Cited by 1,071Psoriasis: Treatment and PathogenesisT-cell and B-cell ImmunologyMultiple Sclerosis Research Studies

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The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF

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El-Behi, Mohamed, Ciric, Bogoljub, Dai, Hong, Yan, Yaping, Cullimore, Melissa, Safavi, Farinaz, Zhang, Guang-Xian, Dittel, Bonnie N, Rostami, Abdolmohamad·2011·Nature Immunology

DOI 10.1038/ni.2031PMC PMC3116521

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Abstract

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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Exhausted KLRG1hi CD8+ T and pathogenic GZMA+ Th17 cells are associated with the mild Mycoplasma pneumoniae pneumonia in children
Zhan, J.-Y., Luo, R., Li, C., Zhong, L., Wu, Q., Wang, R., Chen, D.-P., Chen, X., Ren, K.-Y., Chen, Z., et al. (2025) · Journal of Infection · doi:10.1016/j.jinf.2025.106642 · Cited by 10
Interplay between fungal infections and autoimmunity: mechanisms and therapeutic perspectives
DiPalma, D. T., Lumbreras, M., & Shinohara, M. L. (2025) · EMBO Molecular Medicine · doi:10.1038/s44321-025-00262-y · Cited by 10
“…such as G-CSF, M-CSF, and GM-CSF, enhance myelopoiesis and fungal clearance (Bandera et al, 2008; Du et al, 2020; Nemunaitis et al, 1993), but GM-CSF is particularly linked to autoimmune diseases as a detrimental factor in MS (Codarri et al, 2011; El-Behi et al, 2011; McQualter et al, 2001).”
Pathways to Progressive Disability in Multiple Sclerosis: The Role of Glial Cells in Chronic CNS Inflammation
Siffrin, V. (2025) · Glia · doi:10.1002/glia.70044 · Cited by 10
“Key factors include the master transcription factor RORγt which drives Th17 cell differentiation (Ivanov et al. 2006), IL-23, which stabilizes Th17 cells, and GMCSF, which mediates the manifestation of clinical signs of EAE (McGeachy et al. 2009; Codarri et al. 2011; El-Behi et al. 2011).”
The IL-23R and Its Genetic Variants: A Hitherto Unforeseen Bridge Between the Immune System and Cancer Development
Audia, S., Brescia, C., Dattilo, V., Torchia, N., Trapasso, F., & Amato, R. (2024) · Cancers · doi:10.3390/cancers17010055 · Cited by 11
Metabolic Stress Expands Polyfunctional, Proinflammatory Th 17 Cells in Patients With Psoriatic Arthritis for Whom There is Interleukin‐23–Independent Interleukin‐17 Production
Stober, C. B., Ellis, L., GOODALL, J. C., Veldhoen, M., & Gaston, H. (2024) · Arthritis & Rheumatology · doi:10.1002/art.43095 · Cited by 11
“35,36 In contrast to murine studies in which IL-23 augments GM-CSF, 11,12 we show that GM-CSF is negatively regulated by IL-23 in human Th 17 and Th 1 cells.”
Myelin oligodendrocyte glycoprotein reactive Th17 cells drive Janus Kinase 1 dependent transcriptional reprogramming in astrocytes and alter cell surface cytokine receptor profiles during experimental autoimmune encephalomyelitis
Milne, S. M., Lahiri, A., Sanchez, C. L., Marshall, M. J., Jahan, I., & Meares, G. P. (2024) · Scientific Reports · doi:10.1038/s41598-024-63877-0 · Cited by 10
A T H 17-intrinsic IL-1β–STAT5 axis drives steroid resistance in autoimmune neuroinflammation
Miller-Little, W. A., Chen, X., Salazar, V., Liu, C., Bulek, K., Zhou, J. Y., Xiao, L., Stüve, O., Stappenbeck, T. S., Dubyak, G., et al. (2024) · Science Immunology · doi:10.1126/sciimmunol.abq1558 · Cited by 10
GM-CSF+ Tc17 cells are required to bolster vaccine immunity against lethal fungal pneumonia without causing overt pathology
Mudalagiriyappa, S., Sharma, J., Vieson, M. D., & Nanjappa, S. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.111543 · Cited by 9
“Consistent with this idea, studies have identified a non-redundant role for GM-CSF in cooperating with Th17 cells during autoimmune neuroinflammation (Codarri et al., 2011; El-Behi et al., 2011; Lee et al., 2012).”
BackgroundResult
Pathological Role of Pin1 in the Development of DSS-Induced Colitis
Matsunaga, Y., Hasei, S., Yamamotoya, T., Honda, H., Kushiyama, A., Sakoda, H., Fujishiro, M., Ono, H., Ito, H., Okabe, T., et al. (2021) · Cells · doi:10.3390/cells10051230 · Cited by 11
“DC cells and macrophages produce cytokines IL-6, IL-23 and IL-1β and then drive Th17 cells to produce IL-17 [17].”
BackgroundInfluential
Increased IL-2 and Reduced TGF-β Upon T-Cell Stimulation are Associated with GM-CSF Upregulation in Multiple Immune Cell Types in Multiple Sclerosis
Aram, J., Frakich, N., Morandi, E., Alrouji, M., Samaraweera, A. P. R., Onion, D., Spendlove, I., Colombo, S., Tanasescu, R., Gran, B., et al. (2020) · Biomedicines · doi:10.3390/biomedicines8070226 · Cited by 9
Cytokines as Mediators of Neuroinflammation in Experimental Autoimmune Encephalomyelitis
Gogoleva, V. S., Атретханы, К.-С. Н., Drutskaya, M. S., Mufazalov, I. A., Kruglov, A., & Nedospasov, S. A. (2018) · Biochemistry (Moscow) · doi:10.1134/s0006297918090110 · Cited by 13
IL-3 Is a Marker of Encephalitogenic T Cells, but Not Essential for CNS Autoimmunity
Lee, P. W., Xin, M., Pei, W., Yang, Y.-H., & Lovett-Racke, A. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01255 · Cited by 9
“Since the Il3 allele is located in the same gene cluster with Csf2 (encodes GMCSF) on chromosome 11 in mouse and chromosome 5 in human (Figure 1G) and GMCSF was found to be critical for encephalitogenic T cells (17, 21, 23, 24), we analyzed GMCSF+activated CD4 T cells via flow cytometry.”
Background
Translational utility of experimental autoimmune encephalomyelitis: recent developments
Jagodic, M., Guerreiro‐Cacais, A. O., Lindahl, H., Flytzani, S., N’diaye, M., & Olsson, T. P. (2015) · Journal of Inflammation Research · doi:10.2147/jir.s76707 · Cited by 6
“68 Since GM-CSF is the only T-cell effector cytokine shown to date to be absolutely essential for EAE induction, 69,70 the results of this study come to resolve the conundrum.”
Background
T Cell-Derived GM-CSF, Regulation of Expression and Function
Sheng, W. (2015) · Immunome Research · doi:10.4172/1745-7580.1000098 · Cited by 8
“demonstrated that both antigen-specific TH1 and TH17 are encephalitogenic and that GM-CSF expression by either TH1 or TH17 cells was required for their encephalitogenicity in mice [15].”
BackgroundResultInfluential
Mechanisms of immunological tolerance in central nervous system inflammatory demyelination
Mari, E. R., Moore, J. N., Zhang, G., & Rostami, A. M. (2015) · Clinical and Experimental Neuroimmunology · doi:10.1111/cen3.12196 · Cited by 8
Self-citation
TL1A Increases Expression of CD25, LFA-1, CD134 and CD154, and Induces IL-22 and GM-CSF Production from Effector CD4 T-Cells
Reichwald, K., Jørgensen, T. Z., & Skov, S. (2014) · PLoS ONE · doi:10.1371/journal.pone.0105627 · Cited by 9
“GM-CSF is up-regulated in several autoimmune diseases, and is directly responsible for the encephalitogenicity of the Th17 cells mediating disease in an EAE mouse model [24,25].”
Cellular aspects of immunity involved in the development of atherosclerosis
Khalaf, K., Chamieh, M., Welc, N. A., Singh, C., Kaouk, J. L., Kaouk, A., Mackiewicz, A. A., Kaczmarek, M., & Perek, B. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1461535 · Cited by 10
The Effect of Peri-Implant Therapy on the Expression of Th17-Related Cytokines in Patients with Peri-Implant Mucositis and Peri-Implantitis: A Prospective Longitudinal Study
Gonçalves, L. T. C., Neves, G. S. T., da Silva, A. M. P., Telles, D. D. M., Figueredo, C. M., Lourenço, E. J. V., & Teixeira, M. K. S. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14020340 · Cited by 10
IL-37 suppresses CNS autoimmunity by increasing the frequency of Treg cells and reducing CD4 + T cell-derived IL-10 production
Yazdani, R., Naziri, H., Azizi, G., Ciric, B., Askari, M., Ahmadi, A. M., Aseervatham, J., Zhang, G.-X., & Rostami, A. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03295-1 · Cited by 8
Self-citation
The immunologic role of IL-23 in psoriatic arthritis: a potential therapeutic target
Su, Q. Y., Gao, H.-Y., Duan, Y.-R., Luo, J., Wang, W.-Z., Qiao, X.-C., & Zhang, S. (2024) · Expert Opinion on Biological Therapy · doi:10.1080/14712598.2024.2401148 · Cited by 9
Serum GM-CSF level is a predictor of treatment response to tocilizumab in rheumatoid arthritis patients: a prospective observational cohort study
Su, J., Hu, W., Ding, Y., Zhang, P., Li, T.-F., Liu, S., & Xing, L. (2024) · Arthritis Research & Therapy · doi:10.1186/s13075-024-03373-y · Cited by 8
“Proinflammatory cytokines (IL-6, IL-1 and IL-23) are well characterized as an enhancer and stabilizer of effector Th17 cells [30, 31].”
Background
Investigation into Cardiac Myhc-α 334–352-Specific TCR Transgenic Mice Reveals a Role for Cytotoxic CD4 T Cells in the Development of Cardiac Autoimmunity
Sur, M., Rasquinha, M. T., Mone, K., Massilamany, C., Lasrado, N., Gurumurthy, C. B., Sobel, R. A., & Reddy, J. (2024) · Cells · doi:10.3390/cells13030234 · Cited by 10
GM-CSF Protects Macrophages from DNA Damage by Inducing Differentiation
Vico, T., Youssif, C., Zare, F., Comalada, M., Sebastián, C., Lloberas, J., & Celada, A. (2022) · Cells · doi:10.3390/cells11060935 · Cited by 12
“Ly6Chigh monocytes in an inflammatory locus differentiate into macrophages with a proinflammatory profile, releasing a number of molecules (IL-1α, IL-1β, TNF-α and IL-12) that activate helper T cells and induce the production of GM-CSF [66,67].”
Background
Stimulation of a subset of natural killer T cells by CD103+ DC is required for GM-CSF and protection from pneumococcal infection
Murray, M. P., Crosby, C., Marcovecchio, P. M., Hartmann, N., Chandra, S., Zhao, M., Khurana, A., Zahner, S., Clausen, B., Coleman, F., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2021.110209 · Cited by 8
“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
Myocarditis and carotidynia caused by Granulocyte-Colony stimulating factor administration
de la Fuente, E. C., Barquín, A., Saavedra, C., Domingo, J. J. S., Huertas, R. M., Fernández-Abad, M., & Martínez-Jáñez, N. (2020) · Modern Rheumatology Case Reports · doi:10.1080/24725625.2020.1754552 · Cited by 9
The Effects of Anti-IL-23p19 Therapy on Atherosclerosis Development in ApoE −/− Mice
Wang, J., Zhao, P., Gao, Y., Zhang, F., Yuan, X., Jiao, Y., & Gong, K. (2019) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2019.0050 · Cited by 11
Effect of 50-Hz Magnetic Fields on Serum IL-1β and IL-23 and Expression of BLIMP-1, XBP-1, and IRF-4
Molaei, S., Behzad, M., Gholamian-Hamadan, M., Zaerieghane, Z., & Zamani, A. (2019) · Inflammation · doi:10.1007/s10753-019-01042-w · Cited by 8
Novel Therapeutic Targets in Axial Spondyloarthritis
Worth, C., Bowness, P., & Al-Mossawi, M. (2018) · Current Treatment Options in Rheumatology · doi:10.1007/s40674-018-0095-1 · Cited by 8
Interleukin 23 in IBD Pathogenesis
Eken, A., & Oukka, M. (2016) · InTech eBooks · doi:10.5772/64882 · Cited by 7
“More importantly, independent studies revealed that GMCSF is required for classical EAE development in mice, especially by activating microglia or mobilizing inflammatory myeloid lineages to the inflammation site [109, 110].”
Background
Exposure to inflammatory cytokines selectively limits GM ‐ CSF production by induced T regulatory cells
Reynolds, B. C., Turner, D. G., McPherson, R. C., Prendergast, C. T., Phelps, R. G., Turner, N. A., O’Connor, R. A., & Anderton, S. M. (2014) · European Journal of Immunology · doi:10.1002/eji.201444687 · Cited by 9
Macrophages orchestrate elimination of Shigella from the intestinal epithelial cell niche via TLR-induced IL-12 and IFN-γ
Eislmayr, K., Langner, C. A., Liu, F. L., Yuvaraj, S., Babirye, J. P., Roncaioli, J. L., Vickery, J., Barton, G. M., Lesser, C. F., & Vance, R. E. (2025) · Cell Host & Microbe · doi:10.1016/j.chom.2025.08.001 · Cited by 10
SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation
Hu, W., Kwon, L., Jeong, Y. S., Bae, G. H., Kim, Y. S., Zabel, B. A., & Bae, Y. (2025) · Immune Network · doi:10.4110/in.2025.25.e19 · Cited by 8
“We examined IL-6, known to collaborate with TGF-β in promoting Th17 differentiation, along with IL-23 and IL-1 β , which have been implicated in inducing pathogenic GM-CSF-producing Th17 subsets (29).”
Early involvement of peripherally derived monocytes in inflammation in an NMO-like mouse model
Kim, M., Kim, W., Cha, H., Kim, B., Kwon, Y. N., & Kim, S. M. (2024) · Scientific Reports · doi:10.1038/s41598-024-51759-4 · Cited by 10
“IL-1β plays a role in the expansion of GM-CSF-producing Th17 cells 29 , breakdown of the blood–brain barrier (BBB) 30 , activation of microglia 31 , and promotion of IL-1β production/secretion to amplify inflammation.”
The roles of lncRNAs in Th17-associated diseases, with special focus on JAK/STAT signaling pathway
Wang, H., Yu, L., Cheng, L., & Guo, Z. (2023) · Clinical and Experimental Medicine · doi:10.1007/s10238-023-01181-3 · Cited by 6
“Given that GM-CSF plays a vital function in Th17 cells for encephalitogenicity in mice [19, 21], the observation that active MS patients with relapsing–remitting type had increased levels of GM-CSF in their cerebrospinal fluid and serum as well as enhanced GM-CSF production of T cells from their…”
Background
Histamine H4 Receptor Agonist, 4-Methylhistamine, Aggravates Disease Progression and Promotes Pro-Inflammatory Signaling in B Cells in an Experimental Autoimmune Encephalomyelitis Mouse Model
Alsaad, A. M. S., Ansari, M. A., Nadeem, A., Attia, S. M., Bakheet, S. A., Alomar, H. A., & Ahmad, S. F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241612991 · Cited by 5
“Recent data have also shown that GM-CSF is activated in the disease progression and pathogenicity of EAE [19].”
Background
GATA3 induces the pathogenicity of Th17 cells via regulating GM-CSF expression
Butcher, M. J., Gurram, R. K., Zhu, X., Chen, X., Hu, G., Lazarevic, V., Zhao, K., & Zhu, J. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1186580 · Cited by 7
“As prior work has demonstrated that GM-CSF is an effector cytokine critically required for the recruitment and activation of CNS mononuclear cells and for EAE induction (22, 23, 48), the inability of late tamoxifen-treated Cre-ERT2-Gata3 CD4 effector cells to produce GM-CSF likely explains why these transferred CD4”
Result
GM‐CSF ‐producing CCR2 + CCR6 + Th17 cells are pathogenic in dextran sodium sulfate‐induced colitis model in mice
Ariki, S., Ozaka, S., Sachi, N., Chalalai, T., Soga, Y., Fukuda, C., Kagoshima, Y., Ekronarongchai, S., Mizukami, K., Kamiyama, N., et al. (2023) · Genes to Cells · doi:10.1111/gtc.13008 · Cited by 9
New insights into the immunologic role of oligodendrocyte lineage cells in demyelination diseases
Li, H., Chen, Y., Niu, J., & Yi, C. (2022) · Journal of Biomedical Research · doi:10.7555/jbr.36.20220016 · Cited by 10
Interferon-β Intensifies Interleukin-23-Driven Pathogenicity of T Helper Cells in Neuroinflammatory Disease
Agasing, A. M., Quinn, J. L., Kumar, G., & Axtell, R. (2021) · Cells · doi:10.3390/cells10082139 · Cited by 7
“Rec ntly, it has been reported that GM-CSF is a key cytokine produc by TH cells which pro otes neuroinflammation [17].”
Background
Pertussis Toxin Inhibits Encephalitogenic T-Cell Infiltration and Promotes a B-Cell-Driven Disease during Th17-EAE
Maria, Z., Turner, E., Agasing, A. M., Kumar, G., & Axtell, R. C. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22062924 · Cited by 9
“Since GM-CSF-producing Th17 cells have been reported to be crucial for the induction of EAE [31,32], we speculated that the delayed disease onset and severity could be attributed to the restricted entry of this encephalitogenic T cell subset into the CNS.”
Background
The Effect of Cannabis on the Clinical and Cytokine Profiles in Patients with Multiple Sclerosis
Mustafa, W., Elgendy, N., Salama, S., Jawad, M., & Eltoukhy, K. (2021) · Multiple Sclerosis International · doi:10.1155/2021/6611897 · Cited by 7
“It induces polarization of T cells toward Th17 cells, which are the key cells in MS [64].”
Background
Regulation of mRNA stability by RBPs and noncoding RNAs contributing to the pathogenicity of Th17 cells
Zhang, Y., Wei, Z., Dong, H. F., Zhou, J., Yuan, J., Ni, B., Wu, Y., Han, C., & Tian, Y. (2020) · RNA Biology · doi:10.1080/15476286.2020.1862567 · Cited by 17
“induce autoimmune neuroinflammation [67,68].”
Cytokines and Transgenic Matrix in Autoimmune Diseases: Similarities and Differences
Szewczak, L., & Donskow-Łysoniewska, K. (2020) · Biomedicines · doi:10.3390/biomedicines8120559 · Cited by 7
“GM-CSF production by Th17 cells is stimulated by IL-23 and further GM-CSF production gives a positive feedback loop for APC (antigen presenting cells) to produce IL-23 [30].”
BackgroundInfluential
GRIM-19 Ameliorates Multiple Sclerosis in a Mouse Model of Experimental Autoimmune Encephalomyelitis with Reciprocal Regulation of IFNγ/Th1 and IL-17A/Th17 Cells
Moon, J., Lee, S. H., Lee, S.-Y., Ryu, J., Jhun, J., Choi, J., Kim, G. N., Roh, S., Park, S., & Cho, M. (2020) · Immune Network · doi:10.4110/in.2020.20.e40 · Cited by 7
“Myelin-reactive T cells that produce IFNγ, IL-17, and GM-CSF are associated with the disabilities of EAE (32-37).”
Background
Pharmacological inhibition of GSK3 promotes TNFα-induced GM-CSF via up-regulation of ERK signaling in nasopharyngeal carcinoma (NPC).
Zhao, W., Xiang, Y.-G., Zhang, Z., Liu, X., Jiang, M.-L., Jiang, B., Song, Y., & Hu, J.-Y. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.106447 · Cited by 7
Usefulness of animal models of aspergillosis in studying immunity against Aspergillus infections
Mirkov, I. I., Aleksandrov, A. P., Lazovic, B., Glamočlija, J., & Kataranovski, M. V. (2019) · Journal de Mycologie Médicale · doi:10.1016/j.mycmed.2019.01.006 · Cited by 10
Presenilin1 regulates Th1 and Th17 effector responses but is not required for experimental autoimmune encephalomyelitis
Cummings, M., Arumanayagam, A., Zhao, P., Kannanganat, S., Stüve, O., Karandikar, N., & Eagar, T. (2018) · PLoS ONE · doi:10.1371/journal.pone.0200752 · Cited by 7
“GSI treatment did not impact the frequency of T cells expressing GM-CSF suggesting a mechanism to explain the lack of clinical efficacy of GSI treatment [7, 13, 14, 76, 77].”
Strain specificities in cellular and molecular immunopathogenic mechanisms underlying development of experimental autoimmune encephalomyelitis in aged rats
Nacka-Aleksić, M., Stojić-Vukanić, Z., Pilipović, I., Vujnović, I., Bufan, B., Dimitrijević, M., & Leposavić, G. (2017) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2017.03.001 · Cited by 8
TGF-β Affects the Differentiation of Human GM-CSF+ CD4+ T Cells in an Activation- and Sodium-Dependent Manner
Éliás, S., Schmidt, A., Kannan, V., Andersson, J., & Tegner, J. N. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00603 · Cited by 6
“level In previous studies, a fraction of GM-CSF+ cells has been found to co-express some other cytokines, but this has not been tested on single-cell level in all studies (5, 11, 13, 14, 18, 35).”
BackgroundInfluential

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: Yan, Yaping
Cullimore, Melissa
Safavi, Farinaz
Zhang, Guang-Xian
Dittel, Bonnie N
Rostami, Abdolmohamad
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2011-04-24
Volume: 12
Issue: 6
Pages: 568-575
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.2031
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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The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF

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