OBJECTIVE: Pemphigus Vulgaris (PV) is a mucocutaneous autoimmune disease mediated by autoantibodies that often affects oral mucosa. However, little is known about the connection between oral infections and PV. The present study addresses the hypothesis that immune responses following bacterial infections may cross-react with PV autoantigens, thus providing the pathogenic stimulus, eventually leading to clinical manifestations.METHODS: Available proteomic resources and immunologic data were explored. Searching for common peptides that underlie immune cross-reactions, the analyses focused on pathogenic oral bacteria and PV autoantigens, i.e., Desmoglein-3 (Dsg3).RESULTS: It was found that the analysed bacteria share numerous immunoreactive heptapeptide sequences with Dsg3.CONCLUSION: These data seem to support the hypothesis that the oral microbiome may also contribute to the pathogenesis of PV, with important implications for the treatment of this disease.

Oral Microbioma and Pemphigus vulgaris

Romano, A;Baroni, A;Donnarumma, G;Contaldo, M;Serpico, R
2022

Abstract

OBJECTIVE: Pemphigus Vulgaris (PV) is a mucocutaneous autoimmune disease mediated by autoantibodies that often affects oral mucosa. However, little is known about the connection between oral infections and PV. The present study addresses the hypothesis that immune responses following bacterial infections may cross-react with PV autoantigens, thus providing the pathogenic stimulus, eventually leading to clinical manifestations.METHODS: Available proteomic resources and immunologic data were explored. Searching for common peptides that underlie immune cross-reactions, the analyses focused on pathogenic oral bacteria and PV autoantigens, i.e., Desmoglein-3 (Dsg3).RESULTS: It was found that the analysed bacteria share numerous immunoreactive heptapeptide sequences with Dsg3.CONCLUSION: These data seem to support the hypothesis that the oral microbiome may also contribute to the pathogenesis of PV, with important implications for the treatment of this disease.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/485417
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