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Review
. 2023 Feb 14;9(1):62.
doi: 10.1038/s41420-023-01344-x.

T cells in idiopathic pulmonary fibrosis: crucial but controversial

Lishan Deng #  1 , Teng Huang #  1 , Lei Zhang  2
Affiliations
Review

T cells in idiopathic pulmonary fibrosis: crucial but controversial

Lishan Deng et al. Cell Death Discov. .

Erratum in

Abstract

Idiopathic pulmonary fibrosis (IPF) has been extensively studied in recent decades due to its rising incidence and high mortality. Despite an abundance of research, the mechanisms, immune-associated mechanisms, of IPF are poorly understood. While defining immunopathogenic mechanisms as the primary pathogenesis is controversial, recent studies have verified the contribution of the immune system to the fibrotic progression of IPF. Extensive evidence has shown the potential role of T cells in fibrotic progression. In this review, we emphasize the features of T cells in IPF and highlight the controversial roles of different subtypes of T cells or even two distinct effects of one type of T-cell in diverse settings, and multiple chemokines and cell products are discussed. Furthermore, we discuss the potential development of treatments targeting the immune molecules of T cells and the feasibility of immune therapies for IPF in clinical practice.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Graphic illustration of important T-cell subtypes in IPF.
When the immune system is stimulated by external risk factors, T cells migrate to the interstitium and play different roles as a result of various secreted chemokines. Th1 cells are antifibrotic due to the suppressor IFN-γ. Th2 cells can activate fibroblasts and myofibroblasts. IL-17 produced by Th17 cells extensively promotes ECM production and collagen deposition. Tregs inhibit immunoreaction and may have opposing functions in the early and late stages of fibrosis. Th T helper cell, Treg regulatory T-cell, TGF transforming growth factor, IFN interferon, ECM extracellular matrix.
See this image and copyright information in PMC

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