0000000000267935
AUTHOR
A Starzinski-powitz
Generation of Cytotoxic T Lymphocytes Against Ly Alloantigen
Cytotoxic T lymphocytes specific for immune alloantigens controlled by alleles of the Ly system have been induced in vivo. These results were obtained either in a secondary type of response or by treating mice before immunization with a single dose of cyclophosphamide (80 mg/kg).
Shared determinants between virus-infected and trinitrophenyl-conjugated H-2-identical target cells detected in cell-mediated lympholysis
Infection of H-2-identical mice with either lymphocytic choriomeningitis (LCM) virus, vaccinia virus, or paramyxo (Sendai) virus resulted in the generation of specifically sensitized cytotoxic T lymphocytes (CTL). CTL generated in vitro against 2,4,6-trinitrophenyl (TNP)-conjugated syngeneic stimulator cells were specifically cytotoxic for TNP-conjugated H-2K (D) region identical targets. Both LCM and vaccinia-induced CTL, however, were found to be strongly cytotoxic towards TNP-conjugated, H-2K(D) region-identical target cells. In contrast, Sendai virus-induced CTL did not lyse TNP-conjugated, syngeneic target cells. Inhibition experiments using cold targets suggested that shared antigenic…
Virion Antigens Introduced Exogeneously into the Cell Membrane Render Syngeneic Target Cells Susceptible for T Cell-Mediated Cytolysis
Non-infectious sendai virus renders H-2 matched target cells susceptible to the lytic effect of sendai virus immune cytotoxic T lymphocytes. This observation suggests that exogeneous insertion of virion antigen in the membrane of the target cell is sufficient for T cell cytotoxicity. The finding is incompatible with the concept that H-2K or H-2D gene products of the target cells must be altered in their primary structure (pretranslational effect of the virus infection) for T cell-mediated cytolysis to occur.
T-cell-mediated cytotoxicity against herpes simplex virus-infected target cells
THE control of herpes simplex virus (HSV) infection by immunological mechanisms seems to be complex and is poorly understood. Neutralising antibodies to HSV plus complement seem to have no effect on the propagation of HSV infection, because HSV spreads to adjacent cells by passing through intercellular bridges1–3. Anti-HSV antibodies plus complement, however, destroy virus-infected cells, but cannot prevent the spread of HSV, suggesting that the virus must be transferred to neighbouring cells before immune lysis occurs1,5. Therefore if lymphocyte-mediated cytolytic mechanisms are instrumental in blocking the spread of HSV in vivo, they ought to destroy infected cells at a very early stage i…
T-T cell collaboration during in vivo responses to antigens coded by the peripheral and central region of the MHC.
MIXED lymphocyte culture (MLC)1 has been used extensively as an in vitro model to analyse the reactivity of T cells to antigens coded by the major histocompatibility complex (MHC). When murine T responder cells are exposed in vitro to allogeneic lymphoid cells (stimulator cells) they proliferate and cytotoxic T lymphocytes (CTL) are generated2,3. Antigens coded by the central I region of the MHC are chiefly responsible for triggering proliferation4,5, whereas the target antigen of the CTL generated is either a H–2K or H–2D region or a I–A subregion gene product5–8. This dichotomy in the antigenic requirement of a MLC seems to be reflected at the level of the responding T lymphocytes. Two di…