Role of autophagy in the pathogenesis of systemic lupus erythematosus

Abstract

Autophagy, a highly conserved lysosome-mediated catabolic process, is responsible for degradation of various abnormal cytoplasmic contents, participates in almost every step of immune responses, and plays a vital role in maintaining immune system homeostasis. As a typical autoimmune disease, systemic lupus erythematosus (SLE) shows multiple immunological dysfunctions. Autophagy may be involved in the initiation and progression of SLE via regulating immune responses. Actually, autophagy levels have been reported to be abnormal in multiple peripheral blood immunocytes from patients with lupus, such as T lymphocytes, B lymphocytes, neutrophils and macrophages. Furthermore, polymorphisms in autophagy-related genes are associated with SLE susceptibility. In addition, multiple environment factors which induce or exacerbate SLE may affect autophagy levles. Some drugs which are used to treat SLE can regulate autophagy via different ways. Therefore, autophagy may play an essential role in the occurrence and development of SLE. Key words: Lupus erythematosus, systemic; Autophagy; Immunity; Heredity; Cytokines