Modification of H-2 Antigenic Sites by Enzymatic Treatment Influences Virus-Specific Target Cell Lysis

Vaccinia virus-infected cells were treated enzymatically to remove H-2 antigenic sites. The effect of this procedure on virus-specific cell-mediated cytolysis (CMC) and virus-specific antibody-mediated cytolysis (AMC) was tested. Due to the inhibition of cellular proteinsynthesis by the vaccinia virus infection, H-2 antigenic sites were not resynthesized while there was a continuous production of viral surface antigens. These cells with a high concentration of viral surface antigens and decreased H-2 determinants could be used as targets in the virus specific AMC. But they were not lysed in the virus specific CMC which emphasizes the significance of H-2 antigens during recognition of virus-specific determinants by T cells

Role of early viral surface antigens in cellular immune response to vaccinia virus

Infection of mice with the vaccinia virus strain WR, Elstree or DIs, a conditional lethal mutant of vaccinia virus, resulted in the generation of vaccinia virus-specific sensitized cytolytic T lymphocytes (CTL). It could be shown by cross-reactivity between the three strains and by inhibition experiments with specific antisera that early vaccinia surface antigens are sufficient for the generation of specific CTL in vivo and for the lysis of infected target cells in vitro

Monoclonal antibodies reactive with swine lymphocytes

A panel of monoclonal antibodies (mAb) with specificity for swine leukocytes was prepared by somatic cell hybridization with the use of spleen cells from mice immunized with swine thymocytes. The reactivity of two mAb (295/33 and 122/28), which both immunoprecipitated from the surface of swine leukocytes an antigen termed S-L2 with an apparent m.w. of 33 to 35 kilodaltons under reducing and 65 to 70 kilodaltons under nonreducing conditions, was investigated in detail. These mAb were reactive in indirect immunofluorescence with 50 to 60% of thymocytes, 35% of peripheral blood lymphocytes, and 55% of E rosette- positive cells; they were nonreactive with bone marrow cells, Ig+ B cells, nonrosetting lymphocytes, granulocytes, and monocytes. In functional studies, the elimination of S-L2+ cells partially reduced the proliferative response to concanavalin A and pokeweed mitogen but not to Staphylococcus aureus and lipopolysaccharide. The S-L2- subset proliferated well to alloantigens. Both cytolytic T effector cells and precursor cells carried the antigen S-L2 and could be depleted from heterogeneous cell populations by both antibodies in the presence of complement. These data suggest that the mAb 295/33 and 122/28 recognize a specific polypeptide present on the surface of swine cytolytic T cells. These antibodies will be useful in studies on the swine immune system

T cell-specific suppressor factor(s) with regulatory influence on interleukin 2 production and function

In this study we report that alloantigen-activated spleen cells produce both amplifying and suppressive factors under the same conditions. Both types of soluble mediators--as detected in different assay systems-- were present in the supernatants of in vivo sensitized and in vitro restimulated spleen cell populations and were separable by gel filtration. As shown by others, the amplifying factor (IL 2) was eluted in the size range of 30,000 m.w. The suppressive factor(s) (SF) was eluted in the size range of 10,000 m.w. SF was shown to inhibit the proliferative response of T cells to alloantigen, as well as the generation of regulatory T cells and cytotoxic T cells from their precursors when added at the beginning of the in vitro culture. Furthermore, SF inhibited the release of IL 2 from producer T cells but had no detectable effect on the interaction of IL 2 with receptive T cells. In addition it was shown that SF does not affect the generation of PFC from their precursors after activation by T cell-independent antigens. The results indicate that SF selectively acts on T cells and that it is involved in the regulation of the immune response by modulating early events in T cell activation