ArticleInternational journal of chronic obstructive pulmonary disease2017
Soluble common gamma chain exacerbates COPD progress through the regulation of inflammatory T cell response in mice.
Article in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Particulate matter exposure induces pulmonary TRedox biology · 2025Article
- Rapamycin attenuates Tc1 and Tc17 cell responses in cigarette smoke-induced emphysema in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Aquatic Exercise at Thermoneutral Water Temperature Enhances Antitumor Immune Responses.Immune network · 2019Article
- Review
- ILC2s Induce Adaptive Th2-Type Immunity in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.Mediators of inflammation · 2019Article
- CD4Frontiers in immunology · 2019Article
- Analysis of curative effect of adjuvant therapy with bronchoalveolar lavage on COPD patients complicated with pneumonia.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking (CS) is a major cause of considerable morbidity and mortality by inducing lung cancer and COPD. COPD, a smoking-related disorder, is closely related to the alteration of immune system and inflammatory processes that are specifically mediated by T cells. Soluble common gamma chain (sγc) has recently been identified as a critical regulator of the development and differentiation of T cells. We examined the effects of sγc in a cigarette smoke extract (CSE) mouse model. The sγc level in CSE mice serum is significantly downregulated, and the cellularity of lymph node (LN) is systemically reduced in the CSE group. Overexpression of sγc enhances the cellularity and IFNγ production of CD8 T cells in LN and also enhances Th1 and Th17 differentiation of CD4 T cells in the respiratory tract. Mechanistically, the downregulation of sγc expression mediated by CSE is required to prevent excessive inflammatory T cell responses. Therefore, our data suggest that sγc may be one of the target molecules for the control of immunopathogenic progresses in COPD.
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