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Specificity of anti-T cell antibodies from BCG infected mice
BCG infected mice were found to produce anti-T cell cytotoxic autoantibodies (CAA)6. Absorption studies with intact or desialyzed thymocytes and splenic T cells showed that CAA consisted of two kinds of antibody with different target cell specificities, one (CAA-2) able to recognize determinants on desialyzed T cells, and another (CAA-1) able to bind to both intact and desialyzed thymocytes. Normal thymocytes did not remove the antibodies specific to desialyzed lymphocytes. These two antibodies were separated by affinity chromatography on agarose. Cytotoxicity inhibition, using various sugars as inhibitors, indicated that lactose and lactosamine were potent inhibitors of CAA-2. In contrast CAA-1 was not inhibited by any of the sugars tested. Functional experiments revealed that CAA-2 inhibited the secondary anti-SRBC IgG antibody response without effecting the IgM response. The anti-SRBC antibody production (both IgM and IgG) was not affected by CAA-1. The possible interference of these antibodies with carbohydrate specific cell interactions are discussed.
BCG infected mice were found to produce anti-T cell cytotoxic autoantibodies (CAA)6. Absorption studies with intact or desialyzed thymocytes and splenic T cells showed that CAA consisted of two kinds of antibody with different target cell specificities, one (CAA-2) able to recognize determinants on desialyzed T cells, and another (CAA-1) able to bind to both intact and desialyzed thymocytes. Normal thymocytes did not remove the antibodies specific to desialyzed lymphocytes. These two antibodies were separated by affinity chromatography on agarose. Cytotoxicity inhibition, using various sugars as inhibitors, indicated that lactose and lactosamine were potent inhibitors of CAA-2. In contrast CAA-1 was not inhibited by any of the sugars tested. Functional experiments revealed that CAA-2 inhibited the secondary anti-SRBC IgG antibody response without effecting the IgM response. The anti-SRBC antibody production (both IgM and IgG) was not affected by CAA-1. The possible interference of these antibodies with carbohydrate specific cell interactions are discussed.