Anti-C1q receptor/calreticulin autoantibodies in patients with systemic lupus erythematosus (SLE)
Authors: Van Den Berg,1; Siegert1; Faber-Krol1; Huizinga2; Van ES,1; Daha1
Source: Clinical & Experimental Immunology, Volume 111, Number 2, February 1998 , pp. 359-364(6)
Publisher: Blackwell Publishing
Abstract:
SLE is a disease characterized by the presence of multiple autoantibodies and high levels of circulating immune complexes. We studied the presence and functional relevance of autoantibodies directed against a receptor for the collagen-like stalks of the first subcomponent of complement, also known as calreticulin (cC1qR/CaR), in patients with SLE. In a cross-sectional study it was found that higher titres of antibodies against cC1qR/CaR are present in sera of SLE patients compared with normal donors. No association between anti-cC1qR/CaR titres and SLE disease activity was found. Following gel filtration of SLE serum it was found that anti-cC1qR/CaR reactivity is associated with the peak of monomeric IgG. Purified IgG from patients was able to specifically immunoprecipitate cC1qR/CaR. Since we have shown previously that cC1qR/CaR is able to inhibit the haemolytic activity of C1q, we determined a possible pathogenic role for anti-cC1qR/CaR on complement regulation. IgG derived from SLE serum reversed the inhibitory capacity of cC1qR/CaR in a dose-dependent fashion up to 63%, whereas IgG from normal donors had no significant effect. With respect to the capacity of anti-cC1qR/CaR antibodies to activate neutrophils, it was found that incubation of normal neutrophils with F(ab′)2 anti-cC1qR/CaR resulted in a very limited oxidative burst. However, cross-linking of F(ab′)2 anti-cC1qR/CaR on the neutrophils clearly induced neutrophil activation. Pre-incubation of the SLE-derived F(ab′)2 with cC1qR/CaR prevented activation of neutrophils up to 81 ± 5%. These results suggest that the presence of anti-cC1qR/CaR antibodies in patients with SLE may modulate complement and neutrophil activation.Keywords: human; neutrophils; lupus; autoantibodies; complement; calreticulin; C1q receptor
Document Type: Original article
DOI: 10.1046/j.1365-2249.1998.00473.x
Affiliations: 1: Departments of Nephrology, 2: Rheumatology, Leiden University Hospital, Leiden, The Netherlands

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