Lymphocyte-dependent ‘natural’ immunity to virus infections mediated by both natural killer cells and memory T cells
Abstract The replication and dissemination of viruses in the host can be retarded at early stages of infection by lymphocytes not previously exposed to the invading pathogen. Natural killer (NK) cells responding to virus-induced cytokines can mediate profound antiviral effects. Studies with murine cytomegalovirus suggest that NK cells may mediate anti-viral functions by different mechanisms in different organs. T cells may also mediate a rapidly-inducible natural immunity against viral infections. A subpopulation of memory T cells specific for one infectious agent may be stimulated through crossreactive determinants encoded by a heterologous infectious agent and thereby play an active role in the early host response to infection. This heterologous T cell-dependent ‘natural’ immunity may in part be due to the liberation of antiviral cytokines such as interferon γ, as there is much higher production of this cytokine early in infection in mice immune and previously exposed to heterologous infectious agents. Thus, both NK cells and memory T cells may act early in infection to delay the spread of virus, allowing time for high affinity antigen-specific responses to develop and cure the host of infection.
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