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discussed in relation to the occurrence and expression of cross-reacting embryonic antigens associated with the cell surface of these rat tumours.
suggested that they were macrophages, granulocytes and lymphoid cells. Surface changes in the erythrocytes during contact with K cells indicate that mechanical factors may be involved in cell lysis in this system.
B AND T CELLS IN CANINE LYMPHOSARCOMA. D. E. ONIoNs, Department of THERAPY OF METHYL CHOLANClinical Veterinary Medicine, University of THRENE INDUCED CBA MOUSE TUCambridge. MOURS WITH CORYNEBACTERIUM Canine multicentric lymphosarcoma is a PAR VUM AND IRRADIATED TUcommon spontaneous neoplasm of dogs. MOUR CELLS. R. BOMFORD, DepartCanine lymphoma cells, like normal canine ment of Experimental Immunobiology, lymphocytes, may be divided into two classes, Wellcome Research Laboratories, Beckenham. T and B, based on the spontaneous rosette Mice were injected subcutaneously with formation between canine T cells and human 2 x 104 tumour cells and 2 days later given erythrocytes, and the presence of a receptor C. parvum, irradiated tumour cells, or both for (human) complement on the surface of B admixed, into the footpad. Tumour growth cells. was unaffected by C. parvum or tumour cells The presence of an Fc receptor on canine alone, but was suppressed by appropriate lymphocytes appears to be an unreliable mixtures. The conditions for successful marker for B cells as many complement therapy were: 1. sufficient tumour cells receptor lymphocytes (EACL) lack a (> 5 x 104); 2. sufficient, but not excessive, detectable Fc receptor for using a rosetting C. parvum (optimally between about 5 to technique with antibody coated eryth- 20 [kg, increasing with the dose of tumour rocytes. cells); 3. the same tumour cells in the tumour challenge and treatment mixture; other SCANNING ELECTRON MICROS- MCA tumour cells were ineffective; 4. mice COPY OF K CELL ACTIVITY ON RED with an intact T cell system; tumour growth CELL MONOLAYERS. A. E. WILLIAMS, was not suppressed in T cell depleted mice. Western General Hospital, Edinburgh, J. R. The results suggest that the therapeutic INGLIS, W. J. Penhale, A. FARMER and W. J. effect depends on the potentiation by C. IRVINE, Department of Therapeutics, Uni- parvum of a T cell dependent component of the immune response to TSTAs. versity of Edinburgh. K cell activity against syngeneic cells (De Landazuriet et al., Cell Immunol. 1974, ROLE OF IMMUNOCOMPETENCE IN 14, 193) and defects in K cell activity in LOCALIZED BCG SUPPRESSION OF cancer patients (Wisloff et al., Scand. J. TUMOUR GROWTH. M. V. PIMM and Immunol., 1973, 2, 325) have been demon- D. G. Hopper, Cancer Research Campaign strated. However, the identity of the K cell Laboratories, University of Nottingham. is still uncertain and conflicting evidence Admixture of BCG organisms with cells of supports B lymphocytes, monocytes, macro- syngeneically transplanted rat tumours prephages and other leucocytes. vents their development and this leads to We have used the SEM to examine the immunologically specific rejection of tumour interaction between human leucocytes deposits at distant sites. Immunosuppres(separated in Ficoll-Triosil and pre-incubated sion by whole body irradiation did not preon glass) and antibody coated sheep erythro- vent suppression of growth from mixed BCG: cyte monolayers (Kennedy and Axelrad, tumour cell inocula but did abrogate the Immunology, 1971, 20, 253). Only a small concomitant rejection of distant challenge proportion of the leucocyte suspension inocula. Tumour suppression at the site of adhered to the monolayer and the non- BCG was, however, prevented by macrophage adherent cells lacked antibody dependent depletion of the host by silica treatment. cytotoxic activity. Three morphologically These observations suggest that local BCG distinct cell types were associated with areas suppression of tumour does not require of lysis in the erythrocyte monolayer within lymphocyte mediated immune responses and 4 h and correlation with light microscopy probably depends on less specific macrophage 17