Induction and molecular signature of pathogenic TH17 cells

By Youjin Lee, A. Awasthi, Nir Yosef, F. Quintana, S. Xiao, A. Peters, Chuan Wu, Markus Kleinewietfeld, Sharon Kunder, David A. Hafler and 3 more. Nature Immunology, 2012

1,152 citations recorded by the source corpus.

Interleukin 17 (IL-17)-producing helper T cells (TH17 cells) are often present at the sites of tissue inflammation in autoimmune diseases, which has led to the conclusion that TH17 cells are main drivers of autoimmune tissue injury. However, not all TH17 cells are pathogenic; in fact, TH17 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 TH17 cells was dependent on IL-23, which together with IL-6 induced very pathogenic TH17 cells. Moreover, TGF-β3-induced TH17 cells were functionally and molecularly distinct from TGF-β1-induced TH17 cells and had a molecular signature that defined pathogenic effector TH17 cells in autoimmune disease.

Subfields: Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/fabc2f28e52b3e702ac67c4d1d753a3a0dbafcaa

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Citations in the corpus

TGF-β Activation and Function in Immunity (2013, background): “Indeed, recent evidence has suggested that, during differentiation of Th17 cells, different isoforms of TGF-β may activate different Smad signaling pathways (12).”
The intestinal microbiota modulates the anticancer immune effects of cyclophosphamide (2013, background): “CTX increased the frequency of “pathogenic “Th17 (pTh17) cells, which share hallmarks of Th1 cells (nuclear expression of the transcription factor T-bet, cytoplasmic expression of IFNγ and surface exposure of the chemokine receptor CXCR3) and Th17 cells (expression of RORγt, IL-17 and CCR6) (17, 18)”
Single-cell Genomics Unveils Critical Regulators of Th17 cell Pathogenicity (2015, neutral): “A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript of signature genes of pathogenic T cells (Lee et al., 2012) or of other CD4+ lineages (columns) and the single-cell expression of any other ”
Regulation of the immune response by the aryl hydrocarbon receptor (2018, background): “Collectively, these data identify a role for AhR during the early stages of the differentiation of Th17 cells, at a stage when they produce IL-10 and their pathogenic potential has not fully developed (McGeachy et al., 2007; Lee et al., 2012).”