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Up‐regulation of ICAM‐1 expression on human dermal fibroblasts by IFN β in the presence of TNF‐α
Author(s) -
Horikoshi Takashi,
Ezoe Kyori,
Nakagawa Hidemi,
Eguchi Hiroaki,
Hanada Niro,
Hamaoka Shuji
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00299-o
Subject(s) - peripheral blood mononuclear cell , tumor necrosis factor alpha , icam 1 , dermis , cytokine , beta (programming language) , chemistry , interferon , fibroblast , interferon gamma , immunology , microbiology and biotechnology , medicine , biology , intracellular , pathology , in vitro , biochemistry , computer science , programming language
Unstimulated human fibroblasts show low or undetectable ICAM‐1 expression. Interferon‐beta (IFN‐β) at concentrations of 10,100, and 1000 IU/ml in the presence of tumor necrosis factor‐alpha (TNF‐α) significantly increased the ICAM‐I expression of fibroblasts in a dose‐dependent manner. Treatment with IFN‐β alone, however, did not up‐regulate the ICAM‐1 expression. Furthermore the attachment of peripheral blood mononuclear cells (PBMCs) to cytokine‐treated fibroblasts was increased. This augmented attachment was partly inhibited by anti‐ICAM‐1 antibody. These results suggest that IFN‐β and TNF‐α may cooperatively modulate the attachment of PBMCs in the dermis.