Immunoconglutinin in various rheumatic diseases and certain diseases suspected of an autoimmune pathogenesis

Bienenstock, John; Bloch, Kurt J.

doi:10.1002/art.1780100304

Cited by 23 publications

(7 citation statements)

References 40 publications

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“…Several studies have also shown that the levels of IgM IKs are elevated but quickly returned to normal without evidence of a secondary antibody response, during infections and exacerbations of autoimmune diseases in humans or after repeated i.v. injections of various bacteria in animals [1,20]. In contrast to other autoimmune diseases, SLE patients have previously been shown to exhibit a decrease in the agglutination titre of IKs during an acute exacerbation, although the titre remains higher than in normal individuals (201.…”

Section: Discussionmentioning

confidence: 99%

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Detection and characterization of immunoconglutinins in patients with systemic lupus erythematosus (SLE): serial analysis in relation to disease course

Nilsson

Ekdahl

Sjöholm

et al. 1992

Clinical and Experimental Immunology

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SUMMARYThe levels of IgA. IgG and IgM immunoconglulinins (IK) were assessed in sera from 20 palienls wilh SLE which were followed for 8-monlh periods. Al the time of the exacerbation, IgG IKs were significantly increased to 226 + 90 arbitrary units (mean±s.e.m.) compared wilh both the minimum value of 75 + 28 in the SLE patients and with 31+2 in healthy controls (/*<005). There was no difference between SLE patients and controls in the levels of IgM and IgA IKs. Most of the SLE patients in this material showed maximal IgG IK levels before exacerbation, but there was no correlation between the clinical disease index and the levels of IgG IK. The specificity of IgG IKs showed a broad diversity for microtit re-fixed C3b, iC3b. C3c and C3dg. The antibodies were of IgG 1, IgG3 and in two patients. lgG4 subclass. IgG IKs were correlated to the C3d/C3 ratio which suggested that the IK responses were secondary to C3 activation. In summary, unlike other conditions associated with complement activation where elevated IgM 1 Ks are common, an increase in IgG IK levels was observed. It is possible that this diverging IK response contributes to the pathophysiology of the disease.

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Section: Discussionmentioning

confidence: 99%

“…injections of various bacteria in animals [1,20]. In contrast to other autoimmune diseases, SLE patients have previously been shown to exhibit a decrease in the agglutination titre of IKs during an acute exacerbation, although the titre remains higher than in normal individuals (201.…”

Section: Discussionmentioning

confidence: 99%

Detection and characterization of immunoconglutinins in patients with systemic lupus erythematosus (SLE): serial analysis in relation to disease course

Nilsson

Ekdahl

Sjöholm

et al. 1992

Clinical and Experimental Immunology

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“…Such a change in structure to reveal a neoepitope may follow proteolytic cleavage, a conformational change following activation or following binding of the protein to another protein. Amongst the earliest autoantibodies to complement proteins to be identified were immunoconglutinins and these have been found in the sera of patients with SLE [71,72]. These autoantibodies bind to an activation product of C3 known as iC3b and are something of an esoteric curiosity since, although quite common, they have never been shown to play any direct role in disease.…”

Section: Complement and Sle: The Clinical Observationsmentioning

confidence: 99%

Untitled

Walport

2002

Arthritis Res

247

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Chapter summaryComplement is implicated in the pathogenesis of systemic lupus erythematosus (SLE) in several ways and may act as both friend and foe. Homozygous deficiency of any of the proteins of the classical pathway is causally associated with susceptibility to the development of SLE, especially deficiency of the earliest proteins of the activation pathway. However, complement is also implicated in the effector inflammatory phase of the autoimmune response that characterizes the disease. Complement proteins are deposited in inflamed tissues and, in experimental models, inhibition of C5 ameliorates disease in a murine model. As a further twist to the associations between the complement system and SLE, autoantibodies to some complement proteins, especially to C1q, develop as part of the autoantibody response. The presence of anti-C1q autoantibodies is associated with severe illness, including glomerulonephritis. In this chapter the role of the complement system in SLE is reviewed and hypotheses are advanced to explain the complex relationships between complement and lupus.

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“…Our experiences with simultaneous determination of serum CH and Cc may suffice to prove that it would be worth while, with the use of modern methods, to reformulate the concept of the conglutinating complement and especially the role of the conglutinin‐immunoconglutinin system in the functioning of the complement system. Bienenstock and Bloch (11) suggest that immunoconglutinin could interact with the complement sequence at several steps and they speculate that immunoconglutinin might have either beneficial or detrimental effects on the host under different circumstances.…”

Section: Discussionmentioning

confidence: 99%