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Interferon‐γ‐induced HLA‐DR, but not ICAM‐1, Expression of Human Keratinocytes Is Down‐regulated by Calmodulin Antagonist
Author(s) -
Saitoh Atsushi,
Osada Atsushi,
Kitajima Yasuo,
Furue Masutaka,
Tamaki Kunihiko
Publication year - 1994
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/j.1346-8138.1994.tb03274.x
Subject(s) - icam 1 , calmodulin , mhc class ii , human leukocyte antigen , hla dr , microbiology and biotechnology , intercellular adhesion molecule 1 , inhibitory postsynaptic potential , biology , interferon , major histocompatibility complex , intracellular , chemistry , immunology , antigen , biochemistry , endocrinology , enzyme
Interferon‐γ (IFN‐γ) has been shown to induce or enhance the expression of MHC class II and intercellular adhesion molecule‐1 (ICAM‐1) in a variety of human and murine cell types, including epidermal keratinocytes (KC). However, the expression of MHC class II and ICAM‐1 molecules induced by IFN‐γ is not necessarily coordinated. We investigated the inhibitory effects of the calmodulin antagonist, W‐7, and its chlorine deficient inactive analogue, W‐5, on the expression of MHC class II (HLA‐DR) and ICAM‐1 by human KC incubated with IFN‐γ. We found that the IFN‐γ‐induced expression of HLA‐DR was reproducibly and dose‐dependently inhibited by W‐7. However, the expression of ICAM‐1 was highly resistant to the inhibitory effects of W‐7. Neither HLA‐DR nor ICAM‐1 expression was affected by W‐5. These data suggest that the IFN‐γ‐induced HLA‐DR, but not ICAM‐1, expression is mediated, if not exclusively, by calmodulin in human KC.