Dermatitis herpetiformis bodies. Ultrastructural study on the skin of patients using direct preembedding immunogold labeling

Kárpáti, Sarolta

doi:10.1001/archderm.126.11.1469

Cited by 16 publications

(9 citation statements)

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“…According to structure and staining characteristics, DH bodies were suggested representing immune complex aggregates. 27 Ultrastructural studies also demonstrated perivascular granular IgA around the mucosal blood vessels in DH patients. 28 The observation of IgA deposits in the kidney of 11 DH patients, which did not induce clinical symptoms or signs, supports the possibility that DH can be a skin disease mediated by immune complexes.…”

Section: Discussionmentioning

confidence: 93%

Immunoglobulin, complement and epidermal transglutaminase deposition in the cutaneous vessels in dermatitis herpetiformis

Preisz

Sárdy

Horváth

et al. 2004

Acad Dermatol Venereol

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Section: Discussionmentioning

confidence: 93%

Immunoglobulin, complement and epidermal transglutaminase deposition in the cutaneous vessels in dermatitis herpetiformis

Preisz

Sárdy

Horváth

et al. 2004

Acad Dermatol Venereol

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“…The gene coding for fibrillin (FBN1) was also upregulated in our DH skin samples. This protein constitutes the major backbone of multifunctional microfibrils in elastic and nonelastic extracellular matrices and may be one of the structural components bound by IgA-reactive deposits in the skin of patients with DH [39]. …”

Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions

Dolcino

Cozzani

Riva

et al. 2012

Clinical and Developmental Immunology

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Dermatitis herpetiformis (DH) is an autoimmune blistering skin disease associated with gluten-sensitive enteropathy (CD). In order to investigate the pathogenesis of skin lesions at molecular level, we analysed the gene expression profiles in skin biopsies from 6 CD patients with DH and 6 healthy controls using Affymetrix HG-U133A 2.0 arrays. 486 genes were differentially expressed in DH skin compared to normal skin: 225 were upregulated and 261 were downregulated. Consistently with the autoimmune origin of DH, functional classification of the differentially expressed genes (DEGs) indicates a B- and T-cell immune response (LAG3, TRAF5, DPP4, and NT5E). In addition, gene modulation provides evidence for a local inflammatory response (IL8, PTGFR, FSTL1, IFI16, BDKRD2, and NAMPT) with concomitant leukocyte recruitment (CCL5, ENPP2), endothelial cell activation, and neutrophil extravasation (SELL, SELE). DEGs also indicate overproduction of matrix proteases (MMP9, ADAM9, and ADAM19) and proteolytic enzymes (CTSG, ELA2, CPA3, TPSB2, and CMA1) that may contribute to epidermal splitting and blister formation. Finally, we observed modulation of genes involved in cell growth inhibition (CGREF1, PA2G4, and PPP2R1B), increased apoptosis (FAS, TNFSF10, and BASP1), and reduced adhesion at the dermal epidermal junction (PLEC1, ITGB4, and LAMA5). In conclusion, our results identify genes that are involved in the pathogenesis of DH skin lesions.

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“…Ultrastructurally, the granular IgA staining corresponds to small amorphous grains, the so-called ''dermatitis herpetiformis bodies'', which show an apparently irregular distribution within the papillary dermis. They could be detected along collagenous and reticulin fibres, within the elastic tissues, and also around small capillaries when studied in the oral mucosa [35,36]. A recent study indicates a significant small vessel IgA staining in the papillary skin of 116 patients with DH [37].…”

Section: Skin Iga and The Theory Of Other Transglutaminases In Dermatmentioning

confidence: 99%

Dermatitis herpetiformis: close to unravelling a disease

Kárpáti

2004

Journal of Dermatological Science

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Dermatitis herpetiformis bodies. Ultrastructural study on the skin of patients using direct preembedding immunogold labeling

Cited by 16 publications

References 0 publications

Immunoglobulin, complement and epidermal transglutaminase deposition in the cutaneous vessels in dermatitis herpetiformis

Immunoglobulin, complement and epidermal transglutaminase deposition in the cutaneous vessels in dermatitis herpetiformis

Gene Expression Profiling in Dermatitis Herpetiformis Skin Lesions

Dermatitis herpetiformis: close to unravelling a disease

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