Membranous Glomerulopathy

Bruijn, Jan A.

doi:10.1007/978-0-387-31127-2_2

Cited by 1 publication

(1 citation statement)

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“…Indeed, many anti-dsDNA antibodies cross-react with glomerular antigens [4]. Clinical involvement of the kidneys occurs in 50–80% of lupus patients during the course of their disease and renal pathology is found in as many as 90% of patients at autopsy [5]. …”

Section: Introductionmentioning

confidence: 99%

Anti-DNA antibodies cross-react with C1q

Franchin

Son

Kim

et al. 2013

Journal of Autoimmunity

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Systemic lupus erythematosus (SLE) is an autoimmune disorder that involves multiple organ systems and typically presents as a chronic inflammatory disease. Antibodies to double-stranded (ds) DNA are present in approximately 70% of patients and form nucleic acid containing immune complexes which activate dendritic cells through engagement of toll-like receptors, leading to a pro-inflammatory, pro-immunogenic milieu. In addition, anti-dsDNA antibodies deposit in kidneys to initiate glomerulonephritis. Antibodies to C1q have also been implicated in lupus nephritis and are found in 30–50% of patients. C1q is a known suppressor of immune activation and C1q deficiency is the strongest risk factor for SLE. We previously identified a subset of anti-DNA antibodies that binds the N-methyl-d-aspartate receptor. We now show that both mouse and human anti-DNA antibodies with this specificity bind C1q. These antibodies bind to Clq in glomeruli and exhibit decreased glomerular deposition in the absence of C1q. We propose that this subset of anti-DNA antibodies participates in lupus pathogenesis through direct targeting of C1q on glomeruli and also through removal of soluble C1q thereby limiting the ability of C1q to mediate immune homeostasis.

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Section: Introductionmentioning

confidence: 99%