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Programmed death-1 promotes contused skeletal muscle regeneration by regulating Treg cells and macrophages

Authors :
Weihua Xiao
Yingjie Chen
Xinjuan Shi
Xiaoguang Liu
Jian Shou
Peijie Chen
Source :
Laboratory Investigation; a Journal of Technical Methods and Pathology
Publication Year :
2021
Publisher :
Elsevier BV, 2021.

Abstract

Immune cells are involved in skeletal muscle regeneration. The mechanism by which Treg cells are involved in the regeneration of injured skeletal muscle is still unclear. The purpose of this study was to explore the role of programmed death-1 in contused skeletal muscle regeneration, and to clarify the regulation of programmed death-1 on Treg cell generation and macrophage polarization, in order to deepen our understanding of the relationship between the immune system and injured skeletal muscle regeneration. The results show that programmed death-1 knockdown reduced the number of Treg cells and impaired contused skeletal muscle regeneration compared with those of wild-type mice. The number of pro-inflammatory macrophages in the contused skeletal muscle of programmed death-1 knockout mice increased, and the expression of pro-inflammatory factors and oxidative stress factors increased, while the number of anti-inflammatory macrophages and the expression of anti-inflammatory factors, antioxidant stress factors, and muscle regeneration-related factors decreased. These results suggest that programmed death-1 can promote contused skeletal muscle regeneration by regulating Treg cell generation and macrophage polarization.<br />Immune cells are involved in skeletal muscle regeneration, but the mechanisms are unclear. In this paper, the authors show that programmed death-1 (PD-1), a key immunosuppressive receptor that is involved in adaptive immune responses, can promote contused skeletal muscle regeneration by regulating Treg cell generation and macrophage polarization.

Details

ISSN :
00236837
Volume :
101
Database :
OpenAIRE
Journal :
Laboratory Investigation
Accession number :
edsair.doi.dedup.....5e158b093d023e7b05e8881403e30132
Full Text :
https://doi.org/10.1038/s41374-021-00542-4