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  3. The role of B-cell ferroptosis in the pathogenesis of systemic lupus erythematosus

The role of B-cell ferroptosis in the pathogenesis of systemic lupus erythematosus

  • Clin Immunol. 2023 Sep 18;256:109778. doi: 10.1016/j.clim.2023.109778.
Qian Chen 1,  Mengmeng Xiang 1,  Zhanyan Gao 1,  Fan Lvu 1,  Zhan Sun 1,  Yilun Wang 1,  Xiangguang Shi 1,  Jinhua Xu 2,  Jie Wang 3,  Jun Liang 4
Affiliations

Affiliations

  • 1 Department of Dermatology, Huashan Hospital, Fudan University, PR China.
  • 2 Department of Dermatology, Huashan Hospital, Fudan University, Shanghai Institute of Dermatology, Shanghai, PR China.
  • 3 Department of Dermatology, Huashan Hospital, Fudan University, PR China. Electronic address: wangjie16@fudan.edu.cn.
  • 4 Department of Dermatology, Huashan Hospital, Fudan University, PR China. Electronic address: Liangjun1976@medmail.com.cn.
PMID: 37730009 DOI: 10.1016/j.clim.2023.109778
Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the dysregulation of B cell subpopulation and function. Recent studies have suggested a potential role of Ferroptosis, an iron-dependent form of regulated cell death, in the pathogenesis of SLE. Here, we demonstrate that B-cell Ferroptosis occurs both in lupus patients and MRL/lpr mice. Treatment with liproxstatin-1, a potent Ferroptosis inhibitor, could reduce autoantibody production, improve renal damage, and alleviate lupus symptoms in vivo. Furthermore, our results suggest that Ferroptosis may regulate B cell differentiation and plasma cell formation, indicating a potential mechanism for its involvement in SLE. Taken together, targeting Ferroptosis in B cells may be a promising therapeutic strategy for SLE.

Keywords

B lymphocytes; Ferroptosis; Plasma cells; Systemic lupus erythematosus.

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