Calcium-dependent and calcium-independent signals in the conglutinin-binding assay (KgBa) for immune complexes

Holmskov, Uffe; Haas, Helmut; Teisner, B.; Andersen, Ove; Jensenius, Jens C.

doi:10.1016/0022-1759(92)90176-t

Cited by 22 publications

(4 citation statements)

References 24 publications

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“…Immune responses to alimentary antigens, including bovine plasma proteins are not uncommon [30], which could be one reason for the occurrence of antibodies against BK. In a previous study, detection of anti-BK antibodies by ELISA was inhibited by soluble BK as might be expected if the antibodies recognize epitopes of native protein [31]. We confirmed the presence of such anti-BK antibodies in the sera of SLE patients and healthy controls.…”

Section: Discussionsupporting

confidence: 85%

Human Autoantibodies Against C1q: Lack of Cross‐Reactivity with the Collectins Mannan‐Binding Protein, Lung Surfactant Protein A and Bovine Conglutinin

et al. 1996

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The collectins, a group of humoral C-type lectins, have globular and collagen-like regions and share structural features with the complement protein C1q. The question was asked if autoantibodies to the collagen-like region of C1q (anti-C1qCLR) might cross-react with collectins, such as mannan-binding protein (MBP), lung surfactant protein A (SP-A) and bovine conglutinin (BK). Anti-C1qCLR antibodies of the systemic lupus erythematosus (SLE) type and anti-C1qCLR antibodies of the hypocomplementemic urticarial vasculitis syndrome (HUVS) type were investigated. Cross-absorption and elution experiments combined with antibody detection by enzyme-linked immunosorbent assay (ELISA) and immunoblot analysis gave no evidence of cross-reactive anti-C1qCLR antibodies. However, one serum with HUVS type anti-C1qCLR antibodies contained anti-MBP antibodies that were cross-reactive with SP-A. Judging from results of ELISA inhibition experiments and immunoblot analysis, four SLE sera contained antibodies to native BK, while two sera with HUVS type anti-C1qCLR antibodies contained antibodies to epitopes of denatured BK. This might imply that autoimmunity to collagen-like structures is not restricted to C1qCLR in HUVS and HUVS/SLE overlap syndromes.

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Section: Discussionsupporting

confidence: 85%

Human Autoantibodies Against C1q: Lack of Cross‐Reactivity with the Collectins Mannan‐Binding Protein, Lung Surfactant Protein A and Bovine Conglutinin

et al. 1996

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“…Finally, the C. pneumoniae-specific monoclonal antibody was used to detect antigen in serum IC that were tested with and without EDTA. EDTA inhibits calcium-dependent iC3b binding to conglutinin but not the adherence of cross-reacting antibodies (calcium-independent binding), which may be formed against dietary conglutinin [38]. Therefore, we only determined a sample to be positive for C. pneumoniae-specific IC if, in the presence of EDTA, the OD was reduced by more than 20%.…”

Section: Discussionmentioning

confidence: 99%

Chlamydia pneumoniae-specific serum immune complexes in patients with multiple sclerosis

et al. 2008

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The significance of Chlamydia pneumoniae infection in patients with multiple sclerosis (MS) is unclear. We determined the frequency of serum C. pneumoniae-specific immune complexes in patients with MS, neurological (OND) and healthy controls in a blinded, cross-sectional study. C. pneumoniae immune complexes were detected in 24% (38/156) of MS patients, 16% (11/69) of OND and 15% (77/499) of healthy controls. The odds ratio for all MS patients was 3.95 (95% CI: 2.15 to 7.24; P < 0.0001) accounting for the covariates: sex, age, socio-economic status and area of residence. The odds ratio for recently diagnosed MS patients was 4.33 (95% CI: 1.76 to 10.64; P = 0.001). Systemic C. pneumoniae infection is more frequent in MS patients than the healthy population and occurs early in the course of the disease.

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“…Like the C1q-binding assay, this assay is prone to interference, in particular from anti-collagen II antibodies. 25 As these antibodies are frequently found in connective tissue diseases, 26 the utility of the assay is restricted. One study has advocated the use of the ratio of calciumdependent to calcium-independent binding to overcome the interference from conglutininbinding antibodies.…”

Section: Conglutinin-binding Assaysmentioning

confidence: 99%

Measurement of immune complexes is not useful in routine clinical practice

Lock¹,

Unsworth²

2000

Ann Clin Biochem

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The vogue for the determination of immune complexes (ICs) in the clinical setting has now passed, as can be seen from the fact that only two of the regional immunology reference laboratories in the UK still offer a service. This is partly due to the lack of speci®city seen in the assays available, which, apart from minor modi®cations, have remained essentially unchanged. They have not lived up to their initial promise and are unlikely to be offered by service laboratories in the future. In this review we consider when these assays may still have a role and which might be the most useful in a particular clinical setting.An IC is formed when an antibody reacts speci®cally with its corresponding antigen. The size of the complex formed is dependent on many factors, including the ratio of antibody to antigen, the valency of the antigen and the avidity of the antibody±antigen reaction. IC formation is an integral part of the normal immune response to infection and usually takes place without adverse pathological consequences. ICs are captured by speci®c receptors, in particular on erythrocytes, and transported to the reticuloendothelial system for processing and removal. The events leading to IC formation and subsequent removal are summarized in Fig. 1. There are, however, various disorders in which ICs play an important role in the disease process. These include some forms of vasculitis (e.g. Henoch±SchoÈ nlein purpura), infectious disorders (e.g. bacterial endocarditis, shunt nephritis) and connective tissue autoimmune disorders [e.g. rheumatoid arthritis (RA), systemic lupus erythematosus (SLE)]. The pathology generally arises from inappropriate clearance or deposition of ICs. Thus, vasculitis DETECTION OF CIC IN BODY FLUIDS (USUALLY SERUM)At least 40 different assays for CICs have been described. They vary widely in terms of disease sensitivity, speci®city and clinical applicability. Possibly the major area of investigation has been in autoimmune disease, in particular SLE. SLE has been considered the archetypal IC disease. Many of the disease manifestations, including

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Calcium-dependent and calcium-independent signals in the conglutinin-binding assay (KgBa) for immune complexes

Cited by 22 publications

References 24 publications

Human Autoantibodies Against C1q: Lack of Cross‐Reactivity with the Collectins Mannan‐Binding Protein, Lung Surfactant Protein A and Bovine Conglutinin

Human Autoantibodies Against C1q: Lack of Cross‐Reactivity with the Collectins Mannan‐Binding Protein, Lung Surfactant Protein A and Bovine Conglutinin

Chlamydia pneumoniae-specific serum immune complexes in patients with multiple sclerosis

Measurement of immune complexes is not useful in routine clinical practice

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