清除凋亡细胞以预防狼疮性肾炎：非典型自噬在自身免疫中的新作用。

LAPping up dead cells to prevent lupus nephritis: a novel role for noncanonical autophagy in autoimmunity.

机构信息

Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA; Renal Division, James J. Peters Bronx Veterans Affairs Medical Center, Bronx, New York, USA.

出版信息

Kidney Int. 2016 Aug;90(2):238-239. doi: 10.1016/j.kint.2016.06.001.

DOI:10.1016/j.kint.2016.06.001

PMID:27418084

Abstract

The mechanisms underlying the development of systemic lupus erythematosus and lupus nephritis remain poorly understood. A recent study demonstrates that deficiencies in the immune system's ability to degrade scavenged dead cells via noncanonical autophagy is sufficient to break immune tolerance and produce features commonly seen in lupus, including circulating autoantibodies, inflammatory cytokines, and nephritis. This work provides a possible mechanism for the association of polymorphisms in autophagy genes with the risk of lupus.

摘要

系统性红斑狼疮和狼疮性肾炎的发病机制仍不清楚。最近的一项研究表明，免疫系统降解被吞噬的死细胞的能力缺陷足以打破免疫耐受，并产生狼疮常见的特征，包括循环自身抗体、炎症细胞因子和肾炎。这项工作为自噬基因多态性与狼疮风险的关联提供了一个可能的机制。