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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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Ghilas, S., O’Keefe, R. N., Mielke, L. A., Raghu, D., Büchert, M., & Ernst, M. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.944982 · Cited by 30
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“This work was supported by grants from the National Natural Science Foundation of China (81570834), the Tianjin Municipal Science and Technology Commission (13JCYBJC23300), and the Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry (48).”
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“directly in the target tissue upon infiltration and reactivation of self-reactive T cells (47, 48) or by target tissue-specific expression of GM-CSF as a transgene (51, 52) fosters autoimmunity.”
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Suppression of Experimental Autoimmune Encephalomyelitis by ILT3.Fc
Xu, Z., Lin, C.-C., Ho, S., Vlad, G., & Suciu-Foca, N. (2020) · Journal of Immunology · doi:10.4049/jimmunol.2000265 · Cited by 16
Zhang, L., Sun, P., Zhang, Y., Xu, Y., & Sun, Y. (2020) · Biochemical and Biophysical Research Communications - BBRC · doi:10.1016/j.bbrc.2020.06.073 · Cited by 16
Deciphering targets of Th17 cells fate: From metabolism to nuclear receptors
Boldrini, V. O., Farias, A. S., & Degasperi, G. (2019) · Scandinavian Journal of Immunology · doi:10.1111/sji.12793 · Cited by 16
Stojić-Vukanić, Z., Pilipović, I., Vujnović, I., Nacka-Aleksić, M., Petrović, R., Arsenović-Ranin, N., Dimitrijević, M., & Leposavić, G. (2016) · PLoS ONE · doi:10.1371/journal.pone.0166498 · Cited by 15
Novel Insights and Therapeutics in Multiple Sclerosis
Wagner, C., & Goverman, J. (2015) · F1000Research · doi:10.12688/f1000research.6378.1 · Cited by 16
GM-CSF production by CD4+ T cells in MS patients: Regulation by regulatory T cells and vitamin D
Peelen, E., Muris, A., Damoiseaux, J. G. M. C., Knippenberg, S. A. M., Broens, K., Smolders, J., Tervaert, J.-W. C., Hupperts, R., & Thewissen, M. M. (2015) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2015.02.007 · Cited by 16
“, 2011), but also in inducing production of granulocyte-macrophage-colonystimulating factor (GM-CSF) by T cells (El-Behi et al., 2011).”
BackgroundResultInfluentialT‐bet or not T‐bet: Taking the last bow on the autoimmunity stage
Spath, S., & Becher, B. (2013) · European Journal of Immunology · doi:10.1002/eji.201344109 · Cited by 16
Cholera Toxin Directly Enhances IL-17A Production from Human CD4+ T Cells
Tsai, H., & Wu, R. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1301079 · Cited by 17
“Whether GM-CSF secreted from CT-treated T cells also has this IL-23/GM-CSF loop to enhance Th17 cell function in vivo needs to be clarified.”
BackgroundInfluentialHuman Aquaporin 4281–300 Is the Immunodominant Linear Determinant in the Context of HLA-DRB1*03:01
Arellano, B., Hussain, R. Z., Zacharias, T., Yoon, J., David, C., Zein, S., Steinman, L., Forsthuber, T., Greenberg, B., Lambracht-Washington, D., et al. (2012) · Archives of Neurology · doi:10.1001/archneurol.2012.1300 · Cited by 16
“TH17 cells have also been shown to play a critical role in the production of GM-CSF in the periphery and CNS.(27,28) Our group and other investigators recently found that GM-CSF may play a critical role in different models of active and passive experimental autoimmune encephalomyelitis.”
BackgroundDefective autophagy in CD4 T cells drives liver fibrosis via type 3 inflammation
Sayegh, R. A., Wan, J., Caër, C., Azoulai, M., Gasperment, M., Baweja, S., Chouillard, M.-A., Kandiah, J., Cadoux, M., Mabire, M., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-59218-y · Cited by 20
Alghibiwi, H. K., Ansari, M. A., Nadeem, A., Algonaiah, M. A., Attia, S. M., Bakheet, S. A., Albekairi, T. H., Almudimeegh, S., Alhamed, A. S., Shahid, M., et al. (2023) · Biomedicines · doi:10.3390/biomedicines11061511 · Cited by 16
“GM-CSF has been demonstrated to be critical for EAE pathogenesis due to the role it plays in driving the mobilization and activation of neutrophils [19].”
BackgroundTranslating the biology of β common receptor-engaging cytokines into clinical medicine
Pant, H., Hercus, T. R., Tumes, D. J., Yip, K. H., Parker, M. W., Owczarek, C. M., Lopez, A. F., & Huston, D. P. (2022) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2022.09.030 · Cited by 21
STAT1 signaling protects self-reactive T cells from control by innate cells during neuroinflammation
Arbelaez, C. A., Palle, P., Charaix, J., & Bettelli, E. (2022) · JCI Insight · doi:10.1172/jci.insight.148222 · Cited by 18
“CD4 + T cells with the potential to induce EAE include subsets secreting IL-17, and GM-CSF with concomitant expression of IFN-γ (3).”
InfluentialDhaliwal, M., Tyagi, R., Malhotra, P., Barman, P., Loganathan, S. K., Sharma, J., Sharma, K., Mondal, S., Rawat, A. K., & Singh, S. (2022) · Frontiers in Pediatrics · doi:10.3389/fped.2022.790273 · Cited by 15
Rasouli, J., Casella, G., Ishikawa, L. L. W., Thomé, R., Boehm, A., Ertel, A., Melo‐Silva, C. R., Mari, E. R., Porazzi, P., Zhang, W., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.679498 · Cited by 17
“As previously described (26), Csf2 mice developed mild clinical EAE, with fewer immune cells in the CNS than in WT mice.”
BackgroundResultSelf-citationE3 Ubiquitin Ligase Von Hippel–Lindau Protein Promotes Th17 Differentiation
Chitrakar, A., Budda, S. A., Henderson, J. G., Axtell, R. C., & Zenewicz, L. A. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.2000243 · Cited by 15
Guo, R., Zhao, Y., Li, J., Gu, Y., Huo, H.-X., Li, S., Song, Y., Zhu, Z., & Tu, P. (2017) · Frontiers in Pharmacology · doi:10.3389/fphar.2017.00281 · Cited by 16
“The initial development of Th17 cells from naive CD4 T cells is directed by TGF-β in combination with IL-6, and this process is enhanced by IL-1β and TNF-α, whereas IL-23 is required for the terminal differentiation of Th17 cells into mature effector cells (Ogura et al., 2008; McGeachy et al., 2009; El-Behi et al., 20…”
BackgroundNa, H., Im, K.-I., Kim, N., Lee, J., Gil, S., Min, G. J., & Cho, S. (2024) · iScience · doi:10.1016/j.isci.2024.109783 · Cited by 13
“59,60 Induction of the Th1 and Th17 pathways suppresses Th2 and Treg cell actions and thus increases the severity of acute GVHD after allo-BMT.”
BackgroundDamage-Associated Molecular Patterns, a Class of Potential Psoriasis Drug Targets
Gao, Y., Gong, B., Chen, Z., Song, J., Xu, N., & Weng, Z. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25020771 · Cited by 15
“Additionally, inflammatory factors such as IL-6 and IL-23 can stimulate Th17 proliferation and induce Th17 to release pro-inflammatory factors such as IL-17A, IL-17F, IL-22, and GM-CSF [38,39].”
BackgroundYang, Z., Wang, T., Wang, B., Gao, H., He, C., Shang, H., Lü, X., Wang, Y., & Xu, J. (2022) · Journal of Inflammation · doi:10.1186/s12950-022-00311-0 · Cited by 15
Decoupling the role of RORγt in the differentiation and effector function of T H 17 cells
Zhong, X., Wu, H., Zhang, W., Gwack, Y., Shang, W., Lee, K. O., Isakov, N., He, Z., & Sun, Z. (2022) · Science Advances · doi:10.1126/sciadv.adc9221 · Cited by 16
“Differentiated TH17 cells are able to induce tissue inflammation involved in the pathogenesis of autoimmune diseases, including psoriasis, inflammatory bowel disease, and multiple sclerosis (2, 3, 14).”
BackgroundPiper, C., Hainstock, E., Yin-Yuan, C., Chen, Y., Khatun, A., Kasmani, M. Y., Evans, J., Miller, J. A., Gorski, J., Cui, W., et al. (2022) · Blood Advances · doi:10.1182/bloodadvances.2021006084 · Cited by 14
SerpinB1 expression in Th17 cells depends on hypoxia-inducible factor 1-alpha
Hou, L., & Yuki, K. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.106826 · Cited by 16
Kuo, P., Brown, D. A., Scofield, B. A., Paraiso, H. C., Wang, P., Yu, I.-C. I., & Yen, J.-H. J. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.03.010 · Cited by 16
“GM-CSF, which was shown to promote neuroinflammation in EAE (El-Behi et al., 2011; Shiomi et al., 2015), was also upregulated in MG activated with LPS, but downregulated in MG activated with LPS in the presence of ACDT (Fig 3B).”
BackgroundSerre, L., Girard, M., Ramadan, A., Menut, P., Rouquié, N., Lucca, L. E., Mahiddine, K., Léobon, B., Mars, L. T., & Guerder, S. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1700667 · Cited by 15
Zielinski, C. E. (2017) · Immunology Letters · doi:10.1016/j.imlet.2017.08.001 · Cited by 13
γδ T Cells and NK Cells – Distinct Pathogenic Roles as Innate-Like Immune Cells in CNS Autoimmunity
Edwards, S. C., McGinley, A. M., McGuinness, N. C., & Mills, K. H. G. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2015.00455 · Cited by 15
Guo, W., Wang, C., Wang, X., Luo, C., Yu, D.-M., Wang, Y.-H., Chen, Y., Lei, W., Gao, X.-D., & Yao, W. (2015) · OncoTarget · doi:10.18632/oncotarget.5164 · Cited by 14
Autoimmunity beyond Th17: GM-CSF producing T cells
Zielinski, C. E. (2014) · Cell Cycle · doi:10.4161/15384101.2014.946377 · Cited by 14
Immunoregulatory Effects of Interferon-β in Suppression of Th17 cells
Pennell, L. M., & Fish, E. N. (2013) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2013.0088 · Cited by 14
Kim, Y., Oh, K., Song, H., Lee, D.-S., & Park, S. (2013) · Journal of Medicinal Chemistry · doi:10.1021/jm400949h · Cited by 14
Adaptive Immune Responses in CNS Autoimmune Disease: Mechanisms and Therapeutic Opportunities
McPherson, R. C., & Anderton, S. (2013) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-013-9453-9 · Cited by 14
Th17 cell promotes apoptosis of IL-23R+ neurons in experimental autoimmune encephalomyelitis
Sonar, S. A., Meitei, H. T., Karmakar, S., Mishra, A., Inamdar, S., Lenka, N., & Lal, G. (2024) · Clinical Immunology · doi:10.1016/j.clim.2024.109898 · Cited by 15
Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis
Pascual, D. W., Goodwin, Z. I., Bhagyaraj, E., Hoffman, C. A., & Yang, X. (2022) · Frontiers in Microbiology · doi:10.3389/fmicb.2022.1018165 · Cited by 18
“Th17 cells have been reported to produce GM-CSF and IL-22 following RORγt activation (Liang et al., 2006; Zheng et al., 2007; Codarri et al., 2011; El-Behi et al., 2011).”
BackgroundInterleukin-38 in atherosclerosis.
Zhang, X.-H., Li, Y., Zhou, L., & Tian, G.-P. (2022) · Clinica chimica acta; international journal of clinical chemistry · doi:10.1016/j.cca.2022.09.017 · Cited by 13
S1P analogues SEW2871, BAF312 and FTY720 affect human Th17 and Treg generation ex vivo
Okuş, F. Z., Azizoğlu, Z. B., Canatan, H., & Eken, A. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.108665 · Cited by 14
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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