Specific Suppression by Antibody Treatment of the Lymphoid Cells* by Erna Moller,* M.d

The central role of immune lymphoid cells in the manifestation of diverse immunological reactions in delayed hypersensitivity, transplantation, and autoimmunity is well established, but the mechanism by which the sensitized cells exert their effect is still largely unknown. The introduction of tissue culture methods represents a major advance in this area, and cell-mediated immunity against histoincompatible target cells can now be demonstrated by the capacity of specifically sensitized lymphoid cells to kill normal or neoplastic target cells in vitro (1-8). Cytotoxicity by sensitized cells fulfils requirements for immunological specificity (9), is preceded as a rule by aggregation of the lymphoid cells around the target cells, and is abolished if the two cell types are separated by impermeable diffusion membranes (8). However, not only specifically sensitized cells but normal allogeneic (though not syngeneic) cells were also found to kill H-2 incompatible target cells of mouse origin in vitro (10-12) if heterologous antibodies or phytohemagglutinin was present in the medium. Although this reaction may represent the induction of a primary immune response in vitro, this seemed less probable since lymphoid cells, which would be genetically unable to react immunologically against the targets, were still capable of mediating target cell death (11). The only variable that determined cytotoxicity in this case seemed to be the presence of foreign histocompatibility antigens on the lymphoid cells. Presumably, target cells were damaged by dose confrontation with cells carrying incompatible surface isoantigenic determinants. An analogous concept was also put forward by HellstrSm et al. (13) as an explanation of the phenomenon of reduced tumor growth in semisyngeneic F1 hybrid mice as compared to tumor growth in syngeneic hosts (14). The reaction was termed "allogeneic inhibition".