Correlation of IgE Autoantibody to BP180 With a Severe Form of Bullous Pemphigoid

Iwata, Y.; Komura, Kazuhiro; Kodera, Masanari; Usuda, Toshikazu; Yokoyama, Yoko; Hara, Toshihide; Muroi, Eiji; Ogawa, Fumihide; Takenaka, Motoi; Sato, Shinichi

doi:10.1001/archdermatol.2007.9

Cited by 126 publications

(98 citation statements)

References 31 publications

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“…None of the 17 patients with IgG 4 as the only positive subclass had IgE antibodies against ADAMTS13, excluding a pathogenic role of IgE autoantibodies in TTP as described in, for example, bullous pemphigoid [14]. IgG subclasses (Fig.…”

Section: Subclass Distribution Of Igg Anti-adamts13 Antibodiesmentioning

confidence: 88%

IgG subclass distribution of anti‐ADAMTS13 antibodies in patients with acquired thrombotic thrombocytopenic purpura

Ferrari

Mudde²,

Rieger

et al. 2009

Journal of Thrombosis and Haemostasis

172

154

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Summary. Background: ADAMTS13‐neutralizing IgG autoantibodies are the major cause of acquired thrombotic thrombocytopenic purpura (TTP). Objective: To analyze the IgG subclass distribution of anti‐ADAMTS13 antibodies and a potential relationship between subclass distribution and disease prognosis. Methodology: An enzyme‐linked immunosorbent assay‐based method was used to quantify the relative amounts of IgG subclasses of anti‐ADAMTS13 antibodies in acquired TTP plasma. Results: IgG4 (52/58, 90%) was the most prevalent IgG subclass in patients with acquired TTP, followed by IgG1 (52%), IgG2 (50%), and IgG3 (33%). IgG4 was found either alone (17/52) or with other IgG subclasses (35/52). IgG4 was not detected in 10% of the patients. There was an inverse correlation between the frequency and abundance of IgG4 and IgG1 antibodies (P < 0.01). Patients with high IgG4 levels and undetectable IgG1 are more prone to relapse than patients with low IgG4 levels and detectable IgG1. Conclusions: All IgG subclasses of anti‐ADAMTS13 antibodies were detected in patients with acquired TTP, with IgG4, followed by IgG1, antibodies dominating the anti‐ADAMTS13 immune response. Levels of IgG4 could be useful for the identification of patients at risk of disease recurrence.

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Section: Subclass Distribution Of Igg Anti-adamts13 Antibodiesmentioning

confidence: 88%

IgG subclass distribution of anti‐ADAMTS13 antibodies in patients with acquired thrombotic thrombocytopenic purpura

Ferrari

Mudde²,

Rieger

et al. 2009

Journal of Thrombosis and Haemostasis

172

154

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“…[102,106] In line, serum levels of anti-NC16A IgE significantly correlated with disease severity in individual BP patients. [96,99,106,107] These data are further supported by Delaporte et al and Kalowska et al, who found the disappearance of IgE anti-BP180 autoantibodies to be associated with clinical remission. [101,102] Interestingly, in two infants with BP, no IgE reactivity against the NC16A domain was detectable.…”

Section: Bp180-specific Ige Autoantibodiesmentioning

confidence: 90%

“…[79] The percentage of BP patients with IgE anti-BP180 NC16A autoantibodies varied substantially in the different reports. [46,83,95,96,[99][100][101][102][103][104][105][106] In the initial report, we identified anti-BP180 NC16A IgE reactivity in 55% of 18 BP sera. [96] Subsequent studies found IgE anti-NC16A in 100% of 10, 83% of 18, 22% of 37, 77% of 43, 30% of 67, 61% of 31, and 71% of 56 BP patients.…”

Section: Bp180-specific Ige Autoantibodiesmentioning

confidence: 99%

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Beek

Schulze

Zillikens

et al. 2015

Expert Review of Clinical Immunology

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Autoimmune bullous diseases (AIBDs) are characterized by autoantibodies against structural proteins of the dermal-epidermal junction (in pemphigoid diseases) and the epidermal/ epithelial desmosomes (in pemphigus diseases). By far, the most common AIBD is bullous pemphigoid, which is immunopathologically characterized by autoantibodies against BP180 (type XVII collagen) and BP230. IgG and, to a lesser extent, IgA autoantibodies are the major autoantibody isotypes in these disorders. IgE autoantibodies are increasingly reported in particular in bullous pemphigoid. The development of specific and sensitive anti-BP180 IgE ELISA systems, the report of two experimental murine models employing IgE autoantibodies against BP180, and the successful treatment of bullous pemphigoid with the anti-IgE antibody omalizumab have raised interest in the role of IgE autoantibodies and the modulation of their production in AIBDs. Here, the relevance of IgE autoantibodies in the diagnosis, pathophysiology, and treatment decisions of AIBDs, with a focus on bullous pemphigoid, is reviewed. ARTICLE HISTORY

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“…Eighty-five percent and 46% of BP sera contained IgG1 and IgG4 Abs against hCOL17, respectively (6). The presence of IgG1 autoantibodies has been associated with active BP phenotypes (5,6), and the autoantibody level has been correlated with the area of skin blistering (29). These clinical findings indicate that IgG1 might be the main pathogenic subclass in BP.…”

mentioning

confidence: 83%

Human IgG1 Monoclonal Antibody against Human Collagen 17 Noncollagenous 16A Domain Induces Blisters via Complement Activation in Experimental Bullous Pemphigoid Model

Ujiie

Shibaki

et al. 2010

The Journal of Immunology

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Correlation of IgE Autoantibody to BP180 With a Severe Form of Bullous Pemphigoid

Abstract: To determine the prevalence, immunoglobulin subclass distribution, and clinical correlation of antibodies (Abs), especially of IgE Abs, to BP180 and BP230 in patients with bullous pemphigoid (BP).

Cited by 126 publications

References 31 publications

IgG subclass distribution of anti‐ADAMTS13 antibodies in patients with acquired thrombotic thrombocytopenic purpura

IgG subclass distribution of anti‐ADAMTS13 antibodies in patients with acquired thrombotic thrombocytopenic purpura

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Human IgG1 Monoclonal Antibody against Human Collagen 17 Noncollagenous 16A Domain Induces Blisters via Complement Activation in Experimental Bullous Pemphigoid Model

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