Endoplasmic reticulum stress interferes with the development of type 1 regulating T cells.

CD4 T cell Colitis Endoplasmic reticulum stress Immune regulation Immunity

Journal

Inflammation research : official journal of the European Histamine Research Society ... [et al.]
ISSN: 1420-908X
Titre abrégé: Inflamm Res
Pays: Switzerland
ID NLM: 9508160

Informations de publication

Date de publication:
24 Jan 2024
Historique:
received: 17 08 2022
accepted: 14 12 2023
revised: 12 12 2023
medline: 24 1 2024
pubmed: 24 1 2024
entrez: 24 1 2024
Statut: aheadofprint

Résumé

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. CD4 The presence of ER stress in peripheral CD4 The synergistic effects of ER stress and MNP interfere with the development of Tr1 cells. The development of Tr1 from CD4

Sections du résumé

BACKGROUND 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 METHODS
CD4
RESULTS RESULTS
The presence of ER stress in peripheral CD4
CONCLUSIONS CONCLUSIONS
The synergistic effects of ER stress and MNP interfere with the development of Tr1 cells. The development of Tr1 from CD4

Identifiants

DOI: 10.1007/s00011-023-01841-w PMID: 38265686
pubmed: 38265686
doi: 10.1007/s00011-023-01841-w
pii: 10.1007/s00011-023-01841-w
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

Références

Ananthakrishnan AN. Epidemiology and risk factors for IBD. Nat Rev Gastroenterol Hepatol. 2015;12:205–17.
doi: 10.1038/nrgastro.2015.34 pubmed: 25732745
Chapman TP, Gomes CF, Louis E, Colombel JF, Satsangi J. De-escalation of immunomodulator and biological therapy in inflammatory bowel disease. Lancet Gastroenterol Hepatol. 2020;5:63–79.
doi: 10.1016/S2468-1253(19)30186-4 pubmed: 31818473
Guan Q. A comprehensive review and update on the pathogenesis of inflammatory bowel disease. J Immunol Res. 2019;2019: 7247238.
doi: 10.1155/2019/7247238 pubmed: 31886308 pmcid: 6914932
Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature. 2007;448:427–34.
doi: 10.1038/nature06005 pubmed: 17653185
Saez A, Gomez-Bris R, Herrero-Fernandez B, Mingorance C, Rius C, Gonzalez-Granado JM. Innate lymphoid cells in intestinal homeostasis and inflammatory bowel disease. Int J Mol Sci. 2021;22: 7618.
doi: 10.3390/ijms22147618 pubmed: 34299236 pmcid: 8307624
Hang S, Paik D, Yao L, Kim E, Trinath J, Lu J, et al. Bile acid metabolites control T(H)17 and T(reg) cell differentiation. Nature. 2019;576:143–8.
doi: 10.1038/s41586-019-1785-z pubmed: 31776512 pmcid: 6949019
Clough JN, Omer OS, Tasker S, Lord GM, Irving PM. Regulatory T-cell therapy in Crohn’s disease: challenges and advances. Gut. 2020;69:942–52.
doi: 10.1136/gutjnl-2019-319850 pubmed: 31980447
Oakes SA, Papa FR. The role of endoplasmic reticulum stress in human pathology. Annu Rev Pathol. 2015;10:173–94.
doi: 10.1146/annurev-pathol-012513-104649 pubmed: 25387057
Bettigole SE, Glimcher LH. Endoplasmic reticulum stress in immunity. Annu Rev Immunol. 2015;33:107–38.
doi: 10.1146/annurev-immunol-032414-112116 pubmed: 25493331
Frakes AE, Dillin A. The UPR(ER): sensor and coordinator of organismal homeostasis. Mol Cell. 2017;66:761–71.
doi: 10.1016/j.molcel.2017.05.031 pubmed: 28622521
Powell N, Pantazi E, Pavlidis P, Tsakmaki A, Li K, Yang F, et al. Interleukin-22 orchestrates a pathological endoplasmic reticulum stress response transcriptional programme in colonic epithelial cells. Gut. 2020;69:578–90.
doi: 10.1136/gutjnl-2019-318483 pubmed: 31792136
Liu C, Mo LH, Feng BS, Jin QR, Li Y, Lin J, et al. Twist1 contributes to developing and sustaining corticosteroid resistance in ulcerative colitis. Theranostics. 2021;11:7797–812.
doi: 10.7150/thno.62256 pubmed: 34335965 pmcid: 8315068
Zhao CN, Xu Z, Wu GC, Mao YM, Liu LN, Qian W, et al. Emerging role of air pollution in autoimmune diseases. Autoimmun Rev. 2019;18:607–14.
doi: 10.1016/j.autrev.2018.12.010 pubmed: 30959217
Cortez JT, Montauti E, Shifrut E, Gatchalian J, Zhang Y, Shaked O, et al. CRISPR screen in regulatory T cells reveals modulators of Foxp3. Nature. 2020;582:416–20.
doi: 10.1038/s41586-020-2246-4 pubmed: 32499641 pmcid: 7305989
de Souza HS, Fiocchi C. Immunopathogenesis of IBD: current state of the art. Nat Rev Gastroenterol Hepatol. 2016;13:13–27.
doi: 10.1038/nrgastro.2015.186 pubmed: 26627550
Cook L, Stahl M, Han X, Nazli A, MacDonald KN, Wong MQ, et al. Suppressive and gut-reparative functions of human type 1 T regulatory cells. Gastroenterology. 2019;157:1584–98.
doi: 10.1053/j.gastro.2019.09.002 pubmed: 31513797
Kühn R, Löhler J, Rennick D, Rajewsky K, Müller W. Interleukin-10-deficient mice develop chronic enterocolitis. Cell. 1993;75:263–74.
doi: 10.1016/0092-8674(93)80068-P pubmed: 8402911
Schmitt H, Ulmschneider J, Billmeier U, Vieth M, Scarozza P, Sonnewald S, et al. The TLR9 agonist cobitolimod induces IL10-producing wound healing macrophages and regulatory T cells in ulcerative colitis. J Crohns Colitis. 2020;14:508–24.
doi: 10.1093/ecco-jcc/jjz170 pubmed: 31630153
Noya Y, Mikami Y, Taneda S, Mori Y, Suzuki AK, Ohkura K, et al. Improvement of an efficient separation method for chemicals in diesel exhaust particles: analysis for nitrophenols. Environ Sci Pollut Res Int. 2008;15:318–21.
doi: 10.1007/s11356-008-0006-3 pubmed: 18437438
Fukushima M, Fujisawa T, Katagi T, Takimoto Y. Metabolism of fenitrothion and conjugation of 3-methyl-4-nitrophenol in tomato plant (Lycopersicon esculentum). J Agric Food Chem. 2003;51:5016–23.
doi: 10.1021/jf034289q pubmed: 12903963
Liu JQ, Li SS, Mo LH, Yu D, Geng XR, Hong JY, et al. Exposure to 3-methyl-4-nitrophenol facilitates development of intestinal allergy. Allergy. 2019;74:610–3.
doi: 10.1111/all.13648 pubmed: 30357863
Liu XY, Wu YJ, Song LJ, Zeng XH, Wang S, Liu JQ, et al. 3-Methyl-4-nitrophenol triggers nasal allergy by modulating dendritic cell properties. J Allergy Clin Immunol. 2019;143:1614-6.e7.
doi: 10.1016/j.jaci.2018.11.012 pubmed: 30472262
Li C, Taneda S, Suzuki AK, Furuta C, Watanabe G, Taya K. Anti-androgenic activity of 3-methyl-4-nitrophenol in diesel exhaust particles. Eur J Pharmacol. 2006;543:194–9.
doi: 10.1016/j.ejphar.2006.06.010 pubmed: 16822498
Li C, Takahashi S, Taneda S, Furuta C, Watanabe G, Suzuki AK, et al. Effects of 3-methyl-4-nitrophenol in diesel exhaust particles on the regulation of reproductive function in immature female Japanese quail (Coturnix japonica). J Reprod Dev. 2007;53:673–8.
doi: 10.1262/jrd.18133 pubmed: 17202750
Yang L, Ma S, Wan Y, Duan S, Ye S, Du S, et al. In vitro effect of 4-pentylphenol and 3-methyl-4-nitrophenol on murine splenic lymphocyte populations and cytokine/granzyme production. J Immunotoxicol. 2016;13:548–56.
doi: 10.3109/1547691X.2016.1140853 pubmed: 27031367
Di Conza G, Ho PC. ER stress responses: an emerging modulator for innate immunity. Cells. 2020;9:695.
doi: 10.3390/cells9030695 pubmed: 32178254 pmcid: 7140669
Cosovanu C, Neumann C. The many functions of Foxp3(+) regulatory T cells in the intestine. Front Immunol. 2020;11: 600973.
doi: 10.3389/fimmu.2020.600973 pubmed: 33193456 pmcid: 7606913

Auteurs

Baisui Feng (B)

Department of Gastroenterology, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China.

Huazhen Liu (H)

Guangdong Provincial Regional Disease Key Laboratory, Shenzhen, China.
Institute of Allergy and Immunology of Shenzhen University, State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China.

Wenkai Yao (W)

Guangdong Provincial Regional Disease Key Laboratory, Shenzhen, China.
Institute of Allergy and Immunology of Shenzhen University, State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China.

Yan Li (Y)

Department of Gastroenterology, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China.

Gaohui Wu (G)

Department of Respirology, The Third Affiliated Hospital, Shenzhen University, Shenzhen, China.

Liteng Yang (L)

Department of Respirology, The Third Affiliated Hospital, Shenzhen University, Shenzhen, China. litengryang@mailnesia.com.

Pingchang Yang (P)

Guangdong Provincial Regional Disease Key Laboratory, Shenzhen, China. pcy2356@szu.edu.cn.
Institute of Allergy and Immunology of Shenzhen University, State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University, Shenzhen, China. pcy2356@szu.edu.cn.

Classifications MeSH