Bullous pemphigoid and dermatitis herpetiformis association: A genetic predisposition

Vaira, Fabrizio; Valle, Valentina; Fanoni, Daniele; Pontini, Paolo; Muratori, Simona

doi:10.1111/1346-8138.12262

Cited by 8 publications

(7 citation statements)

References 5 publications

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“…Several cases of patients with a history of DH and BP have been reported ( 215 – 228 ) (Table 6 ). Van der Meer was the first to describe a patient showing clinically both DH and BP features, but only pathological and DIF BP features were found ( 215 ).…”

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

“…In 11 cases, dual findings for BP and DH were detected by DIF ( 220 – 227 ). On the one hand, BP and DH were described as concomitant in nine cases ( 220 , 221 , 223 – 227 ); on the other hand, in two patients, DIF was performed at different time, showing only one disease per biopsy ( 222 , 228 ). In five of the nine patients, serum antibodies were directed against the BMZ, and in one patient only antiendomysial antibodies were highlighted at the DH onset ( 223 ).…”

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

“…In five of the nine patients, serum antibodies were directed against the BMZ, and in one patient only antiendomysial antibodies were highlighted at the DH onset ( 223 ). Only two patients with serum autoantibodies compatible with both BP and DH have been described, however, sera were not taken at the same time ( 222 , 228 ). Indeed, only Schulze et al detected both BP and DH serum autoantibodies at the same time ( 227 ).…”

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

“…In addition, Vaira et al analyzed the HLA profile in a patient, who developed DH several years after the BP diagnosis. HLA alleles were HLA-DQB1 03:01 (predisposing to BP), HLA-DQA1 05:05/05:01 (predisposing to CD) and HLA-DQB1 02:01 (predisposing to CD and to DH) ( 228 ). The authors concluded that those findings highlighted a specific genetic susceptibility to both diseases in the same patient ( 228 ).…”

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

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Humoral Epitope Spreading in Autoimmune Bullous Diseases

Didona

Zenzo

2018

Front. Immunol.

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Autoimmune blistering diseases are characterized by autoantibodies against structural adhesion proteins of the skin and mucous membranes. Extensive characterization of their autoantibody targets has improved understanding of pathogenesis and laid the basis for the study of antigens/epitopes diversification, a process termed epitope spreading (ES). In this review, we have reported and discussed ES phenomena in autoimmune bullous diseases and underlined their functional role in disease pathogenesis. A functional ES has been proposed: (1) in bullous pemphigoid patients and correlates with the initial phase of the disease, (2) in pemphigus vulgaris patients with mucosal involvement during the clinical transition to a mucocutaneous form, (3) in endemic pemphigus foliaceus, underlining its role in disease pathogenesis, and (4) in numerous cases of disease transition associated with an intermolecular diversification of immune response. All these findings could give useful information to better understand autoimmune disease pathogenesis and to design antigen/epitope specific therapeutic approaches.

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Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

Section: Humoral Es In Autoimmune Bullous Diseasesmentioning

confidence: 99%

See 2 more Smart Citations

Humoral Epitope Spreading in Autoimmune Bullous Diseases

Didona

Zenzo

2018

Front. Immunol.

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“…01 foi associado ao PB em diversas etnias, incluindo americanos(DELGADO et al, 1996), britânicos(BANFIELD et al, 1998), espanhóis (ZAKKA; RECHE; AHMED, 2011), italianos(VAIRA et al, 2013), japoneses (MINAGAWA et al, 2015, chineses(FANG et al, 2018) e brasileiros(CHAGURY et al, 2018). Provavelmente, o alelo -DQB1*03:01 leva à perda da autotolerância e desencadeia o PB, uma vez que as células Th1, Th2 e B autorreativas reconhecem diferentes domínios do epítopo da proteína BP180(ANTIGA et al, 2014;PICKFORD et al, 2015;XU et al, 2001; ZAKKA; RECHE; AHMED, 2011).…”

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