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LTB4-induced anti-apoptosis and infiltration of neutrophils in rheumatoid arthritis


1, 2, 3, 4, 5

 

  1. Department of Physiology, College of Medicine, Nanchang University, Nanchang, Jiangxi, China.
  2. Department of Physiology, College of Medicine, Nanchang University, Nanchang, Jiangxi, China.
  3. Department of Physiology, College of Medicine, Nanchang University, Nanchang, Jiangxi, China.
  4. Department of Experimental Teaching Center, Nanchang University, Nanchang, Jiangxi, China. hongfenfang@126.com
  5. Department of Physiology, College of Medicine, Nanchang University, Nanchang, Jiangxi, China. slyang@ncu.edu.cn

CER12287
2020 Vol.38, N°3
PI 0543, PF 0551
Reviews

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PMID: 32105594 [PubMed]

Received: 31/03/2019
Accepted : 31/07/2019
In Press: 14/02/2020
Published: 26/05/2020

Abstract

Rheumatoid arthritis (RA) is the most common autoimmune disease, resulting in synovitis, joint pain and stiffness, even deformity and disability. The interactions between leukotriene B4 (LTB4) and neutrophils in RA progression have not been elucidated in detail. Our review focuses on the correlation of LTB4 and neutrophils in the development of RA especially in terms of infiltration and delayed life span of neutrophils. In this article, the roles of LTB4 in the anti-apoptosis of neutrophils will be detailed, which is achieved by suppressed pro-apoptotic Bax and up-regulated anti-apoptotic Mcl-1, and several key molecules, as well as signalling pathways and factors relevant to the enhancement of LTB4 production and functions. The mechanisms of LTB4-induced anti-apoptosis and infiltration of neutrophils provide more potential targets in the treatment of RA and recent therapeutic strategies are also discussed.

Rheumatology Article