Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Apr 28:11:723.
doi: 10.3389/fimmu.2020.00723. eCollection 2020.

Role of Regulatory T Cells in Disturbed Immune Homeostasis in Patients With Chronic Obstructive Pulmonary Disease

Affiliations
Review

Role of Regulatory T Cells in Disturbed Immune Homeostasis in Patients With Chronic Obstructive Pulmonary Disease

Jia Hou et al. Front Immunol. .

Abstract

Chronic obstructive pulmonary disease (COPD) is a complex chronic disease in which T cell-mediated pulmonary inflammation has been shown to play a key role. Accumulating evidence shows that COPD has many of the characteristics of an autoimmune response. An adaptive immune response directed against lung self-antigens, which are released during the initial innate inflammatory response and are triggered by constant exposure to cigarette smoke and epithelial injury, drives the persistent inflammatory response found in smokers. The development and severity of adaptive inflammation depend on the level of tolerance to self-antigens. For these reasons, the effect of regulatory T (Treg) cells on adaptive immunity in COPD patients is of particular interest and could be targeted therapeutically. The disturbance in immune homeostasis caused by changes in the number or function of Treg cells, which is related to cigarette smoke exposure, may be of importance in understanding the development and progression of COPD.

Keywords: COPD; T-regulatory cells; adaptive immunity; aging; immune homeostasis; smoking.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Disturbed immune homeostasis in patients with chronic obstructive pulmonary disease (COPD). In smokers, although smoke exposure triggers the pro-inflammatory response, the compensatory anti-inflammatory mechanism keeps immune homeostasis intact as in healthy non-smokers. In smoking COPD patients, long-term smoking can lead to exhaustion of the compensatory anti-inflammatory compacity, which leads to the imbalance between pro- and anti-inflammatory mechanisms, and eventually disrupts the immune homeostasis.

Similar articles

Cited by

References

    1. Vogelmeier CF, Criner GJ, Martinez FJ, Anzueto A, Barnes PJ, Bourbeau J, et al. . Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 report: GOLD executive summary. Eur Resp J. (2017) 49:1700214. 10.1164/rccm.201701-0218PP - DOI - PubMed
    1. Cosio MG, Saetta M, Agusti A. Immunologic aspects of chronic obstructive pulmonary disease. N Eng J Med. (2009) 360:2445–54. 10.1056/NEJMra0804752 - DOI - PubMed
    1. Núñez B, Sauleda J, Antó JM, Julià MR, Orozco M, Monsó E, et al. . Anti-tissue antibodies are related to lung function in chronic obstructive pulmonary disease. Am J Resp Crit Care Med. (2011) 183:1025–31. 10.1164/rccm.201001-0029OC - DOI - PubMed
    1. Bonarius H, Brandsma C, Kerstjens H, Koerts J, Kerkhof M, Nizankowska-Mogilnicka E, et al. Antinuclear autoantibodies are more prevalent in COPD in association with low body mass index but not with smoking history. Thorax. (2011) 66:101–7. 10.1136/thx.2009.134171 - DOI - PubMed
    1. Arnson Y, Shoenfeld Y, Amital H. Effects of tobacco smoke on immunity, inflammation and autoimmunity. J Autoimm. (2010) 34:J258–J65. 10.1016/j.jaut.2009.12.003 - DOI - PubMed

Publication types