Autoantibody-induced intestinal inflammation and weight loss in experimental epidermolysis bullosa acquisita (Q47387894)

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title

Autoantibody-induced intestinal inflammation and weight loss in experimental epidermolysis bullosa acquisita (English)

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epidermolysis bullosa

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7

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Detlef Zillikens

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object named as

Detlef Zillikens

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5

Takashi Hashimoto

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author name string

Norito Ishii

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Andreas Recke

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Sidonia Mihai

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Misa Hirose

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publication date

7 March 2011

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published in

Journal of Pathology

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volume

224

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issue

2

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page(s)

234-244

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Genetic linkage of type VII collagen (COL7A1) to dominant dystrophic epidermolysis bullosa in families with abnormal anchoring fibrils

cites work

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Mutation analysis and characterization of COL7A1 mutations in dystrophic epidermolysis bullosa

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Autoimmunity to type VII collagen: epidermolysis bullosa acquisita

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Mechanisms of blister induction by autoantibodies

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Epidermolysis bullosa acquisita antigen is the globular carboxyl terminus of type VII procollagen

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Epitope mapping of type VII collagen. Identification of discrete peptide sequences recognized by sera from patients with acquired epidermolysis bullosa

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Epitope mapping for epidermolysis bullosa acquisita autoantibody by molecularly cloned cDNA for type VII collagen

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Granulocyte-derived elastase and gelatinase B are required for dermal-epidermal separation induced by autoantibodies from patients with epidermolysis bullosa acquisita and bullous pemphigoid

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Organ-specific, phylogenetic, and ontogenetic distribution of the epidermolysis bullosa acquisita antigen.

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The epidermolysis bullosa acquisita antigen (type VII collagen) is present in human colon and patients with crohn's disease have autoantibodies to type VII collagen.

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Evidence that anti-type VII collagen antibodies are pathogenic and responsible for the clinical, histological, and immunological features of epidermolysis bullosa acquisita

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Induction of epidermolysis bullosa acquisita in mice by passive transfer of autoantibodies from patients

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PS3, a semisynthetic beta-1,3-glucan sulfate, diminishes contact hypersensitivity responses through inhibition of L- and P-selectin functions.

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Neutrophils are essential for early anti-Listeria defense in the liver, but not in the spleen or peritoneal cavity, as revealed by a granulocyte-depleting monoclonal antibody

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Junctional adhesion molecules (JAM)-B and -C contribute to leukocyte extravasation to the skin and mediate cutaneous inflammation

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The immunological and genetic basis of inflammatory bowel disease

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Autoimmunity to tropomyosin isoforms in ulcerative colitis (UC) patients and unaffected relatives

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Anti-Saccharomyces cerevisiae mannan antibodies combined with antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease: prevalence and diagnostic role

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Animal models for autoimmune bullous dermatoses.

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Use of autoantigen-knockout mice in developing an active autoimmune disease model for pemphigus

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Identifiers

DOI

10.1002/PATH.2857

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15 January 2018

PubMed ID

21381035

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15 January 2018