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Med1 controls CD8 T cell maintenance through IL-7R-mediated cell survival signalling.

Lei LeiXiaofeng YangYanhong SuHuiqiang ZhengJun LiuHaiyan LiuYujing ZouAnjun JiaoXin WangCangang ZhangXingzhe ZhangJiahui ZhangDan ZhangXiaobo ZhouLin ShiEnqi LiuLiang BaiChenming SunBaojun Zhang
Published in: Journal of cellular and molecular medicine (2021)
Under steady-state conditions, the pool size of peripheral CD8+ T cells is maintained through turnover and survival. Beyond TCR and IL-7R signals, the underlying mechanisms are less well understood. In the present study, we found a significant reduction of CD8+ T cell proportion in spleens but not in thymi of mice with T cell-specific deletion of Mediator Subunit 1 (Med1). A competitive transfer of wild-type (WT) and Med1-deficient CD8+ T cells reproduced the phenotype in the same recipients and confirmed intrinsic role of Med1. Furthermore, we observed a comparable degree of migration and proliferation but a significant increase of cell death in Med1-deficient CD8+ T cells compared with WT counterparts. Finally, Med1-deficient CD8+ T cells exhibited a decreased expression of interleukin-7 receptor α (IL-7Rα), down-regulation of phosphorylated-STAT5 (pSTAT5) and Bim up-regulation. Collectively, our study reveals a novel role of Med1 in the maintenance of CD8+ T cells through IL-7Rα/STAT5 pathway-mediated cell survival.
Keyphrases
  • wild type
  • cell death
  • cell proliferation
  • poor prognosis
  • bone mineral density
  • adipose tissue
  • regulatory t cells
  • skeletal muscle
  • postmenopausal women
  • long non coding rna