Stress hormone signalling inhibits Th1 polarization in a CD4 T‐cell‐intrinsic manner via mTORC1 and the circadian gene PER1 [* Cross-Reference *]

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Christophe Capelle; Anna Chen; Ni Zeng; Alexandre Baron; Kamil Grzyb; Thaís Arns; Alexander Skupin; Markus Ollert; Feng He, 2026, "Stress hormone signalling inhibits Th1 polarization in a CD4 T‐cell‐intrinsic manner via mTORC1 and the circadian gene PER1 [* Cross-Reference *]", https://lore.list.lu/citation?persistentId=perma:LIST.DW9FJ9, LIST Open Repository, V1
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Description
Stress hormones are believed to skew the CD4 T-cell differentiation towards a Th2 response via a T-cell-extrinsic mechanism. Using isolated primary human naïve and memory CD4 T cells, here we show that both adrenergic- and glucocorticoid-mediated stress signalling pathways play a CD4 naïve T-cell-intrinsic role in regulating the Th1/Th2 differentiation balance. Both stress hormones reduced the Th1 programme and cytokine production by inhibiting mTORC1 signalling via two parallel mechanisms. Stress hormone signalling inhibited mTORC1 in naïve CD4 T cells (1) by affecting the PI3K/AKT pathway and (2) by regulating the expression of the circadian rhythm gene, period circadian regulator 1 (PER1). Both stress hormones induced the expression of PER1, which inhibited mTORC1 signalling, thus reducing Th1 differentiation. This previously unrecognized cell-autonomous mechanism connects stress hormone signalling with CD4 T-cell differentiation via mTORC1 and a specific circadian clock gene, namely PER1. (2022-02-10)
***This entry has been automatically imported via OpenAlex by LIST harvest scripts. Please refer to https://doi.org/10.1111/imm.13448 for the original and latest version of the publication*** (2026-07-01)
Subject Medicine, Health and Life Sciences
Keyword mTORC1, PER1, Circadian rhythm, Cell biology, Hormone, Biology, Endocrinology, Internal medicine, Signal transduction, Circadian clock, Medicine, CLOCK, PI3K/AKT/mTOR pathway
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