ArticleRespiratory research2025
TIGIT/SHIP-1/RelB regulating Th1 inflammation in smoking induced COPD.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe 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.
methodsThis 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 cytometry, immunofluorescence, and chromatin immunoprecipitation.
resultsWe found that CD4 + T cells in smoking COPD exhibit upregulated expression of TIGIT/SHIP-1, and specific knockout of CD4-Tigit and short-term in vivo inhibition of SHIP-1 significantly elevated Th1 levels in emphysematous mice. Through single-cell and bulk-RNA bioinformatics analysis, we identified RelB that regulates COPD-Th1 inflammation by regulates TBX21 in transcriptional level and confirmed its excessive activation in COPD-Th1 inflammation. The PI3K/AKT signaling, acting downstream of TIGIT/SHIP-1, influences the activation of RelB in Th1 cells.
conclusionsIn smoking-induced COPD, TIGIT/SHIP-1 affects the activation of RelB through the PI3K/AKT pathway, thereby regulating the expression of Th1. It offers insights underlying the immune mechanism of COPD.
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