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Induction of Intercellular Adhesion Molecule‐1 and Adherence of HTLV‐1‐Infected T‐cells to Cultured Keratinocytes
Author(s) -
Fenxiang Jin,
Iwatsuki Keiji,
Takigawa Masahiro,
Yamada Mizuho
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.tb01716.x
Subject(s) - keratinocyte , cell adhesion molecule , biology , monoclonal antibody , intracellular , intercellular adhesion molecule 1 , cell culture , microbiology and biotechnology , t cell , antibody , immunology , immune system , genetics
Cutaneous lesions of T‐cell proliferative disorders are characterized by epidermotropic infiltration of the neoplastic cells and expression of intercellular adhesion molecule‐1 (ICAM‐1) and HLA‐DR by lesional keratinocytes. Using cloned HTLV‐1‐infected T‐cells obtained from patients with adult T‐cell leukemia (ATL), we have studied immunobiological activities of cytokines released from the T‐cell lines and their ability to adhere to cultured keratinocytes. Three out of the five CD‐4‐positive, HTLV‐1‐infected T‐cell clones secreted both IFN‐γ and IL‐4, similar to murine Th0 clones. The other two clones did not produce such cytokines. ICAM‐1 and HLA‐DR molecules were induced on cultured normal human keratinocytes and organ‐cultured skin specimens by co‐cultivation with IFN‐γ‐producing T‐cell clones or their culture supernatants. Induction of both molecules was markedly inhibited by pretreatment of the supernatants with excess amounts of anti‐IFN‐γ monoclonal antibody. The number of cells adherent to the normal cultured keratinocytes was greater in the IFN‐γ‐producing clones than in the non‐producing ones. These data suggest that some HTLV‐1‐infected clones produce cytokines, including IFN‐γ, which in turn induce ICAM‐1 on keratinocytes, thereby enhancing the ability of the T‐cell clones to adhere to the keratinocytes.