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Comment
. 2022 Mar;43(3):167-169.
doi: 10.1016/j.it.2022.01.005. Epub 2022 Jan 17.

Th17 cells: from gut homeostasis to CNS pathogenesis

Jane H Buckner  1 , Oliver J Harrison  2
Affiliations
Comment

Th17 cells: from gut homeostasis to CNS pathogenesis

Jane H Buckner et al. Trends Immunol. 2022 Mar.

Abstract

Th17 cells play crucial roles in host-microbe interactions, but can also promote chronic inflammation and tissue pathology. Factors influencing Th17 cell heterogeneity and effector functions in different inflammatory contexts remain unclear. Schnell et al. demonstrate that intestinal Th17 cells form a reservoir from which pathogenic Th17 cells can be elicited during severe tissue inflammation.

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Conflict of interest statement

Declaration of interests No interests are declared.

Figures

Figure 1:
Figure 1:. Intestinal Th17 cells contribute to the pathogenic Th17 cell pool during CNS inflammation in mice.
Homeostatic Th17 cells are enriched within intestinal tissues during homeostasis and recirculate through the spleen. During inflammation IL-23 acts directly upon SLAMF6+ Th17 cells to promote their conversion to pathogenic Th17 and ex-Th17 cells that produce IFN-γ and GM-CSF, and promote CNS tissue destruction.
See this image and copyright information in PMC

Comment on

References

    1. Ceribelli A et al. (2021) Clinical Trials Supporting the Role of the IL-17/IL-23 Axis in Axial Spondyloarthritis. Front Immunol 12, 622770. - PMC - PubMed
    1. Hueber W et al. (2012) Secukinumab, a human anti-IL-17A monoclonal antibody, for moderate to severe Crohn’s disease: unexpected results of a randomised, double-blind placebo-controlled trial. Gut 61 (12), 1693–700. - PMC - PubMed
    1. Veldhoen M et al. (2006) TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity 24 (2), 179–89. - PubMed
    1. Ghoreschi K et al. (2010) Generation of pathogenic T(H)17 cells in the absence of TGF-β signalling. Nature 467 (7318), 967–71. - PMC - PubMed
    1. Hirota K et al. (2011) Fate mapping of IL-17-producing T cells in inflammatory responses. Nat Immunol 12 (3), 255–63. - PMC - PubMed

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