Strong induction of ICAM‐1 in human T cells transformed by human T‐cell‐leukemia virus type 1 and depression of ICAM‐1 or LFA‐1 in adult T‐cell‐leukemia‐derived cell lines

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Abstract
Sixteen human T‐cell lines were studied for the expression of a cell‐adhesion molecule ICAM‐1 and its counter‐receptor LFA‐1. The cell lines included 3 human T‐cell‐leukemia‐virus‐type‐1 (HTLV‐1)‐negative cell lines derived from acute lymphoblastic leukemia (ALL) and 13 HTLV‐1‐positive cell lines, 7 of them established from cord‐ or peripheral‐blood T cells by in vitro transformation with HTLV‐1, 2 derived from HTLV‐1 carriers, and 4 derived from patients with adult T‐cell leukemia (ATL). In sharp contrast to a basal level of ICAM‐1 in 3 HTLV‐1‐negative ALL cell lines, strong induction of ICAM‐1 was seen in all HTLV‐1‐positive T‐cell lines except for MT‐1, one of the 4 ATL cell lines used in the present study. On the other hand, the expression of LFA‐1 (CD11a and CD18) was more or less similar among the cell lines with and without HTLV‐1. Interestingly, however, 3 out of 4 ATL cell lines (TL‐Oml, H582, HUT102) revealed striking depression of LFA‐1 expression. Several lines of evidence strongly argued against direct involvement of the viral transactivator p40tax or some autocrine cytokines in the induction of ICAM‐1 in HTLV‐1‐positive T‐cell lines. It was also found that ICAM‐1 and LFA‐1 were involved in syncytium formation induced in the co‐culture of HTLV‐1‐positive and HTLV‐1‐negative human T‐cell lines. Implications of constitutive expression of ICAM‐1 for certain clinical manifestations of ATL and of depression of either ICAM‐1 or LFA‐1 during progression of ATL are discussed.
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