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Down‐regulation of transforming growth factor‐β receptors I and II is seen in lesional but not non‐lesional psoriatic epidermis
Author(s) -
Leivo,
Kariniemi,
Keski-Oja,
A. Virtanen
Publication year - 1998
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1998.02026.x
Subject(s) - epidermis (zoology) , psoriasis , receptor , immunohistochemistry , transforming growth factor , pathogenesis , biology , transforming growth factor beta , basal (medicine) , signal transduction , tgf alpha , endocrinology , microbiology and biotechnology , pathology , medicine , growth factor , immunology , anatomy , genetics , insulin
Transforming growth factor‐βs (TGF‐βs) are a family of growth factors with inhibitory effects on epithelial cell proliferation. Their effects are mediated by two interacting receptors, of which type I (TβR‐I) mediates signal transduction after interaction with type II (TβR‐II) carrying the TGF‐β ligand. We have studied the expression of TβR‐I and TβR‐II in psoriatic and normal human skin by using polyclonal rabbit antisera and immunohistochemistry. Immunohistochemical analysis revealed an intense immunoreactivity for both receptors in the basal and often also suprabasal layer of normal and non‐lesional psoriatic epidermis. In contrast, all psoriatic lesions studied lacked detectable immunoreactivity of either receptor in the epidermis. The results suggest that lack of TGF‐β‐mediated growth inhibition by down‐regulation of TGF‐β receptor expression may play an important part in the pathogenesis of psoriasis.