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T-cell deficiency in immune complex glomerulonephritis
Mice chronically infected with the virus of lymphocytic choriomeningitis (LCM) develop immune complex glomerulonephritis. Others have shown that adoptive immunization of these mice by the i.p. injection of syngeneic immune spleen cells terminates the chronic viral carrier state. The present studies were designed to define the effector cell from the immune spleen responsible for adoptive immunization and to determine the effect of this procedure upon the immune complex nephritis which occurs in LCM carrier mice. The results indicate that the effector cell in adoptive immunization is a T-cell that functions directly as a killer cell when transferred to LCM carrier mice. Sixteen of nineteen adoptively immunized mice examined had less immune complex material deposited in their glomeruli than control unmanipulated litter mates. These data demonstrate that this animal model of immune complex glomerulonephritis is immunodeficient with respect to LCM virus-specific killer T-cells. Transfer of this cell population to the LCM carrier mouse diminishes the animal's viremia and improves its immune complex nephritis. In view of these observations, it is suggested that the rationale for the use of immunosuppressive therapy in spontaneously occurring glomerulonephritis should be carefully reconsidered.
Mice chronically infected with the virus of lymphocytic choriomeningitis (LCM) develop immune complex glomerulonephritis. Others have shown that adoptive immunization of these mice by the i.p. injection of syngeneic immune spleen cells terminates the chronic viral carrier state. The present studies were designed to define the effector cell from the immune spleen responsible for adoptive immunization and to determine the effect of this procedure upon the immune complex nephritis which occurs in LCM carrier mice. The results indicate that the effector cell in adoptive immunization is a T-cell that functions directly as a killer cell when transferred to LCM carrier mice. Sixteen of nineteen adoptively immunized mice examined had less immune complex material deposited in their glomeruli than control unmanipulated litter mates. These data demonstrate that this animal model of immune complex glomerulonephritis is immunodeficient with respect to LCM virus-specific killer T-cells. Transfer of this cell population to the LCM carrier mouse diminishes the animal's viremia and improves its immune complex nephritis. In view of these observations, it is suggested that the rationale for the use of immunosuppressive therapy in spontaneously occurring glomerulonephritis should be carefully reconsidered.