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Signalling pathways in pemphigus vulgaris
Author(s) -
Li Xiaoguang,
Ishii Norito,
Ohata Chika,
Furumura Minao,
Hashimoto Takashi
Publication year - 2014
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12317
Subject(s) - acantholysis , pemphigus vulgaris , desmoglein 3 , pemphigus , epidermal growth factor receptor , in vivo , autoantibody , kinase , medicine , receptor , microbiology and biotechnology , biology , immunology , chemistry , cancer research , antibody , genetics
Acantholysis in pemphigus vulgaris is induced by binding of autoantibodies to desmoglein 3 (Dsg3). The roles of signalling pathways on development of acantholysis have recently been extensively studied. In the study by Sayar et al., recently published in Exp Dermatol, epidermal growth factor receptor (EGFR) signalling was activated in both in vivo and in vitro pemphigus vulgaris experimental models. However, while EGFR inhibitors suppressed activity of p38 mitogen‐activated protein kinase (p38MAPK) linearly, they suppressed activity of c‐ M yc and acantholysis in a non‐linear, V‐shaped relationship. These findings indicated complicated interactions among EGFR, p38MAPK and c‐ M yc in pemphigus vulgaris pathology.