# Role of Regulatory T Cells in Chronic Obstructive Pulmonary Disease

## TL;DR

This study explores how regulatory T cells function in COPD patients, finding impaired suppression and altered cytokine levels compared to healthy individuals.

## Contribution

The study reveals compromised Treg function in COPD patients, particularly in smokers and reformed smokers, offering new insights into the disease's immune mechanisms.

## Key findings

- COPD patients showed significantly lower Treg suppression of T responder cells compared to controls.
- COPD smokers had reduced IL-2, IL-10, and TGF-β1 levels in suppression assays compared to other groups.
- COPD smokers exhibited a higher frequency of iTregs with a specific phenotype compared to reformed smokers.

## Abstract

Background: Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder characterized by poorly reversible airway obstruction. COPD being an inflammatory disorder has been proposed to have an imbalance between proinflammatory and anti-inflammatory factors. Regulatory T cells (Tregs) being a negative regulator of immune response have been observed to play an important role in other inflammatory diseases as well as animal models of inflammation.

Objective: This study is aimed at assessing the suppressive functions of circulatory Tregs and examining the inductive capacity of naive CD4+ T cells to generate induced Tregs.

Methods: The study was conducted in 20 COPD patients (smokers n = 10; reformed smokers n = 10) and 20 age-matched healthy controls (smokers n = 10; nonsmokers n = 10). Peripheral blood mononuclear cells were isolated from blood using Ficoll density gradient separation. The suppressive functions were evaluated by assessing the proliferation of T responder cells (CD4+CD25−) in the presence of circulatory Tregs (CD4+CD25+) under polyclonal stimulation. In addition, cytokine-mediated suppression was assessed in the culture supernatants of the suppression assay. Inductive capacity was assessed by stimulating naive CD4+ T cells to generate iTregs in the presence of anti-CD3, IL-2, and TGF-β1.

Results: The percent suppression of T responder cells by Tregs was significantly lower in COPD smokers (p = 0.03) and COPD reformed smokers (p = 0.04) as compared to control smokers. On the assessment of cytokine-mediated suppression, significantly reduced IL-2 in COPD S as compared to COPD RS (p < 0.05) and reduced IL-10 and TGFß1 in COPD S as compared to CNS (p < 0.05) and CS (p < 0.05) was observed in the culture supernatants of suppression assay. In addition, a significantly higher frequency of iTregs with phenotype CD4+CD25+CD45RA+CD127− was observed in COPD S as compared to COPD RS (p < 0.01).

Discussion: Characteristics changes were observed in patients with COPD. The compromised Tregs function, despite the increase in systemic inflammation, suggests a potential role of these cells in the pathogenesis of the disease.