Characterization of C1q-binding IgG complexes in systemic lupus erythematosus

Uwatoko, Shu; Aotsuka, S; Okawa, Masako; Egusa, Yasuo; Yokohari, R; Aizawa, Chikara; Suzuki, Keiji

doi:10.1016/0090-1229(84)90011-4

Cited by 86 publications

(53 citation statements)

References 27 publications

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“…Anti-C1q antibodies were first described by Uwatoko et al in 1984 (5). Whereas complexed IgG mainly binds to the globular portion of C1q, anti-C1q antibodies bind to the collagenous portion, which apparently is the main immunogenic region of the molecule and its Fab fragments (6).…”

mentioning

confidence: 99%

Anti‐C1q antibodies are associated with systemic lupus erythematosus global activity but not specifically with nephritis: A controlled study of 126 consecutive patients

Katsumata

Miyake

Kawaguchi

et al. 2011

Arthritis & Rheumatism

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Objective. Several studies have shown that antiC1q antibodies correlate with the occurrence and activity of nephritis in systemic lupus erythematosus (SLE). However, the significance of anti-C1q antibodies in SLE has not been fully characterized. The aim of this study was to investigate associations between anti-C1q antibodies and clinical and serologic parameters of SLE.Methods. An enzyme-linked immunosorbent assay kit was used to measure anti-C1q antibodies in the sera of 126 consecutive patients with active SLE who were admitted to our university hospital from 2007 through 2009. Sera obtained from patients with high titers of anti-C1q antibodies at the initial evaluation (n ‫؍‬ 20) were reevaluated following treatment. Control sera were obtained from patients with other autoimmune diseases and from normal healthy control subjects (n ‫؍‬ 20 in each group). Associations between anti-C1q antibodies and clinical and serologic parameters of SLE were statistically analyzed.Results. Anti-C1q antibodies were detected in the sera of 79 of 126 patients with SLE. The prevalence and titers of anti-C1q antibodies were significantly (P < 0.0001) higher in SLE patients than in patients with rheumatoid arthritis, patients with systemic sclerosis, and normal healthy control subjects. The prevalence and titers of anti-C1q antibodies were not significantly associated with active lupus nephritis (P ‫؍‬ 0.462 and P ‫؍‬ 0.366, respectively). Anti-C1q antibody titers were significantly correlated with SLE Disease Activity Index 2000 scores and the levels of anti-doublestranded DNA antibodies, C3, C4, CH50, and C1q (P < 0.0001 for all comparisons). Moreover, anti-C1q antibody titers significantly decreased as clinical disease was ameliorated following treatment (P ‫؍‬ 0.00097).Conclusion. These findings indicate that anti-C1q antibodies are associated with SLE global activity but not specifically with active lupus nephritis.

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confidence: 99%

Anti‐C1q antibodies are associated with systemic lupus erythematosus global activity but not specifically with nephritis: A controlled study of 126 consecutive patients

Katsumata

Miyake

Kawaguchi

et al. 2011

Arthritis & Rheumatism

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“…Several groups demonstrated the presence of IgG anti-ClqAb in sera of approximately 50% of patients with SLE [13][14][15]. In 1971 Agnello et al [16] reported that in sera patients with SLE monomeric IgG with reactivity for Clq could be found.…”

Section: Discussionmentioning

confidence: 99%

“…In 1971 Agnello et al [16] reported that in sera patients with SLE monomeric IgG with reactivity for Clq could be found. Other studies on F(ab')2 fragments of IgG were shown to react with the collagen-like region (CLR) of Clq [13,17]. Binding of serum IgG was demonstrated in the presence of 1 M NaCl which excludes aspecific binding of serum IgG to Clq [9].…”

Section: Discussionmentioning

confidence: 99%

Antibodies against C1q in anti-glomerular basement membrane nephritis

Coremans

Daha

Voort

et al. 1992

Clinical and Experimental Immunology

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SUMMARYThe prevalenee of antibodies against the collagen-like region of the subeomponent of the first component of complement, Clq, was investigated in 11 patients with anti-glomerular basement membrane (GBM) nephritis. Anti-Clq antibodies (anti-ClqAb) were deteeted in seven patients. IgG anti-C 1 q Ab were found in four and IgA anti-C 1 q Ab in five patients. During follow up of the patients a relationship was observed between the levels of IgG anti-ClqAb and the levels of anti-GBM antibodies (anti-GBMAb). Gelfiltration experiments indicated that both IgG anti-ClqAb as well as IgG anti-GBMAb were monomeric and that binding also occurred with the F(ab')2 fragments of the antibodies. Although anti-ClqAb and anti-GBMAb are both directed against a collagen-like structure, it was demonstrated by means of inhibition experiments that anti-ClqAb and antiGBMAb are directed against different antigenic sites. Comparison of patients with anti-GBM nephritis with and without anti-ClqAb revealed that there were no differences in disease activity or disease severity. Therefore, the results of this study suggest that anti-ClqAb do not play a direct pathogenetie role in anti-GBM nephritis.

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“…The presence of IgG class autoantibodies to C1q in lupus was first reported in 1984 [146]. Further investigations revealed that the majority of IgG binding to C1q in solid phase assays was attributable to autoantibodies reacting with an epitope only exposed in structurally modified C1q [147].…”

Section: Development and Pathogenicity Of Antibodies Against Acute-phmentioning

confidence: 94%

Pathogenic implications for autoantibodies against C-reactive protein and other acute phase proteins

Sjöwall

Wetterö

2007

Clinica Chimica Acta

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Systemic lupus erythematosus (SLE) is a systemic rheumatic disease characterized clinically by multiorgan involvement and serologically by the occurrence of antinuclear antibodies. SLE patients may present with multiple autoantibodies to cytoplasmic and cell surface antigens as well as to circulating plasma proteins. Another feature of SLE is that serum levels of C-reactive protein (CRP) often remain low despite high disease activity and despite high levels of other acute phase proteins and interleukin-6, i.e. the main CRP inducing cytokine. Apart from its important role as a laboratory marker of inflammation, CRP attracts increasing interest due to its many intriguing biological functions, one of which is a role as an opsonin contributing to the elimination of apoptotic cell debris, e.g. nucleosomes, thereby preventing immunization against autoantigens. Recently, autoantibodies against CRP and other acute phase proteins have been reported in certain rheumatic conditions, including SLE. Although the presence of anti-CRP autoantibodies does not explain the failed CRP response in SLE, antibodies directed against acute phase proteins have several implications of pathogenetic interest. This paper thus highlights the biological and clinical aspects of native and monomeric CRP and anti-CRP, as well as autoantibodies against mannose-binding lectin, serum amyloid A and serum amyloid P component. © 2006 Elsevier B.V. All rights reserved

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Characterization of C1q-binding IgG complexes in systemic lupus erythematosus

Cited by 86 publications

References 27 publications

Anti‐C1q antibodies are associated with systemic lupus erythematosus global activity but not specifically with nephritis: A controlled study of 126 consecutive patients

Anti‐C1q antibodies are associated with systemic lupus erythematosus global activity but not specifically with nephritis: A controlled study of 126 consecutive patients

Antibodies against C1q in anti-glomerular basement membrane nephritis

Pathogenic implications for autoantibodies against C-reactive protein and other acute phase proteins

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