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Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability.

Programmed death one homolog maintains the pool size of regulatory T cells by promoting their differentiation and stability.
Author Information (click to view)

Wang Q, He J, Flies DB, Luo L, Chen L,


Wang Q, He J, Flies DB, Luo L, Chen L, (click to view)

Wang Q, He J, Flies DB, Luo L, Chen L,

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Scientific reports 2017 07 207(1) 6086 doi 10.1038/s41598-017-06410-w

Abstract

Programmed death one homolog (PD-1H) is an immunoglobulin superfamily molecule and primarily acts as a coinhibitor in the initiation of T cell response to antigens. Here, we report that genetic ablation of PD-1H in mice blocks the differentiation of naive T cells to Foxp3(+) inducible Treg cells (iTreg) with a significant decrease of iTreg in lymphoid organs. This effect of PD-1H is highly specific for iTreg because both naturally generated iTreg in gut-related tissues and in vitro induced iTreg by TGF-β were decreased whereas the genesis of natural Treg (nTreg) remains normal. The suppressive function of both iTreg and nTreg, however, is not affected by the loss of PD-1H. In addition to decreased production, PD-1H deficient iTreg could also rapidly convert to CD4(+) T helper 1 or T helper 17 cells in an inflammatory environment. Our results indicate that PD-1H is required for maintenance of iTreg pool size by promoting its differentiation and preventing its conversion to other CD4(+) T cell subsets. These findings may have important implications for manipulating Tregs to control inflammation.

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