Premium
Incomplete clearance of apoptotic cells in systemic lupus erythematosus: pathogenic role and potential biomarker
Author(s) -
Jung JuYang,
Suh ChangHee
Publication year - 2015
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.12568
Subject(s) - apoptosis , immune system , immunology , inflammation , receptor , medicine , programmed cell death , cancer research , microbiology and biotechnology , biology , biochemistry
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. T yro3‐ A xl‐ M er receptors, their bridging molecules, milk fat globulin epidermal growth factor‐8, T ‐cell immunoglobulin mucin domain protein family, scavenger receptors, C 1q, 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.