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2014 ; 26
(5
): 459-66
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Beyond apoptosis in lupus
#MMPMID25036095
Colonna L
; Lood C
; Elkon KB
Curr Opin Rheumatol
2014[Sep]; 26
(5
): 459-66
PMID25036095
show ga
PURPOSE OF REVIEW: Systemic lupus erythematosus (SLE) is characterized by
autoantibodies directed against nuclear autoantigens normally concealed from
immune recognition in healthy individuals. Here, we summarize recently identified
mechanisms of abnormal cell death leading to exposure and aberrant processing of
nucleoprotein self antigens, and discuss their role in the SLE pathogenesis.
RECENT FINDINGS: During the past few years, the unveiling of several new forms of
cell death has expanded our understanding beyond the simple view of 'apoptotic'
versus 'necrotic' cell death. SLE patients show abnormalities in cell death at
several levels, including increased rates of apoptosis, necrosis, and autophagy,
as well as reduced clearance of dying cells. These abnormalities lead to an
increased autoantigen burden and antigen modifications, such as nucleic acid
oxidation that increases the inflammatory properties of self antigens. Recent
investigations have highlighted the role of opsonins in determining the
immunogenic versus tolerogenic characteristics of self antigens. SUMMARY:
Dysregulation of different forms of programmed cell death contributes to
increased exposure, availability, and immunogenic characteristics of
intracellular self antigens, which all participate in development of lupus
autoimmunity. As our understanding of abnormalities of cell death in SLE
advances, potential therapeutic opportunities await human implementation.
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