ACC1-expressing pathogenic T helper 2 cell populations facilitate lung and skin inflammation in mice.
J Exp Med
; 218(12)2021 12 06.
Article
em En
| MEDLINE
| ID: mdl-34813654
ABSTRACT
T cells possess distinguishing effector functions and drive inflammatory disorders. We have previously identified IL-5-producing Th2 cells as the pathogenic population predominantly involved in the pathology of allergic inflammation. However, the cell-intrinsic signaling pathways that control the pathogenic Th2 cell function are still unclear. We herein report the high expression of acetyl-CoA carboxylase 1 (ACC1) in the pathogenic CD4+ T cell population in the lung and skin. The genetic deletion of CD4+ T cell-intrinsic ACC1 dampened eosinophilic and basophilic inflammation in the lung and skin by constraining IL-5 or IL-3 production. Mechanistically, ACC1-dependent fatty acid biosynthesis induces the pathogenic cytokine production of CD4+ T cells via metabolic reprogramming and the availability of acetyl-CoA for epigenetic regulation. We thus identified a distinct phenotype of the pathogenic T cell population in the lung and skin, and ACC1 was shown to be an essential regulator controlling the pathogenic function of these populations to promote type 2 inflammation.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Acetil-CoA Carboxilase
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Pneumonia
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Toxidermias
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Células Th2
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article