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Publication year
2008Source
Lupus, 17, 5, (2008), pp. 371-375ISSN
Publication type
Article / Letter to editor

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Organization
Nephrology
Journal title
Lupus
Volume
vol. 17
Issue
iss. 5
Page start
p. 371
Page end
p. 375
Subject
IGMD 9: Renal disorder; N4i 4: Auto-immunity, transplantation and immunotherapy; NCMLS 1: Immunity, infection and tissue repair; NCMLS 1: Infection and autoimmunity; NCMLS 3: Tissue engineering and pathology; UMCN 4.2: Chronic inflammation and autoimmunityAbstract
Systemic lupus erythematosus (SLE) is a prototype inflammatory autoimmune disease resulting from autoimmune responses against nuclear autoantigens. During apoptosis many lupus autoantigens congregate inside the cells and are susceptible to modifications. Modified nuclear constituents are considered foreign and dangerous. Therefore, apoptotic cells have to has to be efficiently removed to avoid the accumulation of apoptotic debris and the subsequently development of autoimmune responses. Hence, apoptosis and clearance of apoptotic cells/material are considered key processes in the aetiology of SLE. Clearance deficiencies may account for the development of autoimmunity by inducing a loss of tolerance in lymphoid tissues. Furthermore, phagocytosis of apoptotic cells may lead to a pro-inflammatory response in the presence of autoantibodies. This may sustain inflammatory conditions and the pathology found in overt lupus.
This item appears in the following Collection(s)
- Academic publications [204887]
- Electronic publications [103214]
- Faculty of Medical Sciences [81046]
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