The Mediator of Cellular Immunity
نویسنده
چکیده
Natural and vaccine-induced virus infections often are associated with depression of delayed-type hypersensitivity (DTH),' T-helper cell function, and the in vitro proliferative response of lymphocytes to antigens and phytohemagglutinin (1-3). The underlying mechanisms are complex and have not yet been fully elucidated. However, in certain myxoand paramyxovirus infections, unresponsiveness seems to be related, in part, to virus-induced changes in T-lymphocyte traffic (4, 5). When injected intravenously (i.v.) into rats or mice, Newcastle disease virus (NDV) causes transient lymphocytepenia and depletion of lymphocytes in the thymus-dependent areas of lymphoid tissue (6). Lymphocyte output from the thoracic duct is depressed, but recovery occurs within 72 h after virus injection. These changes are related in some way to adsorption of NDV to recirculating T cells. It is in keeping with this view that lymphocytopenia occurs in mice injected with ultraviolet-irradiated NDV (UV-NDV) which cannot achieve a complete replication cycle in embryonated eggs (6). The results of the current investigation confirm and extend these observations by showing that NDV has a transient influence on T-cell traffic into lymph nodes and inflammatory foci. Cell migration is distorted after brief exposure of thoracic duct lymphocytes (TDL) in vitro to either infectious NDV (I-NDV) or UV-NDV before i.v. injection into syngeneic rats. But I-NDV has another lasting effect upon antigen-activated T cells which cannot be duplicated by irradiated virus. It is revealed in the ability of infectious virus to abrogate the protective immunity and DTH transferred by TDL obtained from rats infected with Listeria monocytogenes. The inhibitory influence of I-NDV is reflected in permanent exclusion of labeled S-phase lymphocytes from Listeria-induced exudates. These effects are observed after treatment of the cells with low virus multiplicities. The mechanism has not been determined; however, there are reasons for thinking that activated T cells are especially vulnerable to I-NDV because they alone provide the appropriate milieu for virus replication (7).
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