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Autologous mixed lymphocyte cultures were set up from nylon non-adherent T-enriched lymphocytes and mitomycin C-treated spleen cells of individual ACI/N rats and the effect on the reaction (AMLR) of sera in the culture medium was studied with regard to the xenogeneic nature of the sera. Not only foetal calf serum, but also sera of adult human, horse and swine stimulated the AMLR response, but autologous or rat serum did not. Albumin fractions of these sera were also effective in inducing the AMLR response. Furthermore, the presence of xenogeneic serum in the culture medium was also required for the blastogenic response of AMLR-primed lymphocytes against the secondary stimulation with syngeneic spleen cells. Both autologous and xenogeneic sera, however, supported the Con-A response of the same responder cell population as used in the AMLR. These results substantiated our previous finding (Endho & Hashimoto, 1981) and suggest that two signals, one from autologous non-T cells and another from the xenogeneic factor in culture medium, are required to cause AMLR, at least in the rat system. [ABSTRACT FROM AUTHOR]

Mixed culture of nylon non-adherent (T-enriched) spleen cells or lymph node cells of ACI/N or F344 rats with mitomycin C-treated autologous spleen cells resulted in the increased DNA synthesis of the responder T cells when they were cultured in medium containing foetal calf serum (FCS) or bovine Serum albumin. This autologous mixed lymphocyte reaction (AMLR), however, proceeds little when the cells were cultured in medium containing autologous or allogeneic rat serum, irrespective of the responder:stimulator cell ratio and to the culture period. Furthermore, the AMLR response in FCS was greatly reduced if a relatively large number of macrophages were present in the responder cell population. These results suggest that the AMLR response is unlikely to occur in a physiological condition or in [ABSTRACT FROM AUTHOR]

The presence of tumor-specific or tumor-associated antigens in primary urinary bladder tumors induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in ACI/N rats was examined by means of mixed lymphocyte-tumor cell culture. Bladder tumors (papilloma with cancer foci or cancer) induced by BBN treatment for 18 weeks or more (BT), epithelial cells from papillary hyperplasia induced by 6-week BBN treatment (PH), and normal bladder epithelial cells (NBE) were isolated from the bladder and used as stimulator cells after mitomycin C treatment. BT, PH and NBE all strongly stimulated the blastogenesis of the autologous lymphocytes on culture in medium containing fetal calf serum (FCS), but the spleen cells also stimulated the autologous lymphocytes in this medium. Although the magnitudes of blastogenesis were lower than those in FCS medium, on culture in medium containing rat serum, BT, PH and NBE, but not spleen cells, stimulated the blastogenesis of the autologous lymphocytes. The response with BT was significantly higher than the response with NBE, but there was no statistically significant difference between the response with BT and the response with PH. These results suggest that FCS medium, but not medium with rat serum, evokes the blastogenic response of lymphocytes cultured with autologous spleen cells, and that blastogenic responses with autologous bladder cancer can be produced by stimulation with some sort of tissue antigen present in normal or pre-neoplastic urinary bladder epithelial cells.