HLA-restricted T-cell recognition of Epstein–Barr virus-infected B cells

Abstract

In mice the cytotoxic T-cell response to several types of virus is influenced by genes within the major histocompatibility complex^1–5; in particular, genetic control is exercised at the effector cell level through a requirement that virus-specific cytotoxic T cells recognise viral antigens in association with H–2K and H–2D region gene products on the surface of infected cells^1,2. In man the restriction which the analogous HLA-A, -B and -C-region gene products might place on virus-specific T-cell function is still in dispute. The earliest and most controversial evidence concerns the Epstein–Barr virus (EBV), a B lympho-tropic agent which causes infectious mononucleosis⁶ (IM) and which induces an unusually vigorous T-cell response⁷; cytotoxic T cells from IM patients' blood were shown to be EBV-specific, yet, in contrast to mouse systems, apparently free of any obvious HLA restriction^8,9. Since then T-cell recognition of EBV-infected B cells has assumed particular significance as a model system for the study of cytotoxic T-cell function in man. This report describes the results of a new approach clearly indicating that HLA-A and -B region products do indeed have a role in this system.