Induction and molecular signature of pathogenic TH17 cells
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Interleukin 17 (IL-17)-producing helper T cells (T(H)17 cells) are often present at the sites of tissue inflammation in autoimmune diseases, which has led to the conclusion that T(H)17 cells are main drivers of autoimmune tissue injury. However, not all T(H)17 cells are pathogenic; in fact, T(H)17 cells generated with transforming growth factor-β1 (TGF-β1) and IL-6 produce IL-17 but do not readily induce autoimmune disease without further exposure to IL-23. Here we found that the production of TGF-β3 by developing T(H)17 cells was dependent on IL-23, which together with IL-6 induced very pathogenic T(H)17 cells. Moreover, TGF-β3-induced T(H)17 cells were functionally and molecularly distinct from TGF-β1-induced T(H)17 cells and had a molecular signature that defined pathogenic effector T(H)17 cells in autoimmune disease.
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Acquisition of the pathogenic phenotype of TH17 cells results from changes in the expression of proteins involved in pathology.
“the acquisition of the pathogenic phenotype of TH17 cells results from changes in the expression of proteins involved in pathology (Lee et al., 2012).”
From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Lee et al., 2012
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Doss, P. M. I. A., Umair, M., Baillargeon, J., Fazazi, R., Fudge, N., Akbar, I., Yeola, A. P., Williams, J. B., Leclercq, M., Joly-Beauparlant, C., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.108833 · Cited by 39 · see citing works
Harpaz, I., Bhattacharya, U., Elyahu, Y., Strominger, I., & Monsonego, A. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00283 · Cited by 22 · see citing works
Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1
Uluçkan, Ö., Jiménez, M., Roediger, B., Schnabl, J., Díez-Córdova, L. T., Troulé, K., Weninger, W., & Wagner, E. F. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.09.042 · Cited by 21 · see citing works
- Authors
- Lee, Y., Awasthi, A., Yosef, N., Quintana, F. J., Xiao, S., Peters, A., Wu, C., Kleinewietfeld, M., Kunder, S., Hafler, D. A., Sobel, R. A., Regev, A., & Kuchroo, V. K.
- Affiliations
- Brigham and Women's Hospital (US)
- Broad Institute (US)
- Yale University (US)
- VA Palo Alto Health Care System (US)
- Corresponding author
- Awasthi, Amit
- Kuchroo, Vijay K
- ORCID
- Venue
- Nature Immunology
- Published
- 2012-09-09
- Volume
- 13
- Issue
- 10
- Pages
- 991-999
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC3459594
- OpenAlex
- W2009675211
- Cited by
- 1,174
- References
- 9
- Citations by year
- 2026: 45 · 2025: 65 · 2024: 76 · 2023: 88 · 2022: 96 · 2021: 114 · 2020: 74 · 2019: 73 · 2018: 96 · 2017: 109 · 2016: 92 · 2015: 83 · 2014: 84 · 2013: 71 · 2012: 6
- FWCI
- 34.13
- 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)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (DP1OD003958)
- National Human Genome Research Institute (P01HG005062)
- National Institute of Allergy and Infectious Diseases (R00AI075285, K99AI075285, R01AI093903, P01AI045757, P01AI073748, AI075285, AI073748, AI045757, R01AI091568, AI093903, R56AI093903, P01AI039671)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK090105)
- National Institute of Neurological Disorders and Stroke (R01NS030843, R29NS030843, NS030843, NS045937, R37NS030843, R01NS045937)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- IL-23, TGF-beta3, TGF-β1, IL-17, interleukin-6, autoimmune disease, molecular signatures, T cell differentiation, tissue inflammation
- MeSH terms
- Animals, Autoimmune Diseases, Cell Differentiation, Humans, Inflammation, Interleukin-6, Interleukin-17, Mice, Interleukin-23, Transforming Growth Factor beta1, Transforming Growth Factor beta3, Th17 Cells
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