Antibodies to the collagen‐like region of C1q in sera of patients with autoimmune rheumatic diseases

Wener, Mark H.; Uwatoko, Shu; Mannik, Mart

doi:10.1002/anr.1780320506

Cited by 92 publications

(58 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For comparison, in unselected series of patients with SLE, the prevalence of IgG antibodies to Clq-CLR has varied from 17% to 46% (13)(14)(15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

“…The presence of antibodies to Clq-CLR was detected with an enzyme-linked immunosorbent assay (ELISA) system, as previously described (13). Briefly, Clq was isolated from outdated plasma and Clq-CLR was prepared with previously described methods (21).…”

Section: Methodsmentioning

confidence: 99%

“…Studies that used Clq as a test for immune complexes, and subsequent studies that used the purified collagen-like region of Clq (Clq-CLR) as antigen have provided definitive evidence for serum antibodies to Clq-CLR in patients with proliferative lupus glomerulonephritis (10)(11)(12)(13). Several independent investigations have established the high prevalence of autoantibodies to Clq-CLR in patients with proliferative lupus glomerulonephritis (14)(15)(16)(17).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Mannik

Wener

1997

Arthritis & Rheumatism

Self Cite

104

View full text Add to dashboard Cite

Objective. To determine if antibodies to the collagen-like region of Clq (Clq-CLR) are present in the glomerular immune deposits of patients with systemic lupus erythematosus (SLE).Methods. Kidney tissues were obtained at autopsy, glomeruli were isolated, and glomerular basement membrane fragments were prepared. Antibodies were extracted with low pH or with DNase.Results. The concentrations of antibodies to Clq-CLR recovered from the glomeruli were 150-fold higher per unit of IgG than that found in the serum or in the serum and interstitial fluid entrained in glomeruli. Antibodies to Clq-CLR were recovered from glomeruli of 4 of 5 patients with proliferative glomerulonephritis at autopsy.Conclusion. This is the first demonstration that antibodies to Clq-CLR are deposited and concentrated in the renal glomeruli of patients with SLE. These antibodies, thus, have the potential of contributing to the pathogenesis of lupus glomerulonephritis.

show abstract

“…For comparison, in unselected series of patients with SLE, the prevalence of IgG antibodies to Clq-CLR has varied from 17% to 46% (13)(14)(15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Mannik

Wener

1997

Arthritis & Rheumatism

Self Cite

104

View full text Add to dashboard Cite

show abstract

“…Addition of fluid phase Clq only partially inhibited the binding of anti-C1 qAb to solid phase Clq. This can be explained by the fact that anti-ClqAb in patients' sera only react with either soHd phase or immune complex (ICs) bound Clq [18]. The fluid phase Clq preparation used can partially inhibit anti-ClqAb activity because of the presence of aggregates of Clq.…”

Section: Discussionmentioning

confidence: 99%

Antibodies against C1q in anti-glomerular basement membrane nephritis

Coremans

Daha

Voort

et al. 1992

Clinical and Experimental Immunology

View full text Add to dashboard Cite

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.

show abstract

“…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]. Such a change in structure, to reveal a 'neo-epitope', may follow proteolytic cleavage, a conformational change following activation or following binding to another protein.…”

Section: Development and Pathogenicity Of Antibodies Against Acute-phmentioning

confidence: 98%

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

Sjöwall

Wetterö

2007

Clinica Chimica Acta

View full text Add to dashboard Cite

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

show abstract

Antibodies to the collagen‐like region of C1q in sera of patients with autoimmune rheumatic diseases

Cited by 92 publications

References 28 publications

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Deposition of antibodies to the collagen‐like region of C1Q in renal glomeruli of patients with proliferative lupus glomerulonephritis

Antibodies against C1q in anti-glomerular basement membrane nephritis

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

Contact Info

Product

Resources

About