Cited by 1,191Multiple Sclerosis Research StudiesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

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RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

Codarri, Laura, Gyülvészi, Gabor, Tosevski, Vinko, Hesske, Lysann, Fontana, Adriano, Magnenat, Laurent, Suter, Tobias, Becher, Burkhard·2011·Nature Immunology

DOI 10.1038/ni.2027

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Abstract

Although the role of the T(H)1 and T(H)17 subsets of helper T cells as disease mediators in autoimmune neuroinflammation remains a subject of some debate, none of their signature cytokines are essential for disease development. Here we report that interleukin 23 (IL-23) and the transcription factor RORγt drove expression of the cytokine GM-CSF in helper T cells, whereas IL-12, interferon-γ (IFN-γ) and IL-27 acted as negative regulators. Autoreactive helper T cells specifically lacking GM-CSF failed to initiate neuroinflammation despite expression of IL-17A or IFN-γ, whereas GM-CSF secretion by Ifng(-/-)Il17a(-/-) helper T cells was sufficient to induce experimental autoimmune encephalomyelitis (EAE). During the disease effector phase, GM-CSF sustained neuroinflammation via myeloid cells that infiltrated the central nervous system. Thus, in contrast to all other known helper T cell-derived cytokines, GM-CSF serves a nonredundant function in the initiation of autoimmune inflammation regardless of helper T cell polarization.

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Method
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BackgroundInfluential
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BackgroundInfluential
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Background
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Background
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JunB is essential for IL-23-dependent pathogenicity of Th17 cells
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“In the EAE model of MS, GM-CSF confers pathogenicity on the CD4+ Th17 cell subset (Codarri et al., 2011; El-Behi et al., 2011; Komuczki et al., 2019), which in turn primes an encephalitogenic phenotype in Ly6C+ monocytes (Croxford et al.”
BackgroundMethod
Rorα Enforces Stability of the T-Helper-17 Cell Effector Program
Hall, J. A., Pokrovskii, M. V., Kroehling, L., Kim, B., Kim, S. Y., Wu, L., Lee, J., & Littman, D. R. (2020) · Immunity · doi:10.1016/j.immuni.2022.09.013 · Cited by 104
“…significant reductions in transcripts encoding proteins that are prominent cell-intrinsic drivers of autoimmune pathogenesis, including Csf2 (Codarri et al., 2011; El-Behi et al., 2011), Il1r1 (Shouval et al., 2016), and Il23r (Abdollahi et al., 2016; Duerr et al., 2006; Gaffen et al.,…”
IL-17A gene transfer induces bone loss and epidermal hyperplasia associated with psoriatic arthritis
Adamopoulos, I. E., Suzuki, É., Chao, C., Gorman, D., Adda, S., Maverakis, E., Zarbalis, K. S., Geissler, R. H., Asio, A., Blumenschein, W. M., et al. (2014) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2013-204782 · Cited by 93
GM‐CSF promotes migration of human monocytes across the blood brain barrier
Vogel, D. Y. S., Kooij, G., Heijnen, P. D. A. M., Breur, M., Peferoen, L. A. N., van der Valk, P., de Vries, H. E., Amor, S., & Dijkstra, C. D. (2015) · European Journal of Immunology · doi:10.1002/eji.201444960 · Cited by 94
GM-CSF as a target in inflammatory/autoimmune disease: current evidence and future therapeutic potential
Hamilton, J. A. (2015) · Expert Review of Clinical Immunology · doi:10.1586/1744666x.2015.1024110 · Cited by 94
GM-CSF primes cardiac inflammation in a mouse model of Kawasaki disease
Stock, A. T., Hansen, J. A., Sleeman, M. A., McKenzie, B. S., & Wicks, I. P. (2016) · The Journal of Experimental Medicine · doi:10.1084/jem.20151853 · Cited by 92
“In contrast to diseases models of MS and inflammatory arthritis, where GM-CSF from autoreactive CD4 T cells is critical (Campbell et al., 2011; Codarri et al., 2011), we find that a population of CFs is the major source of GM-CSF production.”
Result
Immune regulatory effects of high dose vitamin D3 supplementation in a randomized controlled trial in relapsing remitting multiple sclerosis patients receiving IFNβ; the SOLARIUM study
Muris, A., Smolders, J., Rolf, L., Thewissen, M. M., Hupperts, R., & Damoiseaux, J. G. M. C. (2016) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2016.09.018 · Cited by 94
T cell mediated pathogenesis in EAE: Molecular mechanisms
Kurschus, F. C. (2015) · Biomedical Journal · doi:10.4103/2319-4170.155590 · Cited by 95
“[8‑12] Also, the composition of CNS‑infiltrating cell types differs between EAE and MS; for example, CD8+ T cells, which may be seen as the dominating T cell population in MS histology,[13,14] are not essential for EAE.”
BackgroundInfluential
Synovial CD4+ T-cell-derived GM-CSF supports the differentiation of an inflammatory dendritic cell population in rheumatoid arthritis
Reynolds, G., Gibbon, J. R., Pratt, A., Wood, M. J., Coady, D., Raftery, G., Lorenzi, A., Gray, A., Filer, A., Buckley, C., et al. (2015) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2014-206578 · Cited by 87
The histone demethylase inhibitor GSK-J4 limits inflammation through the induction of a tolerogenic phenotype on DCs
Doñas, C., Carrasco, M., Fritz, M., Prado, C. E., Tejón, G., Osorio‐Barrios, F., Manrı́quez, V., Reyes, P., Pacheco, R., Bono, M. R., et al. (2016) · Journal of Autoimmunity · doi:10.1016/j.jaut.2016.07.011 · Cited by 94
Hectd3 promotes pathogenic Th17 lineage through Stat3 activation and Malt1 signaling in neuroinflammation
Cho, J. J., Xu, Z., Parthasarathy, U., Drashansky, T. T., Helm, E. Y., Zuniga, A. N., Lorentsen, K. J., Mansouri, S., Cho, J. Y., Edelmann, M. J., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-08605-3 · Cited by 92
Th17 cells in central nervous system autoimmunity
Sie, C., Korn, T., & Mitsdoerffer, M. (2014) · Experimental Neurology · doi:10.1016/j.expneurol.2014.03.009 · Cited by 95
Autoreactive T Cells from Patients with Myasthenia Gravis Are Characterized by Elevated IL-17, IFN-γ, and GM-CSF and Diminished IL-10 Production
Cao, Y., Amezquita, R. A., Kleinstein, S. H., Stathopoulos, P., Nowak, R. J., & O’Connor, K. C. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1501339 · Cited by 94
“Conversely, T cells producing IL-17 and IL-10 are protective and maintain immune homeostasis (30, 31, 33, 34, 43).”
Background
Targeting interleukin-17 in chronic inflammatory disease: A clinical perspective
Zwicky, P., Unger, S., & Becher, B. (2020) · Journal of Experimental Medicine · doi:10.1084/jem.20191123 · Cited by 91
“Dysregulation of the Cytokine GM-CSF Induces Spontaneous Phagocyte Invasion and Immunopathology in the Central Nervous System.”
BackgroundInfluentialSelf-citation
Recent advances in understanding the molecular mechanisms of the development and function of T h17 cells
Kurebayashi, Y., Nagai, S., Ikejiri, A., & Koyasu, S. (2013) · Genes to Cells · doi:10.1111/gtc.12039 · Cited by 93
“Accordingly, antidiabetic thiazolidinediones pioglitazone, a PPARc agonist, decreases Th17 differentiation and the severity of EAE, and Id3, a corepressor of E2A, also inhibits Th17 differentiation.”
BackgroundInfluential
Twin study reveals non-heritable immune perturbations in multiple sclerosis
Ingelfinger, F., Gerdes, L. A., Kavaka, V., Krishnarajah, S., Friebel, E., Galli, E., Zwicky, P., Furrer, R., Peukert, C., Dutertre, C., et al. (2022) · Nature · doi:10.1038/s41586-022-04419-4 · Cited by 88
Astrocyte response to IFN-γ limits IL-6-mediated microglia activation and progressive autoimmune encephalomyelitis
Savarin, C., Hinton, D. R., Valentin-Torres, A., Chen, Z., Trapp, B. D., Bergmann, C. C., & Stohlman, S. A. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0293-9 · Cited by 90
“EAE is mediated by self-reactive T cells directed toward components of myelin [4] secreting interleukin (IL)-17, interferon-γ (IFN-γ), and granulocyte-macrophage colony-stimulating factor [5,6].”
Background
Physiological and pathophysiological functions of SOCE in the immune system
Feske, S. (2012) · Frontiers in Bioscience-Elite · doi:10.2741/e540 · Cited by 91
T helper 17 cells may drive neuroprogression in major depressive disorder: Proposal of an integrative model
Slyepchenko, A., Maes, M., Köhler, C. A., Anderson, G., Quevedo, J., Alves, G. S., Berk, M., Fernandes, B. S., & Carvalho, A. F. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.02.002 · Cited by 89
Controversies on the role of Th17 in cancer: a TGF-β-dependent immunosuppressive activity?
Martin, F., Apétoh, L., & Ghiringhelli, F. (2012) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2012.09.007 · Cited by 104
Intercellular Adhesion Molecule-1 (ICAM-1) and ICAM-2 Differentially Contribute to Peripheral Activation and CNS Entry of Autoaggressive Th1 and Th17 Cells in Experimental Autoimmune Encephalomyelitis
Jahromi, N. H., Marchetti, L., Moalli, F., Duc, D., Basso, C., Tardent, H., Kaba, E., Deutsch, U., Pot, C., Sallusto, F., et al. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2019.03056 · Cited by 93
IL-23R–activated STAT3/STAT4 is essential for Th1/Th17-mediated CNS autoimmunity
Lee, P. W., Smith, A. J., Yang, Y., Selhorst, A. J., Liu, Y., Racke, M. K., & Lovett‐Racke, A. E. (2017) · JCI Insight · doi:10.1172/jci.insight.91663 · Cited by 93
Polyfunctional, Pathogenic CD161+ Th17 Lineage Cells Are Resistant to Regulatory T Cell–Mediated Suppression in the Context of Autoimmunity
Basdeo, S. A., Moran, B., Cluxton, D., Canavan, M., McCormick, J., Connolly, M. C., Orr, C. K., Mills, K. H. G., Veale, D. J., Fearon, U., et al. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1402990 · Cited by 92
Innate IFN‐γ promotes development of experimental autoimmune encephalomyelitis: A role for NK cells and M1 macrophages
Dungan, L. S., McGuinness, N., Boon, L., Lynch, M. A., & Mills, K. H. G. (2014) · European Journal of Immunology · doi:10.1002/eji.201444612 · Cited by 88
Human T helper type 1 dichotomy: origin, phenotype and biological activities
Annunziato, F., Cosmi, L., Liotta, F., Maggi, E., & Romagnani, S. (2014) · Immunology · doi:10.1111/imm.12399 · Cited by 91
Fatty acid synthase regulates the pathogenicity of Th17 cells
Marks, K. E., Flaherty, S., Woodman, K., Sharma-Walia, N., & Reynolds, J. M. (2017) · Journal of Leukocyte Biology · doi:10.1189/jlb.3ab0417-159rr · Cited by 85
“Although Th17 cells produce IL-17, other reports have demonstrated that Th17-derived IFN-g and GM-CSF are what makes a Th17 cell pathogenic for autoimmune inflammation [21, 22, 32].”
Background
New insights into the IL-12 and IL-23: From a molecular basis to clinical application in immune-mediated inflammation and cancers
Chyuan, I., & Lai, J. (2020) · Biochemical Pharmacology · doi:10.1016/j.bcp.2020.113928 · Cited by 89
Cytokines and transcription factors in the differentiation of CD4+ T helper cell subsets and induction of tissue inflammation and autoimmunity
Pawlak, M., Ho, A. W., & Kuchroo, V. K. (2020) · Current Opinion in Immunology · doi:10.1016/j.coi.2020.09.001 · Cited by 93
GM-CSF as a therapeutic target in inflammatory diseases
van Nieuwenhuijze, A. E. M., Koenders, M. I., Roeleveld, D. M., Sleeman, M. A., van den Berg, W., & Wicks, I. P. (2013) · Molecular Immunology · doi:10.1016/j.molimm.2013.05.002 · Cited by 87
“…inflammation (Wada et al., 1997; Ponomarev t al., 2006; Shi et al., 2006) and it has been found recently that GMSF is linked to the IL-23/IL-17 pathway (Campbell et al., 2011a; odarri et al., 2011; El-Behi et al., 2011; Poppensieker et al., 2012; an Nieuwenhuijze et al., unpublished observations).”
Background
The Pleiotropic Effects of the GM-CSF Rheostat on Myeloid Cell Differentiation and Function: More Than a Numbers Game
Zhan, Y., Lew, A. M., & Chopin, M. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.02679 · Cited by 89
Retina-Specific T Regulatory Cells Bring About Resolution and Maintain Remission of Autoimmune Uveitis
Silver, P. B., Horai, R., Chen, J., Jittayasothorn, Y., Chan, C., Villasmil, R., Kesen, M. R., & Caspi, R. R. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1402650 · Cited by 87
Marking and Quantifying IL-17A-Producing Cells In Vivo
Price, A. E., Reinhardt, R. L., Liang, H.-E., & Locksley, R. M. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039750 · Cited by 89
The meninges: new therapeutic targets for multiple sclerosis
Russi, A. E., & Brown, M. A. (2014) · Translational research · doi:10.1016/j.trsl.2014.08.005 · Cited by 90
“GM-CSF is a cytokine that has recently been shown to be necessary and sufficient to confer encephalitogenicity to T cells.(101,102) Furthermore, mast cells cocultured with previously primed myelin-specific T cells induce GM-CSF production by T cells (Walker et al, unpublished observation, 2012).”
Background
Helicobacter pylori–specific Protection Against Inflammatory Bowel Disease Requires the NLRP3 Inflammasome and IL-18
Engler, D. B., Leonardi, I., Hartung, M. L., Kyburz, A., Spath, S., Becher, B., Rogler, G., & Mueller, A. (2015) · Inflammatory Bowel Diseases · doi:10.1097/mib.0000000000000318 · Cited by 86
Granulocyte-macrophage colony-stimulating factor is a key mediator in inflammatory and arthritic pain
Cook, A. D., Pobjoy, J., Sarros, S., Steidl, S., Dürr, M. C., Lacey, D. C., & Hamilton, J. A. (2012) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2012-201703 · Cited by 86
“27 Networks linking GM–CSF and cytokines, such as IL-1 and IL-23, are beginning to emerge, highlighting the key role of GM–CSF as a pathogenic cytokine in inflammation/autoimmunity,(4) 6 11 13 15 16 with GM–CSF being the only known T-cell-derived cytokine with a non-redundant function in the initiation of EAE.(15) The…”
ResultInfluential
Astrocytic A20 ameliorates experimental autoimmune encephalomyelitis by inhibiting NF-κB- and STAT1-dependent chemokine production in astrocytes
Wang, X., Deckert, M., Xuân, N. T., Nishanth, G., Just, S., Waisman, A., Naumann, M., & Schlüter, D. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1183-9 · Cited by 92
Autoimmune Memory T Helper 17 Cell Function and Expansion Are Dependent on Interleukin-23
Haines, C. J., Chen, Y., Blumenschein, W. M., JAIN, R. K., Chang, C., Joyce-Shaikh, B., Porth, K., Boniface, K., Mattson, J. D., Basham, B., et al. (2013) · Cell Reports · doi:10.1016/j.celrep.2013.03.035 · Cited by 87
“It was recently reported that IL-23 is required for granulocyte-macrophage colony-stimulating factor (GM-CSF) production by Th17 cells in EAE (Codarri et al., 2011; El-Behi et al., 2011).”
Background
Cytokine Signaling in Multiple Sclerosis and Its Therapeutic Applications
Palle, P., Monaghan, K. L., Milne, S. M., & Wan, E. C. K. (2017) · Medical Sciences · doi:10.3390/medsci5040023 · Cited by 91
“This was shown by studies demonstrating that IL-23 induces the production of granulocyte-macrophage colony-stimulating factor (GM-CSF) in IL-17 cells, and GM-CSF is the main pathogenic factor of EAE [120,122].”
Method
Granulocyte-macrophage colony-stimulating factor neuroprotective activities in Alzheimer’s disease mice
Kiyota, T., Machhi, J., Lu, Y., Dyavarshetty, B., Nemati, M., Yokoyama, I., Mosley, R. L., & Gendelman, H. E. (2018) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2018.03.009 · Cited by 80
The regulation of the development and function of dendritic cell subsets by GM-CSF: More than a hematopoietic growth factor
Zhan, Y., Xu, Y., & Lew, A. M. (2012) · Molecular Immunology · doi:10.1016/j.molimm.2012.04.009 · Cited by 87
The Emerging Role of Neutrophil Granulocytes in Multiple Sclerosis
Woodberry, T., Bouffler, S. E., Wilson, A. S., Buckland, R. L., & Brüstle, A. (2018) · Journal of Clinical Medicine · doi:10.3390/jcm7120511 · Cited by 84
“This model is strongly dependent on Th17 cells [43,44] and both GM-CSF and IL-17 are derived from CNS infiltrating T cells [40,45], further underlining the strong interaction between this adaptive cell population and neutrophils in the MS model.”
Do Th17 Lymphocytes and IL-17 Contribute to Parkinson's Disease? A Systematic Review of Available Evidence
Storelli, E., Cassina, N., Rasini, E., Marino, F., & Cosentino, M. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2019.00013 · Cited by 87
Minor Structural Change to Tertiary Sulfonamide RORc Ligands Led to Opposite Mechanisms of Action
René, O., Fauber, B. P., Boenig, G. D. L., Burton, B., Eidenschenk, C., Everett, C., Gobbi, A., Hymowitz, S. G., Johnson, A. R., Kiefer, J. R., et al. (2014) · ACS Medicinal Chemistry Letters · doi:10.1021/ml500420y · Cited by 83
An antigen-specific semi-therapeutic treatment with local delivery of tolerogenic factors through a dual-sized microparticle system blocks experimental autoimmune encephalomyelitis
Cho, J. J., Stewart, J. M., Drashansky, T. T., Brusko, M., Zuniga, A. N., Lorentsen, K. J., Keselowsky, B. G., & Avram, D. (2017) · Biomaterials · doi:10.1016/j.biomaterials.2017.07.029 · Cited by 84
“Defects in Th17 and Th1 cells or GM-CSF production prevented disease in EAE, thus solidifying the central role of proinflammatory CD4+ T cells and the corresponding cytokines IL-17A, IFNγ, and GM-CSF in EAE [13, 15].”
Influential

Authors: Codarri, L., Gyülvészi, G., Tosevski, V., Hesske, L., Fontana, A., Magnenat, L., Suter, T., & Becher, B.
Affiliations: University Hospital Zurich (CH)
University of Zurich (CH)
Merck Serono S.A. (Switzerland) (CH)
Corresponding author: Becher, Burkhard
ORCID: Magnenat, Laurent
Suter, Tobias
Becher, Burkhard
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2011-04-24
Volume: 12
Issue: 6
Pages: 560-567
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.2027
OpenAlex: W2157837362
Cited by: 1,191
References: 44
Citations by year: 2026: 31 · 2025: 48 · 2024: 60 · 2023: 53 · 2022: 61 · 2021: 73 · 2020: 85 · 2019: 83 · 2018: 72 · 2017: 99 · 2016: 96 · 2015: 117 · 2014: 103 · 2013: 98 · 2012: 82
FWCI: 70.23
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Topics: Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: RORγt, GM-CSF, experimental autoimmune encephalomyelitis, T helper cells, IL-23, autoimmune neuroinflammation, Th1 cells, Th17 cells, myeloid cell infiltration, IL-12, interferon-gamma, IL-27, cytokine regulation
MeSH terms: Animals, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Female, Flow Cytometry, Glycoproteins, T-Lymphocytes, Helper-Inducer, Interferon-gamma, Interleukins, Male, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Transgenic, Peptide Fragments, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, Knockout, Th1 Cells, Interleukin-12, Interleukin-17, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Myelin-Oligodendrocyte Glycoprotein

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RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

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