Jung Ju-Yang, Suh Chang-Hee
Department of Rheumatology, Ajou University School of Medicine, Suwon, Korea.
Int J Rheum Dis. 2015 Mar;18(3):294-303. doi: 10.1111/1756-185X.12568. Epub 2015 Apr 17.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with repeated inflammation against multiple organs. Although its pathophysiology is not yet unveiled, uncleared apoptotic cells and their accumulation in tissue contribute to the autoimmune disturbance in SLE. Apoptosis is a programmed cell death process, which maintains tissue homeostasis and inhibits the development of any further immune response against apoptotic remnants. Earlier studies revealed that various 'eat-me' signals on apoptotic cells, bridging molecules and their receptors on phagocytes play a role in such a complicated process. Tyro3-Axl-Mer receptors, their bridging molecules, milk fat globulin epidermal growth factor-8, T-cell immunoglobulin mucin domain protein family, scavenger receptors, C1q, and pentraxins were found to be abnormal in SLE. In this review, apoptosis and clearance of its remnants are summarized, and the molecules involved in the incomplete clearance of apoptotic cells in SLE are discussed.
系统性红斑狼疮（SLE）是一种针对多个器官反复发生炎症的慢性自身免疫性疾病。尽管其病理生理学尚未明确，但未清除的凋亡细胞及其在组织中的积累会导致SLE中的自身免疫紊乱。凋亡是一种程序性细胞死亡过程，它维持组织稳态并抑制针对凋亡残余物的任何进一步免疫反应的发展。早期研究表明，凋亡细胞上的各种“吃我”信号、吞噬细胞上的衔接分子及其受体在这一复杂过程中发挥作用。在SLE中发现酪氨酸激酶3-艾克-美受体、它们的衔接分子、乳脂肪球表皮生长因子-8、T细胞免疫球蛋白粘蛋白结构域蛋白家族、清道夫受体、C1q和五聚体异常。在这篇综述中，总结了凋亡及其残余物的清除，并讨论了SLE中参与凋亡细胞不完全清除的分子。
