TIGIT/SHIP-1/RelB regulating Th1 inflammation in smoking induced COPD.

ABSTRACT:

Background

The airway lesions in COPD are mediated by a variety of inflammatory cells, among which the Th1-dominated delayed-type hypersensitivity response can also cause irreversible damage to normal airways. The immune checkpoint TIGIT and its downstream phosphatase SHIP-1 play a crucial role in coordinating the immune response of CD4 + T cells by regulating the phosphoinositide pathway.

Methods

This study evaluates the expression patterns of TIGIT/SHIP-1 in CD4 + T cells within the context of smoking-induced COPD and investigates the mechanisms by which TIGIT/SHIP-1 affects CD4 + T cells, also the downstream signaling changes regulating Th1 inflammation. In smoking COPD, we established a research framework encompassing clinical, animal, cellular levels including flow cyto

SUBMITTER: Ke J 

PROVIDER: S-EPMC12628621 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature