Jie Fan1, Kaimin Zhang2, Farooq Riaz2, Yiping Hu3,4, Jinjun Liu1, Qinwen Wang3,4 and Fan Pan2*
1Department of Cardiology, Handan Central Hospital, China 2Center for Cancer Research, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China 3Department of Rheumatology and Immunology, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China 4Shenzhen Key Laboratory of Immunity and Inflammatory Diseases, Shenzhen, Guangdong, China
*Corresponding Author: Fan Pan, Center for Cancer Research, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China.
Received: October 12, 2022; Published: October 19, 2022
A classic autoimmune connective tissue disease, Systemic lupus erythematosus (SLE), causes injury to multiple organ systems. It has been demonstrated that tumor necrosis factor-induced protein 3 (TNFAIP3), typically represented as A20, is associated with the progression of SLE. However, it hasn’t been revealed how A20 is involved in modulating the role of A20 in SLE. In the current study, we determined that A20 was reduced in B cells collected from SLE patients, while the responsiveness of B cells was considerably elevated in SLE patients. Further investigation indicated overexpressing A20 in B cells restricted their proliferation and initiated their apoptosis. Moreover, trimethylation of histone H3 Lysine 4 (H3K4me3) was decreased in the A20 promoter of SLE B cells. Lysine demethylase 5A (Kdm5a) was significantly increased in B cells from SLE patients and negatively correlated with A20 expression. Further, Kdm5a knockdown increased the H3K4me3 level and A20 expression. More importantly, Kdm5a promoted the proliferation and inhibited the apoptosis of B cells in SLE via downregulation of A20. In general, Kdm5a promoted the proliferation and inhibited the apoptosis of B cells in SLE via downregulation of A20 by decreasing H3K4me3 enrichment level in the A20 promoter, suggesting a novel mechanism underlying SLE progression, and providing a promising therapeutic target for SLE.
Keywords: Systemic Lupus Erythematosus; Tumor Necrosis Factor-Induced Protein 3; B Cells; Lysine Demethylase 5A
Citation: Fan Pan., et al. “Histone Lysine Demethylase 5A Promotes the Proliferation and Inhibits the Apoptosis of B Cells in SLE". Acta Scientific Microbiology 5.11 (2022): 38-46.
Copyright: © 2022 Fan Pan., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.