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- Title
Endoplasmic reticulum stress interferes with the development of type 1 regulating T cells.
- Authors
Feng, Baisui; Liu, Huazhen; Yao, Wenkai; Li, Yan; Wu, Gaohui; Yang, Liteng; Yang, Pingchang
- Abstract
Background: A variety of stimuli can cause endoplasmic reticulum (ER) stress, which is a common cellular reaction. It is not yet clear how ER stress contributes to the pathogenesis of ulcerative colitis (UC). The deregulation of regulatory T cell (Treg) is associated with UC. The goal of this study is to shed light on how ER stress affects Treg's development. Methods: CD4+ CD25− T cells were isolated from blood samples collected from UC patients and healthy control (HC) subjects. ER stress-associated molecule expression in CD4+ CD25− T cell was assessed by RNA sequencing and RT-qPCR. Results: The presence of ER stress in peripheral CD4+ CD25− T cells was observed in patients with UC compared to HC subjects. The induction of ER stress in HC CD4+ CD25− T cells by polyclonal activation was made worse by the presence of 3-methyl-4-nitrophenol (MNP; a common environmental pollutant). Exposure to MNP in culture resulted in an increase in the expression of ring finger protein 20 (Rnf20) in CD4+ CD25− T cells. The synergistic effects of MNP and ER stress on the reduction of IL-10 levels in CD4+ CD25− T cells are mediated by Rnf20, which prevents the development of Tr1 cells. Inhibition of Rnf20 resulted in the development of Tr1 cells from CD4+ CD25− T cells in UC patients. Conclusions: The synergistic effects of ER stress and MNP interfere with the development of Tr1 cells. The development of Tr1 from CD4+ CD25− T cells in patients with UC is re-established by Rnf20 inhibition.
- Subjects
T cells; REGULATORY T cells; ENDOPLASMIC reticulum; POLLUTANTS; ULCERATIVE colitis; T cell receptors
- Publication
Inflammation Research, 2024, Vol 73, Issue 3, p381
- ISSN
1023-3830
- Publication type
Article
- DOI
10.1007/s00011-023-01841-w