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Review
. 2021 Dec 9:12:804919.
doi: 10.3389/fimmu.2021.804919. eCollection 2021.

Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease: Clinical and Experimental Evidence

Affiliations
Review

Th17/Treg Imbalance in Chronic Obstructive Pulmonary Disease: Clinical and Experimental Evidence

Juliana Dias Lourenço et al. Front Immunol. .

Abstract

The imbalance between pro- and anti-inflammatory immune responses mediated by Th17 and Treg cells is deeply involved in the development and progression of inflammation in chronic obstructive pulmonary disease (COPD). Several clinical and experimental studies have described the Th17/Treg imbalance in COPD progression. Due to its importance, many studies have also evaluated the effect of different treatments targeting Th17/Treg cells. However, discrepant results have been observed among different lung compartments, different COPD stages or local and systemic markers. Thus, the data must be carefully examined. In this context, this review explores and summarizes the recent outcomes of Th17/Treg imbalance in COPD development and progression in clinical, experimental and in vitro studies.

Keywords: COPD; Th17 cells (Th17); Th17/Treg imbalance; immune response; regulatory T cell (Treg).

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Th17/Treg imbalance in COPD. Representative image of Th17/Treg imbalance in clinical and experimental studies, in both stable and exacerbated disease. An increase in both Th17 cell amount and function is observed in clinical and experimental studies, during stable and exacerbated disease. In contrast, the Treg response may present increased cell amounts, however with decreased function and cytokine release, leading to Th17/Treg imbalance. COPD, chronic obstructive pulmonary disease; Treg, regulatory T cell; Th17, T helper-17, IL, interleukin; Foxp3, Forkhead box p3; STAT, signal transducer and activator of transcription; RORγt, retinoic acid orphan receptor; TGF-β, transforming growth factor-β; CS, cigarette smoke; LPS, lipopolysaccharide; NTHi, Haemophilus influenzae.

References

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