Literature DB >> 23127823

Increased expression of CD4+IL-17+ cells in the lung tissue of patients with stable chronic obstructive pulmonary disease (COPD) and smokers.

Jianquan Zhang1, Shuyuan Chu, Xiaoning Zhong, Qifang Lao, Zhiyi He, Yi Liang.   

Abstract

CD4(+)IL-17(+) cells have an important role in controlling immune and inflammatory reactions. The authors of the present study hypothesize that these cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). To characterize the frequency of CD4(+)IL-17(+) cells in the lung alveolar walls, small airways and muscular pulmonary arteries of nonsmokers, smokers with normal lung function and COPD patients, CD4(+)IL-17(+) cell number was assessed using double immunofluorescence staining, and IL-17 and IL-21 expression were measured using real-time quantitative PCR in the peripheral lung tissues of 10 nonsmokers, 10 smokers with normal lung function and 10 smokers with stable COPD. In the lung alveolar walls, the number of CD4(+)IL-17(+) cells was increased in COPD patients compared with nonsmokers and in normal smokers compared with nonsmokers. In the small airways, the CD4(+)IL-17(+) cell numbers were higher in COPD patients than in normal smokers and nonsmokers. A positive correlation was observed between CD4(+)IL-17(+) cell expression and pathological changes in the lung tissue. In the small airways, the number of CD4(+)IL-17(+) cells was positively correlated with airflow limitations. The IL-17 mRNA levels in lung tissues were increased in COPD patients and normal smokers compared with nonsmokers. Increased CD4(+)IL-17(+) cell number in lung tissue is involved in chronic inflammation of the lungs and parallels lung injury aggravation in COPD patients and in smokers without airway limitations. These findings contribute to a better understanding of CD4(+) cell-related pathogenesis in COPD.
Copyright © 2012 Elsevier B.V. All rights reserved.

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Year:  2012        PMID: 23127823     DOI: 10.1016/j.intimp.2012.10.018

Source DB:  PubMed          Journal:  Int Immunopharmacol        ISSN: 1567-5769            Impact factor:   4.932


  30 in total

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2.  Cigarette smoke exposure exacerbates lung inflammation and compromises immunity to bacterial infection.

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Journal:  Chronic Obstr Pulm Dis       Date:  2015-08-23

4.  IL-21 is increased in peripheral blood of emphysema mice and promotes Th1/Tc1 cell generation in vitro.

Authors:  Minchao Duan; Ying Huang; Xiaoning Zhong; Haijuan Tang
Journal:  Inflammation       Date:  2014-06       Impact factor: 4.092

5.  A Novel Animal Model of Emphysema Induced by Anti-Elastin Autoimmunity.

Authors:  Bon-Hee Gu; Maran L Sprouse; Matthew C Madison; Monica J Hong; Xiaoyi Yuan; Hui-Ying Tung; Cameron T Landers; Li-Zhen Song; David B Corry; Maria Bettini; Farrah Kheradmand
Journal:  J Immunol       Date:  2019-06-10       Impact factor: 5.422

6.  Chronic Obstructive Pulmonary Disease Alters Immune Cell Composition and Immune Checkpoint Inhibitor Efficacy in Non-Small Cell Lung Cancer.

Authors:  Nicholas M Mark; Julia Kargl; Stephanie E Busch; Grace H Y Yang; Heather E Metz; Huajia Zhang; Jesse J Hubbard; Sudhakar N J Pipavath; David K Madtes; A McGarry Houghton
Journal:  Am J Respir Crit Care Med       Date:  2018-02-01       Impact factor: 21.405

7.  Secondhand Smoke Induces Inflammation and Impairs Immunity to Respiratory Infections.

Authors:  Tariq A Bhat; Suresh Gopi Kalathil; Paul N Bogner; Austin Miller; Paul V Lehmann; Thomas H Thatcher; Richard P Phipps; Patricia J Sime; Yasmin Thanavala
Journal:  J Immunol       Date:  2018-03-19       Impact factor: 5.422

Review 8.  The formation and function of tertiary lymphoid follicles in chronic pulmonary inflammation.

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Journal:  Immunology       Date:  2016-08-16       Impact factor: 7.397

Review 9.  Type 2 immunity in tissue repair and fibrosis.

Authors:  Richard L Gieseck; Mark S Wilson; Thomas A Wynn
Journal:  Nat Rev Immunol       Date:  2017-08-30       Impact factor: 53.106

10.  Loss of Peripheral Tolerance in Emphysema. Phenotypes, Exacerbations, and Disease Progression.

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