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TIGIT/SHIP-1/RelB regulating Th1 inflammation in smoking induced COPD.
Junyi Ke1,2, Siyu Lei1,2, Zhixiong He1
1Guangxi Medical University, Nanning, Guangxi, China.
Respiratory Research
|November 19, 2025
Summary
In smoking-induced COPD, TIGIT/SHIP-1 upregulates RelB via PI3K/AKT signaling, controlling Th1 inflammation. This reveals key immune mechanisms in COPD pathogenesis.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Chronic Obstructive Pulmonary Disease (COPD) involves airway inflammation mediated by various immune cells.
- Th1-type hypersensitivity responses contribute to irreversible airway damage in COPD.
- The TIGIT (T cell immunoglobulin and ITIM domain) receptor and its downstream phosphatase SHIP-1 regulate CD4+ T cell immunity via phosphoinositide pathways.
Purpose of the Study:
- To investigate TIGIT/SHIP-1 expression patterns in CD4+ T cells in smoking-induced COPD.
- To elucidate the mechanisms by which TIGIT/SHIP-1 influences CD4+ T cells and Th1 inflammation.
- To identify downstream signaling pathways regulated by TIGIT/SHIP-1 in COPD.
Main Methods:
- Clinical and animal models of smoking-induced COPD were utilized.
- Flow cytometry, immunofluorescence, and chromatin immunoprecipitation were employed.
- Single-cell and bulk RNA sequencing bioinformatics analyses were performed.
Main Results:
- CD4+ T cells in COPD showed increased TIGIT/SHIP-1 expression.
- Knockout of CD4-Tigit or SHIP-1 inhibition elevated Th1 levels in mice.
- RelB was identified as a key regulator of COPD-Th1 inflammation, acting downstream of TIGIT/SHIP-1 via PI3K/AKT signaling.
Conclusions:
- TIGIT/SHIP-1 regulates Th1 expression in COPD by modulating RelB activation through the PI3K/AKT pathway.
- This study provides novel insights into the immune mechanisms underlying COPD pathogenesis.
- Targeting the TIGIT/SHIP-1/RelB axis may offer therapeutic strategies for COPD.
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