Treg plasticity and human diseases

As a subset of CD4⁺ T cells, regulatory T cells (Tregs) with the characteristic expression of transcription factor FOXP3 play a key role in maintaining self-tolerance and regulating immune responses. However, in some inflammatory circumstances, Tregs can express cytokines of other T help (Th) cells by internal reprogramming, which is called Treg plasticity. These reprogrammed Tregs with impaired suppressive ability contribute to the progression of diseases by secreting pro-inflammatory cytokines. However, in the tumor microenvironment (TME), such changes in phenotype rarely occur in Tregs, on the contrary, Tregs usually display a stronger suppressive function and inhibit anti-tumor immunity. It is important to understand the mechanisms of Treg plasticity in inflammatory diseases and cancers.

In this review, we summarize the characteristics of different Th-like Tregs and discuss the potential mechanisms of these changes in phenotype. Furthermore, we summarize the Treg plasticity in human diseases and discuss the effects of these changes in phenotype on disease progression, as well as the potential application of drugs or reagents that regulate Treg plasticity in human diseases.

Treg plasticity is associated with inflammatory diseases and cancers. Regulating Treg plasticity is a promising direction for the treatment of inflammatory diseases and cancers.