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Proinflammatory phenotype of B10 and B10pro cells elicited by TNF-α in rheumatoid arthritis.

Fanlei HuLianjie ShiXiaohang LiuYingjia ChenXia ZhangYuan JiaXu LiuJianping GuoHuaqun ZhuHongjiang LiuLiling XuYingni LiPing WangXiangyu FangJimeng XueYang XieChaonan WeiJing SongXi ZhengYan-Ying LiuYuhui LiLimin RenDakang XuLiwei LuXiaoyan QiuRong MuJing HeMin WangXuan ZhangWanli LiuZhanguo Li
Published in: Annals of the rheumatic diseases (2024)
TNF-α provoked the proinflammatory phenotype of B10 and B10pro cells by disturbing SHIP-1 in RA, contributing to the disease development. Reinstating the immunosuppressive property of B10 and B10pro cells might represent novel therapeutic approaches for RA.
Keyphrases
  • rheumatoid arthritis
  • induced apoptosis
  • cell cycle arrest
  • disease activity
  • endoplasmic reticulum stress
  • oxidative stress
  • ankylosing spondylitis
  • anti inflammatory
  • signaling pathway
  • cell death
  • pi k akt