Recognition of viral antigens by cytotoxic T lymphocytes

Abstract

Abstract Cytotoxic T lymphocytes (CTLs) are generated during most viral infections. They are detected in vitro by their ability to lyse virus-infected cells and probably act in the same way in vivo (Zinkernagel et al., 1986), although they may also release lymphokines including interferon-gamma (Morris et al., 1982). In acute infections such as with influenza A virus, CTLs have been shown to terminate infection and to contribute to the clearing of virus (Yap et al., 1978; Lin and Askonas, 1981). This was most clearly demonstrated in experiments in which virus-specific CTL clones were transferred to lethally infected mice (Lin and Askonas, 1981). The level of specific CTL responses has been shown to correlate with virus-clearing in humans (McMichael et al., 1983). In Epstein - Barr virus (EBY) infection in vitro, CTLs have been shown to cause regression of the outgrowth of transformed B lymphocytes, and in vivo they probably inhibit infection by persisting virus (Rickinson et al., 1979). This may be a model for other persisting virus infections. The importance of CTLs in vivo has been demonstrated in mice depleted of CD4+ cells by specific monoclonal antibody. These animals generated weak antibody response to infecting influenza virus, because they lacked helper T cells, but a good CTL response was demonstrated and influenza virus-infected irradiated mice were cured by transfer of these CTLs (Lightman et al., 1987). Similarly, mice that are genetically incapable of making a CTL response to a virulent strain of Sendai virus are more likely to die during acute infection (Kast et al., 1986).