The requirements for killer cell production in the course of a mixed leukocyte reaction and the specificity of target cell (PHA‐blasts) lysis in the mouse were investigated using inbred strains carrying intra‐H‐2 recombinant chromosomes. Strong lytic activity was generated in all, and only those, responder‐stimulator combinations which differed at either the H‐2D or the H‐2K, or both regions, even if the MLR incompatibility between responder and stimulator was very weak. Killing activity was specific and directed against determinants controlled by genes in the H‐2K and H‐2D regions. The slope of the killer dose‐response curves is the same for either type of specificity. Quantitative comparison of the lytic activity of a given killer cell population on different targets demonstrated a dose effect of the number of specificities recognized. No significant killing against the Ir or the Ss‐Slp regions of the H‐2 complex could be detected. AntiH2 sera, if directed against the killer cells, do not inhibit their activity, while they can block killing, if directed against the target. This inhibition is specific in that a serum that blocks killing against the H‐2K specificity of a given target does not inhibit the lytic activity directed against the H‐2D determinants on the same target.

Spleen and lymph node cells of BALB/c mice, previously immunized with chicken thymic or bursa cells, were fused with Sp2/0-Ag14 mouse myeloma cells. Hybridomas from two fusions were selected on the basis of reactivity of their secreted antibodies towards thymic or bursal tissues in an indirect immunofluorescence assay. Four monoclonal antibodies reacting with different cell surface proteins of chicken lymphocytes were characterized, as follows. One antibody (IgM X.14) reacted only with cortical thymocytes, and precipitated material of apparent molecular weight (AMW) 65,000 (65 kD), 125 kD, and 180 kD from these cells. A second antibody (IgGl L.17) reacted with both bursa- and thymus-derived lymphocytes, but with different high molecular weight glycoproteins (AMWs 210 kD and 180 kD, respectively) on the two cell types. These proteins may be homologues of the previously described mouse B-220 and T-200 antigens. A third antibody (IgGl L.22) reacted with a protein of AMW 70 kD present on bursa-derived cells of some, but not all, chicken strains. Genetic analysis suggested that the presence of this protein was controlled by a single gene not closely linked to the major histocompatibility complex. A fourth antibody (IgG2b L.43) reacted with bursa-derived cells, macrophages and fibroblasts, but not with thymus-derived lymphocytes. L.43 precipitated material of AMW 23 kD from bursal cells.

No abstract

B6.C-H-2 ba [H (zl)] is a mutant derived from C57BL/6. The two strains mutually reject their skingrafts and are incompatible in the mixed leucocyte reaction (MLR) and in cell-mediated lympholysis (CML) assays. They are serologically indistinguishable. This report shows that H(zl) carries a new, private K end CML specificity clearly distinguishable from that of B6 by a third party strain, HTG. Antisera directed against the private H-2K specificity of B6 present on H(zl) cells) can block CML between the two strains in either direction. The new CML specificities of H(zl) cross-react with (public) CML specificities controlled by both K and D regions of other unrelated haplotypes. The results suggest that H(zl) carries a mutation in the H-2K locus itself or in a closely linked gene, the product of which is also physically associated with the H-2K molecule corresponding to the cis-configuration of the alleles in both loci. These findings indicate that T-and B-cell dictionaries for histocompatibility determinants are different.