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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Background
Central Nervous System Barriers Impact Distribution and Expression of iNOS and Arginase-1 in Infiltrating Macrophages During Neuroinflammation
Ivan, D. C., Walthert, S., & Locatelli, G. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.666961 · Cited by 27
“While the GM-CSF-mediated upregulation of the anti-inflammatory gene Arg1 appears somewhat in contrast wi th the d i sease -dr iv ing func t ion of GM-CSF in neuroinflammatory models (67, 68), MoCs stimulated with GM-CSF have been described as cells sharing pro- and antiinflammatory characteristics (50–52), with a rec…”
Background
NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain
Lee, J., Cho, W., Yu, J., & Hyun, Y. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03468-6 · Cited by 26
Granulocyte-macrophage colony-stimulating factor: an immunotarget for sepsis and COVID-19
Mu, X., Liu, K., Li, H., Wang, F.-S., & Xu, R.-N. (2021) · Cellular & Molecular Immunology · doi:10.1038/s41423-021-00719-3 · Cited by 26
“In another experimental autoimmune encephalomyelitis mouse model, it was reported that GM-CSF is critical for the proinflammatory functions of Th17 cells; GM-CSF blockade, but not IL-17 depletion, may efficiently inhibit tissue inflammation [4].”
Background
Potential for Targeting Myeloid Cells in Controlling CNS Inflammation
Ifergan, I., & Miller, S. D. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.571897 · Cited by 33
“However, in 2011, the CNS pathogenicity of TH17 cells was reported to be primarily associated with their production of GM-CSF (59, 60).”
BackgroundInfluential
Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis
Yang, M., Sun, L., Han, J., Zheng, C., Liang, H., Zhu, J., & Jin, T. (2019) · Molecular Brain · doi:10.1186/s13041-019-0532-6 · Cited by 32
Scopoletin Suppresses Activation of Dendritic Cells and Pathogenesis of Experimental Autoimmune Encephalomyelitis by Inhibiting NF-κB Signaling
Zhang, F., Zhang, Y., Yang, T., Ye, Z.-Q., Tian, J., Fang, H.-R., Han, J., Wang, Z.-Z., & Li, X. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00863 · Cited by 26
The Multiple Roles of B Cells in Multiple Sclerosis and Their Implications in Multiple Sclerosis TherapiesPreprint
Li, R., & Bar‐Or, A. (2018) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a029108 · Cited by 32
“GM-CSF knockoutmice are resistant to active EAE induction (McQualter et al. 2001) and GM-CSF-deficient Th17 cells fail to induce passive EAE (Ponomarev et al. 2007; Codarri et al. 2011; El-Behi et al. 2011).”
Background
Regulation of Th17 Differentiation by IKKα-Dependent and -Independent Phosphorylation of RORγt
He, Z., Wang, F., Zhang, J., Sen, S., Pang, Q., Luo, S., Gwack, Y., & Sun, Z. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1700457 · Cited by 29
Dendritic cells as therapeutic targets in neuroinflammation
Lüssi, F., Zipp, F., & Witsch, E. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2170-9 · Cited by 26
“This approach is currently investigated in phase II clinical trials in patients with rheumatoid arthritis in which two antibodies (MOR103 and KB003) designed to block GM-CSF signalling are being tested, after MOR103 demonstrated preliminary evidence of efficiency in this autoimmune disease [209].”
BackgroundInfluential
Autoreactive Tbet-Positive CD4 T Cells Develop Independent of Classic Th1 Cytokine Signaling during Experimental Autoimmune Encephalomyelitis
Yeh, W.-I., McWilliams, I. L., & Harrington, L. E. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1100031 · Cited by 26
“expression of this cytokine by CD4 T cells is essential for the development of EAE (18, 19).”
Background
Transgenic Expression of GM-CSF in T Cells Causes Disseminated Histiocytosis
van Nieuwenhuijze, A. E. M., Coghill, E., Gray, D. H. D., Prato, S., Metcalf, D., Alexander, W. S., & Wicks, I. P. (2013) · American Journal Of Pathology · doi:10.1016/j.ajpath.2013.09.014 · Cited by 27
Prevention effect of total ginsenosides and ginseng extract from Panax ginseng on cyclophosphamide‐induced immunosuppression in mice
Zhang, H., Sun, Y., Fan, M., Zhang, Y., Liang, Z., Zhang, L.-C., Gao, X., He, X., Li, X., Zhao, D.-Q., et al. (2023) · Phytotherapy Research · doi:10.1002/ptr.7836 · Cited by 25
“IL-1 or TGF-β plus IL-6 stimulate Th17 to produce the IL-17A, IL-10, and GM-CSF, which participate in autoimmune diseases and granulocyte-dependent responses (El-Behi et al., 2011).”
Background
METTL3 inhibits autoreactive Th17 cell responses in experimental autoimmune uveitis via stabilizing ASH1L mRNA
Zhao, L., Liu, Y., Ma, B., Liu, X., Wei, R., & Nian, H. (2023) · The FASEB Journal · doi:10.1096/fj.202201548r · Cited by 26
Advancements in the Alcohol-Associated Liver Disease Model
Zhu, L., Li, H.-D., Xu, J., Li, J., Cheng, M., Meng, X., Huang, C., & Li, J. (2022) · Biomolecules · doi:10.3390/biom12081035 · Cited by 30
“Furthermore, macrophages activate T helper cells to release IL-17 by producing IL-23, which, in turn, mediates neutrophil production/release through an increase in granulocyte colonystimulating factor [88].”
Background
Myeloid caspase-8 restricts RIPK3-dependent proinflammatory IL-1β production and CD4 T cell activation in autoimmune demyelination
Kim, S.-J., Lu, H. C., Steelman, A. J., & Li, J. (2022) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2117636119 · Cited by 25
Neuroinflammation in Autoimmune Disease and Primary Brain Tumors: The Quest for Striking the Right Balance
Mitchell, D. K., Shireman, J. M., Potchanant, E. A. S., Lara-Velazquez, M. A., & Dey, M. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.716947 · Cited by 27
Increased GM‐CSF‐producing NCR‐ ILC3s and neutrophils in the intestinal mucosa exacerbate inflammatory bowel disease
Chang, Y.-N., Kim, J. W., Yang, S., Chung, D., Ko, J., Moon, J., & Kim, H. Y. (2021) · Clinical & Translational Immunology · doi:10.1002/cti2.1311 · Cited by 25
“Although GM-CSF has a protective effect, it also acts as an essential mediator of tissue inflammation.(35,36) GM-CSF exacerbates colitis by promoting the accumulation of Ly-6C inflammatory monocytes(17,18); namely, NCR ILC3s promote inflammation through GM-CSF-induced accumulation of inflammatory monocytes in the anti…”
Background
Invasive fungal disease and the immunocompromised host including allogeneic hematopoietic cell transplant recipients: Improved understanding and new strategic approach with sargramostim
Chu, S., McCormick, T. S., Lazarus, H. M., Leal, L. O., & Ghannoum, M. A. (2021) · Clinical Immunology · doi:10.1016/j.clim.2021.108731 · Cited by 30
REGγ controls Th17 cell differentiation and autoimmune inflammation by regulating dendritic cells
Zhou, L., Yao, L., Zhang, Q., Xie, W., Wang, X., Zhang, H., Xu, J., Lin, Q., Li, Q., Yang, X., et al. (2019) · Cellular and Molecular Immunology · doi:10.1038/s41423-019-0287-0 · Cited by 29
Therapeutic suppression of pulmonary neutrophilia and allergic airway hyperresponsiveness by an RORγt inverse agonist
Whitehead, G. S., Kang, H. S., Thomas, S. Y., Medvedev, A. V., Karcz, T. P., Izumi, G., Nakano, K., Makarov, S., Nakano, H., Jetten, A. M., et al. (2019) · JCI Insight · doi:10.1172/jci.insight.125528 · Cited by 24
“As seen in the previous experiments, TNF was also significantly reduced, whereas GM-CSF was not.”
BackgroundInfluential
In Vitro Th17-Polarized Human CD4+ T Cells Exacerbate Xenogeneic Graft-versus-Host Disease
Delens, L., Ehx, G., Somja, J., Vrancken, L., Belle, L., Seidel, L., Grégoire, C., Fransolet, G., Ritacco, C., Hannon, M., et al. (2018) · Transplantation and Cellular Therapy · doi:10.1016/j.bbmt.2018.10.007 · Cited by 25
STAT-3–independent production of IL-17 by mouse innate-like αβ T cells controls ocular infection
Leger, A. J. S., Hansen, A. M., Karaüzüm, H., Horai, R., Yu, C., Laurence, A. D. J., Mayer-Barber, K. D., Silver, P. B., Villasmil, R., Egwuagu, C. E., et al. (2018) · The Journal of Experimental Medicine · doi:10.1084/jem.20170369 · Cited by 25
“The cytokines IL-23, IL-6, and IL-21 are all known to induce IL-17 production in CD4+ T cells by activation of STAT-3, which is considered to be a critical activating signal for the induction and maintenance of the Th17 lineage (Bettelli et al., 2006; Harris et al., 2007; Huber et al., 2009; Ghoreschi et al., 2010; El…”
Background
Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signaling
Seshadri, S., Allan, D., Carlyle, J. R., & Zenewicz, L. A. (2017) · PLoS Pathogens · doi:10.1371/journal.ppat.1006690 · Cited by 26
“GM-CSF also promotes an inflammatory environment for the adaptive arm of the immune system, especially in Th17 cell biology [64, 65].”
Background
Midkine and multiple sclerosis
Takeuchi, H. (2014) · British Journal of Pharmacology · doi:10.1111/bph.12499 · Cited by 25
“…et al., 2006; Ivanov et al., 2006; Mangan et al., 2006; Weaver et al., 2006; Codarri BJP British Journal ofPharmacology DOI:10.1111/bph.12499 www.brjpharmacol.org British Journal of Pharmacology (2014) 171 931–935 931© 2013 The British Pharmacological Society et al., 2011; El-Behi et al., 2011).”
BackgroundInfluential
Lymphocytes with Cytotoxic Activity Induce Rapid Microtubule Axonal Destabilization Independently and before Signs of Neuronal Death
Miller, N. M., Shriver, L. P., Bodiga, V. L., Ray, A., Basu, S., Ahuja, R., Jana, A., Pahan, K., & Dittel, B. N. (2013) · ASN NEURO · doi:10.1042/an20120087 · Cited by 19
“Although the exact mechanisms whereby CD4 T-cells drive CNS autoimmunity are not well understood, both cell types produce GM-CSF (granulocyte/macrophage colony-stimulating factor), a key cytokine required for the initiation of disease (El-Behi et al. 2011; McQualter et al., 2001; Ponomarev et al., 2007).”
BackgroundSelf-citation
Th17 Cells Induce a Distinct Graft Rejection Response That Does Not Require IL-17A
Agorogiannis, E. I., Regateiro, F. S., Howie, D., Waldmann, H., & Cobbold, S. P. (2012) · American Journal of Transplantation · doi:10.1111/j.1600-6143.2011.03971.x · Cited by 23
“It is also possible that neither IL-17A nor IL-17F are essential to the rejection process mediated by Th17 cells (59), with granulocytemacrophage colony stimulating factor (CSF2) (60,61) and IL-22 (62) as other candidates to be excluded.”
Background
Complexity of enthesitis and new bone formation in ankylosing spondylitis: current understanding of the immunopathology and therapeutic approaches
Kusuda, M., Haroon, N., & Nakamura, A. (2021) · Modern Rheumatology · doi:10.1093/mr/roab057 · Cited by 26
The Involvement of Lactosylceramide in Central Nervous System Inflammation Related to Neurodegenerative Disease
Yu, W. H., Ying, J., Wang, X., Liu, X., Zhao, T., Yoon, S., Zheng, Q., Fang, Y., Yang, D., & Hua, F. (2021) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2021.691230 · Cited by 29
“With the increasing life expectancy and aging of the global population, the number of patients with neurodegenerative diseases is continuously increasing (Feigin et al., 2017; GBD 2015 Neurological Disorders Collaborator Group, 2017).”
Background
Deficiency of IL-27 Signaling Exacerbates Experimental Autoimmune Uveitis with Elevated Uveitogenic Th1 and Th17 Responses
Wu, S., Ma, R., Zhong, Y., Chen, Z., Zhou, H., Zhou, M., Chong, W. P., & Chen, J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22147517 · Cited by 24
“For example, although Th1 cells and their signature cytokine IFN-γ are demonstrated to be pathogenic in EAU [13], innate IFN-γ from natural killer (NK) cells and natural killer T (NKT) cells are protective, as systemic depletion of IFN-γ exacerbates the disease development, in association with elevated Th17 response,…”
BackgroundInfluential
IL-9 Controls Central Nervous System Autoimmunity by Suppressing GM-CSF Production
Yoshimura, S., Thomé, R., Konno, S., Mari, E. R., Rasouli, J., Hwang, D., Boehm, A., Lǐ, Y., Zhang, G., Ćirić, B., et al. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1801113 · Cited by 25
“inflammation by activating CNS-infiltrating myeloid cells, such as monocytes and dendritic cells (DCs), and perpetuating inflammation (4, 5).”
BackgroundSelf-citation
Estrogen Signaling in Bystander Foxp3neg CD4+ T Cells Suppresses Cognate Th17 Differentiation in Trans and Protects from Central Nervous System Autoimmunity
Garnier, L., Laffont, S., Lélu, K., Yogev, N., Waisman, A., & Guéry, J. (2018) · The Journal of Immunology · doi:10.4049/jimmunol.1800417 · Cited by 24
“genic Th17 cells is essential for the induction of neuroinflammation in EAE (34, 35).”
Background
The epigenetic drug Trichostatin A ameliorates experimental autoimmune encephalomyelitis via T cell tolerance induction and impaired influx of T cells into the spinal cord
Jayaraman, A. K., Soni, A., Prabhakar, B. S., Holterman, M., & Jayaraman, S. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.07.015 · Cited by 26
“[50-52] or Th17 cells alone [45-46, 49-51], could mediate EAE.”
Background
Alphavirus Encephalomyelitis: Mechanisms and Approaches to Prevention of Neuronal Damage
Griffin, D. E. (2016) · Neurotherapeutics · doi:10.1007/s13311-016-0434-6 · Cited by 25
“cells and recruits myeloid cells into the CNS, but themechanism by which this leads to disease has not been identified [47, 50, 51].”
Background
The balance of intestinal Foxp3 + regulatory T cells and Th17 cells and its biological significance
Shen, X., Du, J., Guan, W., & Zhao, Y. L. (2014) · Expert Review of Clinical Immunology · doi:10.1586/1744666x.2014.882232 · Cited by 25
Subclinical CNS Inflammation as Response to a Myelin Antigen in Humanized Mice
Zayoud, M., Malki, K., Frauenknecht, K., Trinschek, B., Kloos, L., Karram, K., Wanke, F., Georgescu, J., Hartwig, U., Sommer, C., et al. (2013) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-013-9466-4 · Cited by 24
“We speculate that mouse monocytes cannot replace human monocytes in our model due to lack of compatible receptors for human T cell derived cytokines important in EAE such as GM-CSF (Codarri et al. 2011; El-Behi et al. 2011).”
Background
Adult Onset Still's Disease and Autoinflammation
Efthimiou, P., Moorthy, L. N., Mavragani, C. P., Skokos, D., & Fautrel, B. (2012) · International Journal of Inflammation · doi:10.1155/2012/964751 · Cited by 24
IFN-γ protects from lethal IL-17 mediated viral encephalomyelitis independent of neutrophils
Savarin, C., Stohlman, S., Hinton, D., Ransohoff, R., Cua, D., & Bergmann, C. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-104 · Cited by 24
“These include excessive CNS neutrophil infiltration and release of degrading enzymes, free radicals and pro-inflammatory cytokines, direct IL-17-mediated neuronal toxicity [25] , and/or secretion of granulocyte macrophage colonystimulating factor (GM-CSF) as the pathogenic effector molecule [26] [27] [28] .”
BackgroundInfluential
Adjuvant immunotherapy of Experimental Autoimmune Encephalomyelitis: Immature Myeloid Cells Expressing CXCL10 and CXCL16 attract CXCR3+CXCR6+ and myelin-specific T cells to the draining lymph nodes rather than the CNS ,
O'Connor, R., Li, X., Blumerman, S., Anderton, S., Noelle, R., & Dalton, D. (2012) · Journal of Immunology · doi:10.4049/jimmunol.1101118 · Cited by 24
Unbiased Single‐Cell Sequencing of Hematopoietic and Immune Cells from Aplastic Anemia Reveals the Contributors of Hematopoiesis Failure and Dysfunctional Immune Regulation
Guo, R., Kong, J., Tang, P., Wang, S., Sang, L., Liu, L., Guo, R., Yan, K., Qi, M. Y., Bian, Z., et al. (2023) · Advanced Science · doi:10.1002/advs.202304539 · Cited by 21
JAK inhibition ameliorated experimental autoimmune encephalomyelitis by blocking GM-CSF-driven inflammatory signature of monocytes
Shao, S., Chen, C., Shi, G.-N., Zhou, Y., Wei, Y.-Z., Wu, L., Sun, L., & Zhang, T.-T. (2023) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2023.07.026 · Cited by 23
The Search for the Pathogenic T Cells in the Joint of Rheumatoid Arthritis: Which T-Cell Subset Drives Autoimmune Inflammation?
Yamada, H. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24086930 · Cited by 29
“In mice, GM-CSF is a critical effector cytokine defining the pathogenicity of Th17 cells [25].”
Background
Recombinant human granulocyte macrophage-colony stimulating factor expressed in yeast (sargramostim): A potential ally to combat serious infections
Damiani, G. B., McCormick, T. S., Leal, L. O., & Ghannoum, M. A. (2019) · Clinical Immunology · doi:10.1016/j.clim.2019.108292 · Cited by 26
The connection between the Th17 cell related cytokines and cancer stem cells in cancer: Novel therapeutic targets
Shahid, A., & Bharadwaj, M. (2019) · Immunology Letters · doi:10.1016/j.imlet.2019.07.001 · Cited by 24
GM-CSF producing autoreactive CD4+ T cells in type 1 diabetes
Knoop, J., Gavrisan, A., Kuehn, D., Reinhardt, J., Heinrich, M., Hippich, M., Eugster, A., Ockert, C., Ziegler, A., & Bonifacio, E. E. (2017) · Clinical Immunology · doi:10.1016/j.clim.2017.12.002 · Cited by 21
Granulocyte-Macrophage Colony Stimulatory Factor Enhances the Pro-Inflammatory Response of Interferon-γ-Treated Macrophages to Pseudomonas aeruginosa Infection
Singh, S., Barr, H. L., Liu, Y., Robins, A., Heeb, S., Williams, P. M., Fogarty, A., Cámara, M., & Martínez‐Pomares, L. (2015) · PLoS ONE · doi:10.1371/journal.pone.0117447 · Cited by 23
“Also, recent publications indicate that GM-CSF production by Th17 cells is responsible for their pathological role during chronic inflammation [47,48].”
Background
Similarities and Differences Between Juvenile and Adult Spondyloarthropathies
Fisher, C., Ciurtin, C., Leandro, M. J., Sen, D., & Wedderburn, L. R. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2021.681621 · Cited by 31
“IL23 is less well-studied in ERA.”
BackgroundInfluential
Selective Endocannabinoid Reuptake Inhibitor WOBE437 Reduces Disease Progression in a Mouse Model of Multiple Sclerosis
Reynoso-Moreno, I., Tietz, S., Vallini, E., Engelhardt, B., Gertsch, J., & Chicca, A. (2021) · ACS Pharmacology & Translational Science · doi:10.1021/acsptsci.0c00214 · Cited by 28
PD-1 Blockade Reverses Obesity-Mediated T Cell Priming Impairment
Le, C. T., Khuat, L. T., Caryotakis, S. E., Wang, M., Dunai, C., Nguyen, A. V., Vick, L. V., Stoffel, K. M., Blazar, B. R., Monjazeb, A. M., et al. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.590568 · Cited by 19

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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