. GM-CSF and IL-5 stimulation demonstrated redundancy in eosinophil gene expression. In conclusion, IL-3 produces a distinct eosinophil gene expression program among the β-chain receptor cytokines. IL-3-upregulated genes may provide a foundation for research into therapeutics for patients with eosinophilic asthma who do not respond to anti-IL-5 therapies.Despite recent advances in asthma management with anti-IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a common β subunit receptor with both IL-5 and GM-CSF but, through α-subunit-specific properties, uniquely influences eosinophil biology and may serve as a potential therapeutic target. We aimed to globally characterize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinophils and identify differences in gene expression using advanced statistical modeling. Human eosinophils were isolated from the peripheral blood of healthy volunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h. RNA was then extracted and bulk sequencing performed. DESeq analysis identified differentially expressed genes and weighted gene coexpression network analysis independently defined modules of genes that are highly coexpressed. GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downregulated 553 genes, producing a proinflammatory and survival phenotype that was predominantly mediated through TWEAK signaling. IL-3 stimulation yielded the most numbers of differentially expressed genes that were also highly coexpressed (n = 119). These genes were enriched in pathways involving JAK/STAT signaling. GM-CSF and IL-5 stimulation demonstrated redundancy in eosinophil gene expression. In conclusion, IL-3 produces a distinct eosinophil gene expression program among the β-chain receptor cytokines. IL-3-upregulated genes may provide a foundation for research into therapeutics for patients with eosinophilic asthma who do not respond to anti-IL-5 therapies.
Despite recent advances in asthma management with anti-IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a common β subunit receptor with both IL-5 and GM-CSF but, through α-subunit-specific properties, uniquely influences eosinophil biology and may serve as a potential therapeutic target. We aimed to globally characterize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinophils and identify differences in gene expression using advanced statistical modeling. Human eosinophils were isolated from the peripheral blood of healthy volunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h. RNA was then extracted and bulk sequencing performed. DESeq analysis identified differentially expressed genes and weighted gene coexpression network analysis independently defined modules of genes that are highly coexpressed. GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downregulated 553 genes, producing a proinflammatory and survival phenotype that was predominantly mediated through TWEAK signaling. IL-3 stimulation yielded the most numbers of differentially expressed genes that were also highly coexpressed ( = 119). These genes were enriched in pathways involving JAK/STAT signaling. GM-CSF and IL-5 stimulation demonstrated redundancy in eosinophil gene expression. In conclusion, IL-3 produces a distinct eosinophil gene expression program among the β-chain receptor cytokines. IL-3-upregulated genes may provide a foundation for research into therapeutics for patients with eosinophilic asthma who do not respond to anti-IL-5 therapies.
Author Panwar, Bharat
Vijayanand, Pandurangan
Akuthota, Praveen
Nelson, Ryan K
Liu, Neiman
Alexander, Laura E Crotty
Ay, Ferhat
Brickner, Howard
Herrera-de la Mata, Sara
Ramírez-Suástegui, Ciro
Seumois, Grégory
Diaz, Damaris
Author_xml – sequence: 1
  givenname: Ryan K
  surname: Nelson
  fullname: Nelson, Ryan K
– sequence: 2
  givenname: Howard
  orcidid: 0000-0003-0075-7399
  surname: Brickner
  fullname: Brickner, Howard
– sequence: 3
  givenname: Bharat
  surname: Panwar
  fullname: Panwar, Bharat
– sequence: 4
  givenname: Ciro
  orcidid: 0000-0001-8126-710X
  surname: Ramírez-Suástegui
  fullname: Ramírez-Suástegui, Ciro
– sequence: 5
  givenname: Sara
  orcidid: 0000-0002-9519-9520
  surname: Herrera-de la Mata
  fullname: Herrera-de la Mata, Sara
– sequence: 6
  givenname: Neiman
  orcidid: 0000-0002-7266-2404
  surname: Liu
  fullname: Liu, Neiman
– sequence: 7
  givenname: Damaris
  orcidid: 0000-0002-3347-9578
  surname: Diaz
  fullname: Diaz, Damaris
– sequence: 8
  givenname: Laura E Crotty
  orcidid: 0000-0002-5091-2660
  surname: Alexander
  fullname: Alexander, Laura E Crotty
– sequence: 9
  givenname: Ferhat
  orcidid: 0000-0002-0708-6914
  surname: Ay
  fullname: Ay, Ferhat
– sequence: 10
  givenname: Pandurangan
  surname: Vijayanand
  fullname: Vijayanand, Pandurangan
– sequence: 11
  givenname: Grégory
  orcidid: 0000-0002-8164-6852
  surname: Seumois
  fullname: Seumois, Grégory
– sequence: 12
  givenname: Praveen
  surname: Akuthota
  fullname: Akuthota, Praveen
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31175163$$D View this record in MEDLINE/PubMed
BookMark eNp1kcFu1DAQhi1URLctd07IRy4pHie2kyMK222lRUVAz5bjOKxLbAfbUekb8Dw8CM9EVt29VOI0mtH3_Yf5z9CJD94g9AbIZUWq5v29dW72YbyEmgDn9Qu0AsZIwTnhJ2hFCKUFCC5O0VlK94QQTmj1Cp2WAIIBL1fo9_XslMfrkKwP086OCa9_TdGkhBX-aFO2Xme8Md4c7zZ4_DmG71E5bD3-YtIUfDI4B3yzLUrcBjepaHr8YPNuv7lF-PunaHdqwdvHHH5Yb9IeZlj5Hm8-Fe3Xqwv0clBjMq8P8xzdXa2_tdfF9nZz037YFpoKyEVNVM-quoe-p4JUdTNQ3TTV0DViYA0MwlAYyrpmuiKNBmq6Tpd9xwUHoKph5Tl695Q7xfBzNilLZ5M246i8CXOSlLKyroBysaBvD-jcOdPLKVqn4qM8fm8B-BOgY0gpmkFqm1VePpSjsqMEIvc1yWNN8lDTIpJn4jH7v8o_TmeXdg
CitedBy_id crossref_primary_10_1038_s41385_021_00400_y
crossref_primary_10_3390_ijms241713432
crossref_primary_10_1158_2159_8290_CD_22_1396
crossref_primary_10_1016_j_jaci_2024_05_014
crossref_primary_10_1183_13993003_00582_2022
crossref_primary_10_1016_j_jaci_2024_07_012
crossref_primary_10_1126_sciimmunol_aba6087
crossref_primary_10_1016_j_mucimm_2024_03_005
crossref_primary_10_1016_j_jaci_2022_09_030
crossref_primary_10_1016_j_smim_2021_101510
crossref_primary_10_1002_JLB_3A0920_620R
crossref_primary_10_1021_acsomega_2c00518
crossref_primary_10_1093_jleuko_qiae122
crossref_primary_10_1093_jleuko_qiae188
crossref_primary_10_1111_imr_13430
crossref_primary_10_1053_j_gastro_2020_07_035
crossref_primary_10_1186_s12859_020_3366_4
Cites_doi 10.1186/1471-2105-9-559
10.1002/jcb.26525
10.1038/nprot.2014.006
10.1038/nbt.2957
10.5415/apallergy.2012.2.4.256
10.1164/rccm.200208-789OC
10.1126/science.1176077
10.1038/ncomms15395
10.1006/abbi.2000.1866
10.1126/sciimmunol.aaf9154
10.1038/nature12199
10.1038/nature11267
10.4049/jimmunol.180.2.1199
10.1038/srep25533
10.1182/blood.V87.6.2354.bloodjournal8762354
10.4049/jimmunol.180.11.7622
10.1021/acs.jproteome.8b00057
10.1093/bioinformatics/btt703
10.1056/NEJMoa1403290
10.1080/02770903.2016.1196371
10.1038/s41467-018-05676-6
10.1038/nature25486
10.1620/tjem.241.175
10.4049/jimmunol.169.11.6452
10.1038/ni.3225
10.1126/science.1238279
10.1038/ni.2937
10.2202/1544-6115.1128
10.1016/j.clim.2013.11.009
10.1016/j.bbagrm.2010.05.004
10.1513/AnnalsATS.201703-259OC
10.1186/s12864-018-4933-1
10.1007/s10930-006-9035-2
10.1126/science.1059157
10.1016/j.cyto.2007.09.007
10.1155/2012/376470
10.4238/gmr.15028226
10.1007/978-1-4939-1016-8_2
10.1186/s13059-014-0550-8
10.1371/journal.pone.0067560
10.1007/978-1-4939-7896-0_21
10.1093/bioinformatics/btp120
10.1056/NEJMoa1403291
10.1164/rccm.201611-2234OC
10.1172/JCI85664
10.3389/fmed.2017.00093
ContentType Journal Article
Copyright Copyright © 2019 by The American Association of Immunologists, Inc.
Copyright_xml – notice: Copyright © 2019 by The American Association of Immunologists, Inc.
DBID AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
7X8
DOI 10.4049/jimmunol.1801668
DatabaseName CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
MEDLINE - Academic
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
MEDLINE - Academic
DatabaseTitleList CrossRef
MEDLINE - Academic
MEDLINE
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 337
ExternalDocumentID 31175163
10_4049_jimmunol_1801668
Genre Journal Article
Research Support, N.I.H., Extramural
GrantInformation_xml – fundername: NHLBI NIH HHS
  grantid: K08 HL116429
– fundername: NIAID NIH HHS
  grantid: R01 AI121426
– fundername: NIH HHS
  grantid: S10 OD016262
– fundername: NHLBI NIH HHS
  grantid: R01 HL114093
GroupedDBID ---
-~X
.55
0R~
18M
2WC
34G
39C
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
AFHIN
AFRAH
AGORE
AHMMS
AHWXS
AIZAD
ALMA_UNASSIGNED_HOLDINGS
ARBBW
BAWUL
BCRHZ
BTFSW
CITATION
D0L
DIK
DU5
E3Z
EBS
EJD
F5P
GX1
IH2
K-O
KOP
KQ8
L7B
OCZFY
OK1
OWPYF
P0W
P2P
PQQKQ
R.V
RHI
ROX
RZQ
SJN
TR2
TWZ
W8F
WH7
WOQ
X7M
XSW
XTH
YHG
AFOSN
CGR
CUY
CVF
ECM
EIF
FRP
NPM
RHF
YIN
7X8
ID FETCH-LOGICAL-c271t-80ad548d1dd270489f2c994fb97f591f7e21f3885c409c12ebbc3db676112a953
ISSN 0022-1767
1550-6606
IngestDate Sun Sep 28 01:38:56 EDT 2025
Wed Feb 19 02:31:02 EST 2025
Thu Apr 24 22:53:41 EDT 2025
Wed Sep 10 05:00:49 EDT 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Language English
License https://academic.oup.com/pages/standard-publication-reuse-rights
Copyright © 2019 by The American Association of Immunologists, Inc.
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c271t-80ad548d1dd270489f2c994fb97f591f7e21f3885c409c12ebbc3db676112a953
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ORCID 0000-0002-7266-2404
0000-0001-8126-710X
0000-0002-3347-9578
0000-0002-5091-2660
0000-0002-0708-6914
0000-0002-9519-9520
0000-0003-0075-7399
0000-0002-8164-6852
OpenAccessLink https://www.jimmunol.org/content/jimmunol/203/2/329.full.pdf
PMID 31175163
PQID 2253841267
PQPubID 23479
PageCount 9
ParticipantIDs proquest_miscellaneous_2253841267
pubmed_primary_31175163
crossref_citationtrail_10_4049_jimmunol_1801668
crossref_primary_10_4049_jimmunol_1801668
PublicationCentury 2000
PublicationDate 2019-07-15
20190715
PublicationDateYYYYMMDD 2019-07-15
PublicationDate_xml – month: 07
  year: 2019
  text: 2019-07-15
  day: 15
PublicationDecade 2010
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle The Journal of immunology (1950)
PublicationTitleAlternate J Immunol
PublicationYear 2019
References Gao (2025030417540361200_r37) 2016; 15
Bettigole (2025030417540361200_r33) 2015; 16
Bel (2025030417540361200_r2) 2014; 371
Burkly (2025030417540361200_r25) 2007; 40
Zhu (2025030417540361200_r35) 2018; 119
Kelly (2025030417540361200_r5) 2017; 196
Zhang (2025030417540361200_r22) 2005
Roscioli (2025030417540361200_r36) 2017; 54
Wagner (2025030417540361200_r40) 2007; 26
Aldebert (2025030417540361200_r39) 1996; 87
Mesnil (2025030417540361200_r46) 2016; 126
Kikkawa (2025030417540361200_r38) 2012; 2
Esnault (2025030417540361200_r49) 2014; 150
Alon (2025030417540361200_r30) 2012; 488
Love (2025030417540361200_r18) 2014; 15
Ilani (2025030417540361200_r31) 2013; 341
Hayashizaki (2025030417540361200_r44) 2016; 1
Ortega (2025030417540361200_r3) 2014; 371
Parekh (2025030417540361200_r15) 2016; 6
Wong (2025030417540361200_r32) 2018; 554
Sidler (2025030417540361200_r34) 2017; 8
Picelli (2025030417540361200_r14) 2014; 9
Langfelder (2025030417540361200_r20) 2008; 9
Pan (2025030417540361200_r27) 2009; 325
Geijsen (2025030417540361200_r8) 2001; 293
Rosales (2025030417540361200_r13) 2018; 1799
Yu (2025030417540361200_r29) 2018; 9
Akuthota (2025030417540361200_r10) 2014; 1178
Thomsen (2025030417540361200_r41) 2000; 379
Johansson (2025030417540361200_r47) 2008; 180
Gupta (2025030417540361200_r24) 2010; 1799
SEQC/MAQC-III Consortium (2025030417540361200_r21) 2014; 32
Bhattacharjee (2025030417540361200_r26) 2012; 2012
Asquith (2025030417540361200_r7) 2008; 180
Esnault (2025030417540361200_r45) 2018; 17
McBrien (2025030417540361200_r42) 2017; 4
Trapnell (2025030417540361200_r17) 2009; 25
Fu (2025030417540361200_r16) 2018; 19
Flood-Page (2025030417540361200_r4) 2003; 167
Roychoudhuri (2025030417540361200_r28) 2013; 498
Seumois (2025030417540361200_r12) 2014; 15
Liu (2025030417540361200_r9) 2002; 169
Bastian (2025030417540361200_r23) 2009
Sato (2025030417540361200_r43) 2017; 241
Nurmagambetov (2025030417540361200_r1) 2018; 15
Esnault (2025030417540361200_r6) 2016; 36
Krämer (2025030417540361200_r19) 2014; 30
Seumois (2025030417540361200_r11) 2012; 1
Esnault (2025030417540361200_r48) 2013; 8
References_xml – volume: 9
  start-page: 559
  year: 2008
  ident: 2025030417540361200_r20
  article-title: WGCNA: an R package for weighted correlation network analysis
  publication-title: BMC Bioinformatics
  doi: 10.1186/1471-2105-9-559
– volume: 119
  start-page: 3528
  year: 2018
  ident: 2025030417540361200_r35
  article-title: TWEAK/Fn14 interaction induces proliferation and migration in human airway smooth muscle cells via activating the NF-κB pathway
  publication-title: J. Cell. Biochem.
  doi: 10.1002/jcb.26525
– volume: 9
  start-page: 171
  year: 2014
  ident: 2025030417540361200_r14
  article-title: Full-length RNA-seq from single cells using Smart-seq2
  publication-title: Nat. Protoc.
  doi: 10.1038/nprot.2014.006
– volume: 32
  start-page: 903
  year: 2014
  ident: 2025030417540361200_r21
  article-title: A comprehensive assessment of RNA-seq accuracy, reproducibility and information content by the Sequencing Quality Control Consortium
  publication-title: Nat. Biotechnol.
  doi: 10.1038/nbt.2957
– volume: 2
  start-page: 256
  year: 2012
  ident: 2025030417540361200_r38
  article-title: Interferon-alpha inhibits airway eosinophilia and hyperresponsiveness in an animal asthma model [corrected]
  publication-title: Asia Pac. Allergy
  doi: 10.5415/apallergy.2012.2.4.256
– volume: 167
  start-page: 199
  year: 2003
  ident: 2025030417540361200_r4
  article-title: Eosinophil’s role remains uncertain as anti-interleukin-5 only partially depletes numbers in asthmatic airway
  publication-title: Am. J. Respir. Crit. Care Med.
  doi: 10.1164/rccm.200208-789OC
– volume: 325
  start-page: 1142
  year: 2009
  ident: 2025030417540361200_r27
  article-title: Eos mediates Foxp3-dependent gene silencing in CD4+ regulatory T cells
  publication-title: Science
  doi: 10.1126/science.1176077
– volume: 8
  start-page: 15395
  year: 2017
  ident: 2025030417540361200_r34
  article-title: TWEAK mediates inflammation in experimental atopic dermatitis and psoriasis
  publication-title: Nat. Commun.
  doi: 10.1038/ncomms15395
– volume: 379
  start-page: 147
  year: 2000
  ident: 2025030417540361200_r41
  article-title: The status of half-cystine residues and locations of N-glycosylated asparagine residues in human eosinophil peroxidase
  publication-title: Arch. Biochem. Biophys.
  doi: 10.1006/abbi.2000.1866
– volume: 1
  year: 2016
  ident: 2025030417540361200_r44
  article-title: Myosin light chains 9 and 12 are functional ligands for CD69 that regulate airway inflammation
  publication-title: Sci. Immunol.
  doi: 10.1126/sciimmunol.aaf9154
– volume: 498
  start-page: 506
  year: 2013
  ident: 2025030417540361200_r28
  article-title: BACH2 represses effector programs to stabilize T(reg)-mediated immune homeostasis
  publication-title: Nature
  doi: 10.1038/nature12199
– volume: 488
  start-page: 414
  year: 2012
  ident: 2025030417540361200_r30
  article-title: The dynamic disulphide relay of quiescin sulphydryl oxidase
  publication-title: Nature
  doi: 10.1038/nature11267
– volume: 180
  start-page: 1199
  year: 2008
  ident: 2025030417540361200_r7
  article-title: The IL-3/IL-5/GM-CSF common receptor plays a pivotal role in the regulation of Th2 immunity and allergic airway inflammation
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.180.2.1199
– volume: 6
  start-page: 25533
  year: 2016
  ident: 2025030417540361200_r15
  article-title: The impact of amplification on differential expression analyses by RNA-seq
  publication-title: Sci. Rep.
  doi: 10.1038/srep25533
– volume: 87
  start-page: 2354
  year: 1996
  ident: 2025030417540361200_r39
  article-title: Eosinophils express a functional receptor for interferon alpha: inhibitory role of interferon alpha on the release of mediators
  publication-title: Blood
  doi: 10.1182/blood.V87.6.2354.bloodjournal8762354
– volume: 180
  start-page: 7622
  year: 2008
  ident: 2025030417540361200_r47
  article-title: Up-regulation and activation of eosinophil integrins in blood and airway after segmental lung antigen challenge
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.180.11.7622
– volume: 17
  start-page: 2102
  year: 2018
  ident: 2025030417540361200_r45
  article-title: Proteomic and phosphoproteomic changes induced by prolonged activation of human eosinophils with IL-3
  publication-title: J. Proteome Res.
  doi: 10.1021/acs.jproteome.8b00057
– volume: 30
  start-page: 523
  year: 2014
  ident: 2025030417540361200_r19
  article-title: Causal analysis approaches in ingenuity pathway analysis
  publication-title: Bioinformatics
  doi: 10.1093/bioinformatics/btt703
– volume: 371
  start-page: 1198
  year: 2014
  ident: 2025030417540361200_r3
  article-title: Mepolizumab treatment in patients with severe eosinophilic asthma
  publication-title: N. Engl. J. Med.
  doi: 10.1056/NEJMoa1403290
– volume: 54
  start-page: 116
  year: 2017
  ident: 2025030417540361200_r36
  article-title: BIRC3 single nucleotide polymorphism associate with asthma susceptibility and the abundance of eosinophils and neutrophils
  publication-title: J. Asthma
  doi: 10.1080/02770903.2016.1196371
– volume: 9
  start-page: 3157
  year: 2018
  ident: 2025030417540361200_r29
  article-title: SENP3 maintains the stability and function of regulatory T cells via BACH2 deSUMOylation
  publication-title: Nat. Commun.
  doi: 10.1038/s41467-018-05676-6
– volume: 554
  start-page: 382
  year: 2018
  ident: 2025030417540361200_r32
  article-title: Mitochondria-lysosome contacts regulate mitochondrial fission via RAB7 GTP hydrolysis
  publication-title: Nature
  doi: 10.1038/nature25486
– volume: 241
  start-page: 175
  year: 2017
  ident: 2025030417540361200_r43
  article-title: Bach2 controls homeostasis of eosinophils by restricting the type-2 helper function of T cells
  publication-title: Tohoku J. Exp. Med.
  doi: 10.1620/tjem.241.175
– volume: 169
  start-page: 6452
  year: 2002
  ident: 2025030417540361200_r9
  article-title: Decreased expression of membrane IL-5 receptor alpha on human eosinophils: I. Loss of membrane IL-5 receptor alpha on airway eosinophils and increased soluble IL-5 receptor alpha in the airway after allergen challenge
  publication-title: J. Immunol.
  doi: 10.4049/jimmunol.169.11.6452
– volume: 16
  start-page: 829
  year: 2015
  ident: 2025030417540361200_r33
  article-title: The transcription factor XBP1 is selectively required for eosinophil differentiation
  publication-title: Nat. Immunol.
  doi: 10.1038/ni.3225
– volume: 341
  start-page: 74
  year: 2013
  ident: 2025030417540361200_r31
  article-title: A secreted disulfide catalyst controls extracellular matrix composition and function
  publication-title: Science
  doi: 10.1126/science.1238279
– start-page: 2
  year: 2009
  ident: 2025030417540361200_r23
– volume: 15
  start-page: 777
  year: 2014
  ident: 2025030417540361200_r12
  article-title: Epigenomic analysis of primary human T cells reveals enhancers associated with TH2 memory cell differentiation and asthma susceptibility
  publication-title: Nat. Immunol.
  doi: 10.1038/ni.2937
– volume-title: Stat. Appl. Genet. Mol. Biol.
  year: 2005
  ident: 2025030417540361200_r22
  article-title: A general framework for weighted gene co-expression network analysis
  doi: 10.2202/1544-6115.1128
– volume: 150
  start-page: 90
  year: 2014
  ident: 2025030417540361200_r49
  article-title: Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines
  publication-title: Clin. Immunol.
  doi: 10.1016/j.clim.2013.11.009
– volume: 1799
  start-page: 775
  year: 2010
  ident: 2025030417540361200_r24
  article-title: Inhibiting NF-κB activation by small molecules as a therapeutic strategy
  publication-title: Biochim. Biophys. Acta
  doi: 10.1016/j.bbagrm.2010.05.004
– volume: 15
  start-page: 348
  year: 2018
  ident: 2025030417540361200_r1
  article-title: The economic burden of asthma in the United States, 2008-2013
  publication-title: Ann. Am. Thorac. Soc.
  doi: 10.1513/AnnalsATS.201703-259OC
– volume: 19
  start-page: 531
  year: 2018
  ident: 2025030417540361200_r16
  article-title: Elimination of PCR duplicates in RNA-seq and small RNA-seq using unique molecular identifiers
  publication-title: BMC Genomics
  doi: 10.1186/s12864-018-4933-1
– volume: 26
  start-page: 13
  year: 2007
  ident: 2025030417540361200_r40
  article-title: Human eosinophil major basic protein 2: location of disulfide bonds and free sulfhydryl groups
  publication-title: Protein J.
  doi: 10.1007/s10930-006-9035-2
– volume: 293
  start-page: 1136
  year: 2001
  ident: 2025030417540361200_r8
  article-title: Cytokine-specific transcriptional regulation through an IL-5Ralpha interacting protein
  publication-title: Science
  doi: 10.1126/science.1059157
– volume: 1
  start-page: 70
  year: 2012
  ident: 2025030417540361200_r11
  article-title: An integrated nano-scale approach to profile miRNAs in limited clinical samples
  publication-title: Am. J. Clin. Exp. Immunol.
– volume: 40
  start-page: 1
  year: 2007
  ident: 2025030417540361200_r25
  article-title: TWEAKing tissue remodeling by a multifunctional cytokine: role of TWEAK/Fn14 pathway in health and disease
  publication-title: Cytokine
  doi: 10.1016/j.cyto.2007.09.007
– volume: 2012
  year: 2012
  ident: 2025030417540361200_r26
  article-title: A bioinformatics resource for TWEAK-fn14 signaling pathway
  publication-title: J. Signal Transduct.
  doi: 10.1155/2012/376470
– volume: 15
  year: 2016
  ident: 2025030417540361200_r37
  article-title: A network approach predicts NFKBIA and BIRC3 as pathogenic genes in childhood asthma
  publication-title: Genet. Mol. Res.
  doi: 10.4238/gmr.15028226
– volume: 36
  start-page: 429
  year: 2016
  ident: 2025030417540361200_r6
  article-title: Essential mechanisms of differential activation of eosinophils by IL-3 compared to GM-CSF and IL-5
  publication-title: Crit. Rev. Immunol.
– volume: 1178
  start-page: 13
  year: 2014
  ident: 2025030417540361200_r10
  article-title: Eosinophil purification from peripheral blood
  publication-title: Methods Mol. Biol.
  doi: 10.1007/978-1-4939-1016-8_2
– volume: 15
  start-page: 550
  year: 2014
  ident: 2025030417540361200_r18
  article-title: Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2
  publication-title: Genome Biol.
  doi: 10.1186/s13059-014-0550-8
– volume: 8
  year: 2013
  ident: 2025030417540361200_r48
  article-title: Identification of genes expressed by human airway eosinophils after an in vivo allergen challenge
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0067560
– volume: 1799
  start-page: 275
  year: 2018
  ident: 2025030417540361200_r13
  article-title: A sensitive and integrated approach to profile messenger RNA from samples with low cell numbers
  publication-title: Methods Mol. Biol.
  doi: 10.1007/978-1-4939-7896-0_21
– volume: 25
  start-page: 1105
  year: 2009
  ident: 2025030417540361200_r17
  article-title: TopHat: discovering splice junctions with RNA-Seq
  publication-title: Bioinformatics
  doi: 10.1093/bioinformatics/btp120
– volume: 371
  start-page: 1189
  year: 2014
  ident: 2025030417540361200_r2
  article-title: Oral glucocorticoid-sparing effect of mepolizumab in eosinophilic asthma
  publication-title: N. Engl. J. Med.
  doi: 10.1056/NEJMoa1403291
– volume: 196
  start-page: 1385
  year: 2017
  ident: 2025030417540361200_r5
  article-title: Mepolizumab attenuates airway eosinophil numbers, but not their functional phenotype, in asthma
  publication-title: Am. J. Respir. Crit. Care Med.
  doi: 10.1164/rccm.201611-2234OC
– volume: 126
  start-page: 3279
  year: 2016
  ident: 2025030417540361200_r46
  article-title: Lung-resident eosinophils represent a distinct regulatory eosinophil subset
  publication-title: J. Clin. Invest.
  doi: 10.1172/JCI85664
– volume: 4
  start-page: 93
  year: 2017
  ident: 2025030417540361200_r42
  article-title: The biology of eosinophils and their role in asthma
  publication-title: Front. Med. (Lausanne)
  doi: 10.3389/fmed.2017.00093
SSID ssj0006024
Score 2.401358
Snippet Despite recent advances in asthma management with anti–IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a...
Despite recent advances in asthma management with anti-IL-5 therapies, many patients have eosinophilic asthma that remains poorly controlled. IL-3 shares a...
SourceID proquest
pubmed
crossref
SourceType Aggregation Database
Index Database
Enrichment Source
StartPage 329
SubjectTerms Asthma - immunology
Cytokines - immunology
Down-Regulation - immunology
Eosinophils - immunology
Gene Expression - immunology
Granulocyte-Macrophage Colony-Stimulating Factor - immunology
Humans
Interleukin-3 - immunology
Interleukin-5 - immunology
Signal Transduction - immunology
Up-Regulation - immunology
Title Human Eosinophils Express a Distinct Gene Expression Program in Response to IL-3 Compared with Common β-Chain Cytokines IL-5 and GM-CSF
URI https://www.ncbi.nlm.nih.gov/pubmed/31175163
https://www.proquest.com/docview/2253841267
Volume 203
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3dbtMwFLbKEIgbBANG-ZOR2AUX7hIntptL2hU2oBPaj7S7Kj8Oq0DJ1KVC3RPwPDwIr8CrcI7tpGnFEOMmitzEiXO-nuNjn_MdQl6BxtNghkLGdSJYmAjFkAKahakXe3Gcp0GCicLjA7l3Er4_Faedzq9W1NK8Snrp5R_zSv5HqtAGcsUs2WtItukUGuAc5AtHkDAc_0nGdgV-VIK_X56fTb9eIHOxyf2IkVazmhZpZYil63aU9ScbkYULHYc2QNZUz9j_yAKrHZqIdEweQXAMR9sDzoZnMWYILqryC4bK4w3CbD28G7Ph0Up44DLfzFJSYA6K5XraNjtqXmv94UA3fJELGEyz6jpAvn6XjWNje5e7XcU3GxY-QLbpJm7nELCN2_67M33Jjubm3AcQf56biIXhdFa21zhMWhWzWZ6tnANf2cIdPe1UtQDHV3qyrcu5F7RAy1uaOXADs0Y-sEwz6_YjBH8J7Yf7Lj0f7Le0ZX9WqbrXTGgT2AguFfYxqXuYuB5ukJtcSYklNnb3PzRTBenxsKazx-HZfXTsYWf9HVbnTVc4Q2ZSdHyP3HUypm8sNO-Tji42yS1b33SxSW6PXeTGA_LdYJW2sEodJmlMa6xSxCpdYpU6rNJpQWus0qqkiFVaY5UiVqnFKv35w-KUNjjFiwUFnFKL04fk5O3oeLjHXBUQlnLlVzCFijNwqzM_y7gCexPlPI2iME8ilYvIz5Xmfh70-yINvSj1QeckaZAlUklwJeJIBI_IRlEW-jGhHJwPnnleAr-HKoujLPeVFomQWa4iKbpkp_7Gk9RR5GOlFhDjFXLtktfNHeeWHuYv176sxTYBHY4bc3Ghy_nFBGxq0A99LlWXbFl5Nr0FyKUL7_3kGk96Su4s_0XPyEY1m-vnMHeukhcGf78BEJvD9A
linkProvider Flying Publisher
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=Human+Eosinophils+Express+a+Distinct+Gene+Expression+Program+in+Response+to+IL-3+Compared+with+Common+%CE%B2-Chain+Cytokines+IL-5+and+GM-CSF&rft.jtitle=The+Journal+of+immunology+%281950%29&rft.au=Nelson%2C+Ryan+K&rft.au=Brickner%2C+Howard&rft.au=Panwar%2C+Bharat&rft.au=Ram%C3%ADrez-Su%C3%A1stegui%2C+Ciro&rft.date=2019-07-15&rft.issn=0022-1767&rft.eissn=1550-6606&rft.volume=203&rft.issue=2&rft.spage=329&rft.epage=337&rft_id=info:doi/10.4049%2Fjimmunol.1801668&rft.externalDBID=n%2Fa&rft.externalDocID=10_4049_jimmunol_1801668
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