H–2 gene expression is required for T cell-mediated lysis of virus-infected target cells

Abstract

EFFECTOR T cells generated during the course of virus diseases of mice interact only with virus-infected target cells sharing H–2K or H–2D antigenic specificities with the mouse strain in which the lymphocytes are sensitised^1–3. The current interpretation⁴ of this phenomenon is that the cell membrane component(s) recognised by the T-cell receptor(s) has characteristics of both self (H–2) and non-self (virus). Phenotypic expression of H–2 genes in the target cell would thus be essential for T cell-mediated immunity. Here we test this hypothesis using two teratocarcinoma cell lines (F–9 and PCC4 derived from strain 129 mice^5,6) infected with lymphocytic choriomeningitis virus (LCMV). We show that the F–9 tumour cells apparently do not express H–2K or H–2D antigenic specificities (Fig. 1, Table 1), and are also resistant to attack by lymphocytes sensitised against LCMV. The PCC4 line, however, has remained multipotential and can give rise to various different cell types, at least some of which show evidence of H–2 gene function (Table 1) and are attacked by the appropriately sensitised lymphocytes.