The mitogenic activity of human T-cell leukemia virus type I is T-cell associated and requires the CD2/LFA-3 activation pathway.

摘要: The presence of a high number activated T cells in the bloodstream and spontaneous proliferation peripheral blood mononuclear vitro are striking characteristics human T-cell leukemia virus type I (HTLV-I) infection. HTLV-I regulatory protein Tax envelope gp46 have been implicated mediating activation process. In this study, HTLV-I-producing cell lines purified from were examined for ability to activate lymphocytes (PBLs) Jurkat cells. Antisera monoclonal antibodies against several cellular adhesion proteins involved viral used identify which molecules may be participating First, neither line, MT2, nor produced osteosarcoma line HOS/PL was able induce PBLs proliferate. contrast, both fixed irradiated induced PBLs; did not PBLs. Second, HTLV-I-positive capable activating interleukin-2 mRNA expression Induction inhibited by anti-CD2 anti-lymphocyte function-associated antigen 3 (LFA-3) but anti-human leukocyte antigen-DR, anti-CD4, anti-LFA-1, or anti-intercellular molecule 1. Similar results obtained with as responder Furthermore, antisera various regions gp21 well p40tax block activation. These data indicate that particles intrinsically mitogenic infection target is necessary Instead, activity restricted virus-producing cells, requires cell-to-cell contact, mediated through LFA-3/CD2 pathway.