On the role of the H 2 histocompatibility complex in determining the specificity of cytotoxic effector cells sensitized against syngeneic trinitrophenyl modified targets

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Spleen cells cultured with syngeneic TNP modified stimulator cells display a cytotoxic effect against syngeneic TNP modified targets, but not against modified targets from unrelated H-2 haplotypes. Targets that share the K and I region of the H-2 complex with the stimulator (or effector) cells are lysed to the same extent as the specific targets, while targets that share the I region only are not. When only the D region is shared, a weak cytotoxic effect is observed. Therefore, the stimulator (or effector) and target cell must share the K or D but not the I region of the H-2 complex in order for optimal cytotoxicity to occur. Spleen cells sensitized to irradiated TNP modified H-2 allogeneic cells are cytotoxic to these specific targets, but not against TNP modified targets syngeneic with the effector cells. Coculture of F1 hybrid cells with irradiated TNP modified parental cells results in a cytotoxic effect against only those specific parental cells and not TNP modified cells from the other parent. The cytotoxic effect of the F1 effector cells in the cell mediated lympholysis test is blocked by the addition of unlabeled TNP modified targets that are H-2 syngeneic with the sensitizing parental strain, but not H-2 syngeneic with the other parental strain. These data demonstrate that the specificity of the effector cell in this syngeneic cytotoxicity system is directed against altered self H-2 controlled gene products, rather than a requirement for sharing of histocompatibility genes between effector and target cell in order for lysis to occur. The role of H-2 antigens in determining the sensitivity of a target cell to T cell mediated lysis is discussed.

Original languageEnglish (US)
Pages (from-to)403-418
Number of pages16
JournalJournal of Experimental Medicine
Issue number2
StatePublished - Jan 1 1975


ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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