Apoptosis and NET formation in the pathogenesis of SLE.

Abstract:

:Systemic Lupus Erythematosus is an autoimmune disease characterized by the formation of anti-nuclear autoantibodies, particularly anti-chromatin. Although the aetiology of the disease has not yet been fully elucidated, several mechanisms have been proposed to be involved. Due to an aberrant apoptosis or decreased removal of apoptotic cells, apoptotic blebs containing chromatin are released. During apoptosis, chromatin is modified that increases its immunogenicity. Myeloid dendritic cells (myDC) can take up apoptotic blebs and stimulate autoreactive T helper cells, and subsequently the formation of autoantibodies by autoreactive B cells. Immune complexes formed by anti-chromatin autoantibodies and modified chromatin deposit on basal membranes, and incite a local inflammation, but can also stimulate plasmacytoid dendritic cells to produce IFN-α. In addition to apoptotic blebs, neutrophil extracellular traps released by dying neutrophils, in a process called NETosis, may serve as a source of autoantigens as well. In this review, we describe the role of both apoptosis and NETosis in the pathogenesis of SLE, and show how both processes may interact with each other.

journal_name

Autoimmunity

journal_title

Autoimmunity

authors

Bouts YM,Wolthuis DF,Dirkx MF,Pieterse E,Simons EM,van Boekel AM,Dieker JW,van der Vlag J

doi

10.3109/08916934.2012.719953

subject

Has Abstract

pub_date

2012-12-01 00:00:00

pages

597-601

issue

8

eissn

0891-6934

issn

1607-842X

journal_volume

45

pub_type

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