The 120-kDa soluble ectodomain of type XVII collagen is recognized by autoantibodies in patients with pemphigoid and linear IgA dermatosis

Roh, Joo‐Young; Yee, Carole; Lazarova, Zelmira; Hall, Russell P.; Yancey, Kim B.

doi:10.1046/j.1365-2133.2000.03598.x

Cited by 39 publications

(26 citation statements)

References 28 publications

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“…[16][17][18][19][20][21] Various antigenic sites on the extracellular domain of this anchoring filament protein have been shown to be targeted by autoantibodies in different autoimmune bullous diseases (bullous pemphigoid, cicatricial pemphigoid, and others). The hemidesmosome is a membrane-associated supramolecular dermal epidermal complex linking the cytoskeleton of the basal keratinocyte to structures within the dermis.…”

Section: Discussionmentioning

confidence: 99%

Two Cases of Linear IgA Disease with Clinical Manifestations Limited to the Gingiva

Eguia

Martinez-Sahuquillo

Padrón

et al. 2003

Journal of Periodontology

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Linear IgA disease (LAD) is a chronic, subepithelial blistering disease that is associated with the presence of linear deposits of IgA along the basement membrane zone. Etiopathogenic aspects of LAD are only partially known. LAD is clinically characterized by vesiculobullous skin and mucous lesions. Although more than half of LAD patients present oral mucosal lesions, there are only a few cases reported of oral lesions as the only manifestation of LAD. This study presents 2 of these uncommon cases.

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Section: Discussionmentioning

confidence: 99%

Two Cases of Linear IgA Disease with Clinical Manifestations Limited to the Gingiva

Eguia

Martinez-Sahuquillo

Padrón

et al. 2003

Journal of Periodontology

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“…The involvement of similar molecular targets also explains the presence of the morphological and biological overlap between different diseases such as BP and linear IgA dermatoses [25,26]. In the latter disorder, IgA antibodies usually react with a 285-kDa Ag localised in the sublamina densa.…”

Section: Adhesion Molecules: New Findings and New Entitiesmentioning

confidence: 95%

Autoimmune subepidermal bullous skin diseases: the impact of recent findings for the dermatopathologist

Verdolini

Cerio

2003

Virchows Archiv

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In recent years improved knowledge of the mechanisms of intercellular and cell-matrix adhesion has led to better understanding of the blistering process in many bullous dermatoses. The wide characterisation of adhesion molecules has partially changed some traditional views and invariably has made the routine work of the pathologist more complex. If understanding cell-cell cohesion structures such as desmosomes and adherens junctions is complex enough, the cell-matrix adhesion structures, such as hemidesmosomes and their structural analogues on the basement membrane and superficial dermis, are even more complex. Defects of such structures cause the subepidermal bullous diseases in which there has been most characterisation of the adhesion molecules and has also led to the discovery of new diseases (e.g. p200 pemphigoid). Most of the antigens are also the targets for mutations seen in patients with the inherited type of epidermolysis bullosa, a group of rare blistering genodermatoses. Another important aspect of bullous skin conditions is the more accurate definition of the role of the different inflammatory cells involved in triggering, development and maintenance of these diseases. Recent studies have outlined the important role of T-cell lymphocytes and their cytokines in their pathogenesis. All these studies, based mainly on highly sophisticated ultrastructural and molecular biology techniques, have updated our knowledge of the pathogenesis of blistering diseases. Nevertheless, the diagnostic characterisation of bullous diseases remains sometimes difficult, and some pathological features and mechanisms still represent an enigma. Diseases such as bullous pemphigoid and cicatricial pemphigoid, or anti-laminin cicatricial pemphigoid and acquired bullous epidermolysis share the same molecular target but have very different clinical manifestations. Explaining this phenomenon, probably linked to different expressions of MHC, is one of the challenges for the future.

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“…Durch lineare Ablagerungen von Immunglobulinen ± u Èberwiegend IgA ± kommt es zu einer subepidermalen Spaltbildung, die zum klinischen Bild praller Blasen fu Èhrt (1, 3, 4). Als mo Ègliches Autoantigen der Erkrankung wurde eine soluble Ektodoma Ène des Kollagen Typ XVII identifiziert (5). Als mo Ègliches Autoantigen der Erkrankung wurde eine soluble Ektodoma Ène des Kollagen Typ XVII identifiziert (5).…”

Section: A Ogilvieunclassified

9. Erlanger Dermatologen‐Nachmittag (EDN) am 24. 1. 2001 in der Dermatologischen Klinik mit Poliklinik der Universit?t Erlangen‐N?rnberg

Simon¹,

Schell²

2002

H G Z Hautkrankh

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The 120-kDa soluble ectodomain of type XVII collagen is recognized by autoantibodies in patients with pemphigoid and linear IgA dermatosis

Cited by 39 publications

References 28 publications

Two Cases of Linear IgA Disease with Clinical Manifestations Limited to the Gingiva

Two Cases of Linear IgA Disease with Clinical Manifestations Limited to the Gingiva

Autoimmune subepidermal bullous skin diseases: the impact of recent findings for the dermatopathologist

9. Erlanger Dermatologen‐Nachmittag (EDN) am 24. 1. 2001 in der Dermatologischen Klinik mit Poliklinik der Universit?t Erlangen‐N?rnberg

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