Predominant recognition of human T cell leukemia virus type I (HTLV-I) pX gene products by human CD8+ cytotoxic T cells directed against HTLV-I-infected cells

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Abstract
We established long-term cell lines of cytotoxic T lymphocytes (CTL) specific for human T cell leukemia virus type I (HTLV-I) from peripheral blood lymphocytes (PBL) of a patient with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), an HTLV-l-carrler with Sjögren syndrome, and an asymptomatic HTLV-l-carrier, by repeated stimulation with autologous HTLV-I-Infected T cells In vitro. CTL derived from the patient with HAM/TSP expressed CD8 antigen, and their function was restricted by HLA-A2. They showed cytotoxic effects predominantly against the target cells expressing HTLV-I p40tax among the autologous B cell lines Infected with vaccinia recombinants containing various HTLV-I genes which served as targets. These data are consistent with the previously reported findings that fresh PBL of HAM/TSP patients contain p40tax-specific CTL activity. Furthermore, CTL derived from the patient with Sjögren syndrome without neurological involvement also demonstrated cytotoxicity predominantly to p40tax. The cytotoxicity to the target cells experimentally expressing p40tax was blocked by unlabeled HTLV-I-infected cells possessing HLA-A2. HTLV-l-specific cytotoxicity was also Inhibited by unlabeled B cells bearing p40tax. Thus, HTLV-I p40tax-specific cytotoxicity is mediated by the major CTL population activated by native HTLV-I antigens in patients with HAM/TSP or Sjögren syndrome. In contrast to the CTL of these patients, CTL similarly Induced from the asymptomatic HTLV-l-carrier, which were highly cytotoxic to autologous HTLV-l-infected T cells, did not show significant levels of cytotoxicity to autologous B cells expressing p40tax. These CTL possessed CD4 antigen. It was concluded that the predominant CTL population activated by HTLV-I stimulation differs in phenotype and antigen-specificity among HTLV-I seropositive individuals, and that these differences in CTL response may play a role in determining the susceptibility of the host to various HTLV-I related disorders.

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