Complement-fixing pemphigus antibodies

Hashimoto, T.

doi:10.1001/archderm.114.8.1191

Cited by 7 publications

(3 citation statements)

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“…However, the mechanisms of blister formation in pemphigus after binding of autoantibodies to epidermal cells were largely unknown at that time. The involvement of the complement system and of proteases was intensely debated (25,27,28,(35)(36)(37)(38)(39). Further studies using F(ab 0 ) 2 and Fab fragments of IgG and mice deficient for C5 component have shown that complement is not required for the pathogenicity of pemphigus autoantibodies in vivo (40).…”

Section: Pemphigusmentioning

confidence: 99%

Mechanisms of blister induction by autoantibodies

Sitaru

Zillikens

2005

Experimental Dermatology

149

153

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Autoimmune diseases are characterized by defined self-antigens, organ specificity, autoreactive T cells and/or autoantibodies that can transfer disease. Autoimmune blistering diseases are organspecific autoimmune diseases associated with an immune response directed to structural proteins mediating cell-cell and cell-matrix adhesion in the skin. While both autoreactive T and B cells have been detected and characterized in patients with autoimmune blistering diseases, current evidence generally supports a pathogenic role of autoantibodies for blister formation. The immunopathology associated with blisters induced by autoantibodies relies on several mechanisms of action. Autoantibodies from patients with pemphigus diseases can exert a direct effect just by binding to their target mediated by steric hindrance and/or by triggering the transduction of a signal to the cell. In most subepidermal autoimmune blistering conditions, in addition to the binding to their target antigen, autoantibodies need to interact with factors of the innate immune system, including the complement system and inflammatory cells, in order to induce blisters. Generally, decisive progress has been made in the characterization of the mechanisms of blister formation in autoimmune skin diseases. However, various aspects, including the exact contribution of steric hindrance and signal transduction for pemphigus IgG-induced acantholysis or the fine tuning of the inflammatory cascade triggered by autoantibodies in some subepidermal blistering diseases, still need to be addressed. Understanding the mechanisms by which autoantibodies induce blisters should facilitate the development of more specific therapeutic strategies of autoimmune blistering diseases.

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Section: Pemphigusmentioning

confidence: 99%

Mechanisms of blister induction by autoantibodies

Sitaru

Zillikens

2005

Experimental Dermatology

149

153

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“…Complement fixing IF of normal human skin and indirect immunofluorescence of salt‐split skin for C3 was performed as described previously . cDNA transfection methods for detection of IgG and IgA antibodies to Dsc1–3 were performed by living‐cell staining using COS‐7 cells, as described previously …”

Section: Methodsmentioning

confidence: 99%

Summary of results of serological tests and diagnoses for 4774 cases of various autoimmune bullous diseases consulted to Kurume University

et al. 2016

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“…According to the current view, experimental acantholytic blister formation does not require the complement system (22). Circulating anti-epidermal ICS antibody in the patients' sera has not generally been believed to fix complement in vitro (24,25), although controversy has arisen in the recent literature (26)(27)(28)(29).…”

Section: Horseradish Peroxidase Labeled Antibody Methodfor Light and mentioning

confidence: 99%

Immunopathological Study on Perilesional Pemphigus Skin

Yamasaki

1981

The Journal of Dermatology

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Seven perilesional skin samples which appeared to be normal were obtained from patients with pemphigus and studied by means of direct immunofluorescence and horseradish peroxidase labeled antibody methods. Light microscopic observations revealed that in vivo bound IgG and C3 were localized in the intercellular cement substance region of the epidermis in both the direct immunofluorescence and horseradish peroxidase labeled antibody method in exactly the same fashion. Immunoelectronmicroscopic observations revealed that bound IgG and C3 were localized exclusively in the epidermal intercellular cement substance region, but not in any intracellular organellae, pinocytotic vesicles, cytosol, basal lamina or upper dermis. Bound IgG was detected in all seven cases. Bound C3 was detected in four of the seven cases. Both of these globulins were localized exclusively in the nondesmosomal and desmosomal epidermal intercellular cement substance region, apparently in the same fashion. It was suggested immunoelectronmicroscopically that not only IgG, but also the complement system might be involved in the formation of the skin lesion in pemphigus.

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Complement-fixing pemphigus antibodies

Cited by 7 publications

References 0 publications

Mechanisms of blister induction by autoantibodies

Mechanisms of blister induction by autoantibodies

Summary of results of serological tests and diagnoses for 4774 cases of various autoimmune bullous diseases consulted to Kurume University

Immunopathological Study on Perilesional Pemphigus Skin

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