Abstract:
:T helper-17 (Th17) cells are associated with inflammatory disorders and cancer. We report that environmental conditions resulting in cellular stress, such as low oxygen, glucose, and isotonic stress, particularly enhance the generation of Th17 cells. Pharmacological inhibition of cell stress reduces Th17 cell differentiation while stress inducers enhance the development of Th17 cells. The cellular stress response results in Th17 cell development via sustained cytoplasmic calcium levels and, in part, XBP1 activity. Furthermore, in an inflammatory environment, conditions resulting in cell stress can bring about de novo Th17 cell differentiation, even in the absence of transforming growth factor β (TGF-β) signaling. In vivo, cell stress inhibition enhances resistance to Th17-mediated autoimmunity while stress-exposed T cells enhance disease severity. Adverse metabolic environments during inflammation provide a link between adaptive immunity and inflammation and may represent a risk factor for the development of chronic inflammatory conditions by facilitating Th17 cell differentiation.
journal_name
Cell Repjournal_title
Cell reportsauthors
Brucklacher-Waldert V,Ferreira C,Stebegg M,Fesneau O,Innocentin S,Marie JC,Veldhoen Mdoi
10.1016/j.celrep.2017.05.052subject
Has Abstractpub_date
2017-06-13 00:00:00pages
2357-2370issue
11issn
2211-1247pii
S2211-1247(17)30709-Xjournal_volume
19pub_type
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