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-gamma 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-gamma-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-gamma monoclonal antibody. The number of cells adherent to the normal cultured keratinocytes was greater in the IFN-gamma-producing clones than in the non-producing ones. These data suggest that some HTLV-1-infected clones produce cytokines, including IFN-gamma, which in turn induce ICAM-1 on keratinocytes, thereby enhancing the ability of the T-cell clones to adhere to the keratinocytes.