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The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF
Open accessAbstract
Interleukin 17 (IL-17)-producing helper T cells (T(H)17 cells) require exposure to IL-23 to become encephalitogenic, but the mechanism by which IL-23 promotes their pathogenicity is not known. Here we found that IL-23 induced production of the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) in T(H)17 cells and that GM-CSF had an essential role in their encephalitogenicity. Our findings identify a chief mechanism that underlies the important role of IL-23 in autoimmune diseases. IL-23 induced a positive feedback loop whereby GM-CSF secreted by T(H)17 cells stimulated the production of IL-23 by antigen-presenting cells. Such cross-regulation of IL-23 and GM-CSF explains the similar pattern of resistance to autoimmunity when either of the two cytokines is absent and identifies T(H)17 cells as a crucial source of GM-CSF in autoimmune inflammation.
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“and to promote the production of effector molecules (El-Behi et al., 2011).”
From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as El-Behi et al., 2011
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“(B and C) Normalized counts of autoimmune disease-associated (Il1r1, Il23r, Bhlhe40), pathogenic (Csf2) genes (B) and Rorc (C) in TWT and TAKO Il17aeGFP+ Th17 cells from the DLN (TWT (n = 3) and TAKO (n = 3)) and SC (TWT (n = 3) and TAKO (n = 2)) at peak of EAE.”
BackgroundInfluentialB cells in autoimmune diseases of the central nervous system
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“GM-CSF production in Th17 cells is induced through stimulation of the IL-23 receptor [7,9].”
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DIRECT EFFECTS OF GM-CSF ON THE FUNCTIONS OF HUMAN MONOCYTES/MACROPHAGES
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“В частности, GM-CSF способен поддерживать дифференцировку и выживаемость дендритных клеток, запускающих антигензависимую пролиферацию и дифференцировку Т-лимфоцитов [14, 17] и регулирующих иммунные реакции на всем их протяжении [4, 7].”
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“GM-CSF is essential for CD4-EAE development [23], but its role in CD8-EAE is unknown.”
Self-citationPin1 maintains the effector program of pathogenic Th17 cells in autoimmune neuroinflammation
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Immune-responsive gene 1: The mitochondrial key to Th17 cell pathogenicity in CNS autoimmunity
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“…and is known to include two distinct subsets (22): the pathogenic Th17 (pTh17) subset, which produces high levels of inflammatory mediators, such as IL17a and GMCSF, and induces EAE disease (23–25), and the second nonpathogenic Th17 (npTh17) subset, which has a mild inflammatory profile (26, 27).”
Autotaxin in encephalitogenic CD4 T cells as a therapeutic target for multiple sclerosis
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“These cytokines were chosen based on their known contributions to encephalitogenicity [28–30].”
BackgroundA Compass to Guide Insights into TH17 Cellular Metabolism and Autoimmunity
Wilson, A., Mosure, S., & Solt, L. A. (2021) · Immunometabolism · doi:10.20900/immunometab20220001 · Cited by 2
“The “pathogenic fate” of TH17 cells depends on the cytokine milieu present at the time of T cell activation; IL-6 and TGFβ steer TH17 cells toward a “non-pathogenic” fate, whereas the addition of IL-1β and IL-23 increase TH17 cell pathogenicity [4,6,8].”
BackgroundGene regulatory network of human GM-CSF secreting T helper cells
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T ‐bet is essential for T h1‐mediated, but not T h17‐mediated, CNS autoimmune disease
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Cellular Immunity and Multiple Sclerosis: Current Understanding
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Histamine H4 receptor in neuroinflammation: Dual roles in multiple sclerosis and Parkinson's disease
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Epithelial MLCK deficiency alleviates alcohol-associated liver disease via dendritic–Th17 cell axis
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“47,48 To directly validate Th17 cell functional polarization in vivo , we performed flow cytometry analysis of intestinal CD4 + T cells and found that alcohol exposure increased the proportion of pathogenic Th17 cells (IL-17A + GM-CSF + ), while reducing nonpathogenic Th17 cells (IL-17A + IL-10 +…”
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Role of Neutrophils in the Development of Steatotic Liver Disease
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“122 Further studies are needed to elucidate the role of IL-23 in ALD.”
Siriwardhana, D., & Lanerolle, S. (2023) · Sri Lanka Journal of Obstetrics and Gynaecology · doi:10.4038/sljog.v45i3.8101 · Cited by 1
“…at the University of Philadelphia on the variation of maternal serum and vaginal fluid CRP levels identified that both maternal serum and vaginal fluid CRP determinations after pre-labor preterm rupture of the membrane are of poor predictive value in neonatal early-onset infection prediction 11 .”
BackgroundKim, S. Y., Kim, Y., Kim, S., Han, S.-M., Park, H., Payumo, R. M. P., Kim, H. E., Hyun, J., Kim, K. H., Lee, E. J., et al. (2023) · Human Immunology · doi:10.1016/j.humimm.2022.12.004 · Cited by 1
Luo, Z., Wei, H., & Li, X. (2022) · Pediatric Research · doi:10.1038/s41390-022-02059-y · Cited by 1
Targeting interferon-λ signaling promotes recovery from central nervous system autoimmunity
Manivasagam, S., Williams, J. L., Vollmer, L., Bollman, B., Bartleson, J. M., Ai, S.-J., Wu, G., & Klein, R. (2021) · doi:10.1101/2021.08.17.456642 · Cited by 1
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“Further, IL-23 has been shown to stimulate GM-CSF production by CD4+ Th17 cells, although it is not known if this is true for iNKT cells (Codarri et al., 2011; El-Behi et al., 2011; Rothchild et al., 2014).”
Background
Metadata
- Authors
- El-Behi, M., Ciric, B., Dai, H., Yan, Y., Cullimore, M., Safavi, F., Zhang, G.-X., Dittel, B. N., & Rostami, A.
- Affiliations
- Thomas Jefferson University (US)
- Versiti Blood Center of Wisconsin (US)
- Corresponding author
- Rostami, Abdolmohamad
- ORCID
- Venue
- Nature Immunology
- Published
- 2011-04-24
- Volume
- 12
- Issue
- 6
- Pages
- 568-575
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC3116521
- OpenAlex
- W2084388036
- Cited by
- 1,071
- References
- 44
- Citations by year
- 2026: 25 · 2025: 38 · 2024: 38 · 2023: 58 · 2022: 62 · 2021: 72 · 2020: 82 · 2019: 71 · 2018: 74 · 2017: 96 · 2016: 82 · 2015: 108 · 2014: 91 · 2013: 80 · 2012: 73
- FWCI
- 37.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Multiple Sclerosis Society
- Mary E. Groff Surgical and Medical Research and Education Charitable Trust
- National Institute of Neurological Disorders and Stroke (R01NS046782)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Keywords
- Th17 cells, experimental autoimmune encephalomyelitis, IL-23, GM-CSF, interleukin-1, encephalitogenicity, autoimmune disease, antigen-presenting cells, positive feedback loop, T helper cells
- MeSH terms
- Animals, Antibodies, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Female, Flow Cytometry, Glycoproteins, Interleukin-1, Mice, Inbred C57BL, Mice, Transgenic, Peptide Fragments, CD4-Positive T-Lymphocytes, Granulocyte-Macrophage Colony-Stimulating Factor, Transforming Growth Factor beta, Mice, Knockout, Th1 Cells, Coculture Techniques, CD11c Antigen, Mice, Interleukin-1beta, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Myelin-Oligodendrocyte Glycoprotein
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