The Distribution of IgA Pemphigus Antigen in Human Skin and the Role of IgA Anti-Cell Surface Antibodies in the Induction of Intraepidermal Acantholysis

Supapannachart, Nantapat; Mutasim, Diya F.

doi:10.1001/archderm.1993.01680260075010

Cited by 29 publications

(12 citation statements)

References 15 publications

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“…In extension of previous findings, our case demonstrates that, in addition to IgG autoantibodies, IgA autoantibodies might be associated and play themselves a specific part in the pathogenesis of pemphigus. This has already been suggested by Supapannachart and Mutasim 13 who reported that sera from patients with IgA pemphigus induced intraepidermal acantholysis in a skin explant culture, proving that anti‐intercellular IgA antibody can induce intraepidermal acantholysis in vivo. The part that play IgA anticell antibodies in the pathogenesis of pemphigus has been first reported by Wallach et al.…”

Section: Discussionsupporting

confidence: 61%

IgG/IgA pemphigus with IgG and IgA antidesmoglein 3 antibodies and IgA antidesmoglein 1 antibodies detected by enzyme‐linked immunosorbent assay: a case report and review of the literature

et al. 2010

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Section: Discussionsupporting

confidence: 61%

IgG/IgA pemphigus with IgG and IgA antidesmoglein 3 antibodies and IgA antidesmoglein 1 antibodies detected by enzyme‐linked immunosorbent assay: a case report and review of the literature

et al. 2010

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“…IgA may exert acantholytic properties in IgA pemphigus, as its ultrastructural localization in skin correlates with the site of blister formation. Moreover, IgA from a patient with IgA pemphigus induced acantholysis in skin explant cultures 23,29 . As the concentrations of Dsg3‐reactive IgA in PV sera seem to be much lower than those of Dsg3‐reactive IgG1 and IgG4, the biological role of IgA autoantibodies in PV remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

IgG, IgA and IgE autoantibodies against the ectodomain of desmoglein 3 in active pemphigus vulgaris

et al. 2001

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“…Serum samples from two patients with IgA pemphigus were shown to induce acantholytic blisters in skin explant cultures. Neither bound nor circulating IgA autoantibody was complement fixing (93). Further studies using in vitro and in vivo systems and IgA purified from patients are required to demonstrate the pathogenic potential of IgA autoantibodies and the relevance of their possible interaction with granulocytes in IgA pemphigus.…”

Section: Are Iga Pemphigus Autoantibodies Causing Blisters?mentioning

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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The Distribution of IgA Pemphigus Antigen in Human Skin and the Role of IgA Anti-Cell Surface Antibodies in the Induction of Intraepidermal Acantholysis

Cited by 29 publications

References 15 publications

IgG/IgA pemphigus with IgG and IgA antidesmoglein 3 antibodies and IgA antidesmoglein 1 antibodies detected by enzyme‐linked immunosorbent assay: a case report and review of the literature

IgG/IgA pemphigus with IgG and IgA antidesmoglein 3 antibodies and IgA antidesmoglein 1 antibodies detected by enzyme‐linked immunosorbent assay: a case report and review of the literature

IgG, IgA and IgE autoantibodies against the ectodomain of desmoglein 3 in active pemphigus vulgaris

Mechanisms of blister induction by autoantibodies

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