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Crystalline silica-induced recruitment and immuno-imbalance of CD4⁺ tissue resident memory T cells promote silicosis progression.

ABSTRACT: Occupational crystalline silica (CS) particle exposure leads to silicosis. The burden of CS-associated disease remains high, and treatment options are limited due to vague mechanisms. Here we show that pulmonary CD4⁺ tissue-resident memory T cells (T_RM) accumulate in response to CS particles, mediating the pathogenesis of silicosis. The T_RM cells are derived from peripheral lymphocyte recruitment and in situ expansion. Specifically, CD69⁺CD103⁺ T_RM-Tregs depend more on circulating T cell replenishment. CD69 and CD103 can divide the T_RM cells into functionally distinct subsets, mirroring the immuno-balance within CD4⁺ T_RM cells. However, targeting CD103⁺ T_RM-Tregs do not

SUBMITTER: You Y

PROVIDER: S-EPMC11316055 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature

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Dataset Information

Crystalline silica-induced recruitment and immuno-imbalance of CD4⁺ tissue resident memory T cells promote silicosis progression.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Crystalline silica-induced recruitment and immuno-imbalance of CD4+ tissue resident memory T cells promote silicosis progression.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Crystalline silica-induced recruitment and immuno-imbalance of CD4⁺ tissue resident memory T cells promote silicosis progression.