Zhaoran Wang: China-Japan Friendship Clinical Medical College, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100029, China.
Yi Jiao: Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, 100029, China.
Wenya Diao: Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, 100029, China.
Tong Shi: China-Japan Friendship Clinical Medical College, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100029, China.
Qishun Geng: China-Japan Friendship Clinical Medical College, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100029, China.
Chaoying Wen: China-Japan Friendship Clinical Medical College, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100029, China.
Jiahe Xu: Peking University China-Japan Friendship School of Clinical Medicine, Beijing, 100029, China.
Tiantian Deng: Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, 100029, China.
Xiaoya Li: The Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences/Peking Union Medical College, Beijing, 100193, China.
Lu Zhao: China-Japan Friendship Clinical Medical College, Capital Medical University, Beijing, 100029, China.
Jienan Gu: Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, 100029, China.
Tingting Deng: Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing, 100029, China. ttdeng1983@163.com.
Cheng Xiao: China-Japan Friendship Clinical Medical College, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100029, China. xc2002812@126.com.
Rheumatoid arthritis (RA) is a systemic autoimmune disease involving activation of the immune system and the infiltration of immune cells. As the first immune cells to reach the site of inflammation, neutrophils perform their biological functions by releasing many active substances and forming neutrophil extracellular traps (NETs). The overactivated neutrophils in patients with RA not only directly damage tissues but also, more importantly, interact with various other immune cells and broadly activate innate and adaptive immunity, leading to irreversible joint damage. However, owing to the pivotal role and complex influence of neutrophils in maintaining homoeostasis, the treatment of RA by targeting neutrophils is very difficult. Therefore, a comprehensive understanding of the interaction pathways between neutrophils and various other immune cells is crucial for the development of neutrophils as a new therapeutic target for RA. In this study, the important role of neutrophils in the pathogenesis of RA through their crosstalk with various other immune cells and nonimmune cells is highlighted. The potential of epigenetic modification of neutrophils for exploring the pathogenesis of RA and developing therapeutic approaches is also discussed. In addition, several models for studying cell���cell interactions are summarized to support further studies of neutrophils in the context of RA.
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