Induction of immunocellular resistance to IL-2-activated lymphocytes within ovarian carcinoma cells.

The development of resistance within ovarian carcinoma cells to activated cytotoxic lymphocytes was the objective of this study. Primary ovarian carcinoma cells were obtained from the ascites of a patient. These cells were cocultured with IL-2-activated autologous tumor-associated lymphocytes (TALs) for 1 week.

Induction of foetal lethality in AKR offspring after repeated inoculations into AKR females of anti-TCR/V beta 6 monoclonal antibody.

Female AKR (H-2k, Mlsa) mice were repeatedly injected with monoclonal anti-V beta 6 prior to and during syngeneic pregnancy. The offspring were born non-viable or died within 24 h. Continued injections into the mother resulted in abortions and conception eventually ceased altogether.

Anti-Mlsa-like effect of CBA/J anti DBA2 antibody in in vitro MLRs between Mls incompatible combinations.

Antisera from CBA/J (H-2k,Mlsa) mice hyperimmunised with DBA2 (H-2d,Mlsa) and/or AKR (H-2k,Mlsa) splenocytes, can block in vitro MLRs against Mlsa determinants. These two antisera are furthermore specifically cytotoxic against targets expressing H-2 components but not against Mlsa-bearing targets. In these experimental models the anti-Mlsa-like effects of CBA/J anti-DBA2 and CBA/J anti AKR antibodies seem to be associated with an autoreactive immune response in CBA/J mice elicited by DBA2 and AKR splenocytes, respectively.

Anti-T-cell receptor V beta 6 breaks tolerance in Mlsa mice and induces production of anti-Mlsa antibodies.

Tolerance to the minor lymphocyte stimulating (Mls) self-antigens has been shown to be due to the intrathymic deletion of T-cell clones bearing certain T-cell receptor (TcR) V beta regions. T cells bearing these V beta regions (V beta 6, V beta 7, V beta 8.1, V beta 9) are deleted in Mlsa-positive mice.