SUMMARYThe cell mediated lympholysis (CML) test is normally carried out in 2 steps–first, the lymphoid cells are allowed to interact in mixed allo‐culture (MLC) and secondly, they are reacted against chromium labelled phytohaemagglutinin transformed lymphoblast cells, carrying the appropriate target allo‐determinants. The genetic control of target structures has already been localized to the H‐2D and H‐2K regions of the H‐2 gene complex, but the genetic basis of the generation of effector capacity is not understood and is the subject of this report; the suggestion that there is a separate genetic basis came from the observation that H‐2D and/or H‐2K region incompatibility alone was insufficient for CML to occur and that incompatibility at the Ir‐Ss‐Slp regions of the H‐2 complex was also required. In the Ir region also reside the genetic control for the strong lymphocyte activating determinants (LAD) of the H‐2 gene complex and it was thought possible that they might also be responsible for activating the effector cells for CML.The genetic experiments were done with congenic resistant and recombinant mouse strains, so it was possible to study in relative isolation, and in selected combinations which of the various defined regions of the H‐2 gene complex control the initiation of effector capacity in CML.Five day,‘one‐way’(parent‐F1) mixed lymphocyte cultures–incompatible only for defined regions of the H‐2 gene complex were reacted with51Cr‐labelled PHA blast cells and the specific chromium release was calculated.The results give evidence for a separate but closely linked genetic control for the effector cell stimulating (ECS) and LAD functions. The ECS genes map between the
展开▼
