Cell‐mediated anti‐tumor response in the RL♂ 1 system I. T nature, H‐2 D d involvement and antigenic specificity of the effector cells

After in vivo priming and in vitro secondary stimulation by the radio‐induced RL♂ 1 lymphoma cells, syngeneic BALB/c splenic lymphocytes evidenced a specific but very weak cytolytic activity against RL♂ 1 target cells. Under the same experimental conditions, spleen cells from (B6 x BALB/c)F 1 were a...

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Veröffentlicht in:European journal of immunology 1978-09, Vol.8 (9), p.650-655
Hauptverfasser: Duprez, Veronique, Gomard, Elisabeth, Levy, J. P.
Format: Artikel
Sprache:eng
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Zusammenfassung:After in vivo priming and in vitro secondary stimulation by the radio‐induced RL♂ 1 lymphoma cells, syngeneic BALB/c splenic lymphocytes evidenced a specific but very weak cytolytic activity against RL♂ 1 target cells. Under the same experimental conditions, spleen cells from (B6 x BALB/c)F 1 were at least 100 times more efficient. In both cases, the effector cells were cytolytic T lymphocytes (CTL). Normal H‐2D d antigens of the tumor cell surface were involved in the effector‐to‐target cell interaction since anti‐H‐2 or anti‐H‐2D d antisera abolished the RL♂ 1 cytolysis by immune syngeneic CTL, whereas anti‐H‐2K d were devoid of blocking activity. The testing of a series of lymphoma cells, either virus‐induced or not, belonging to different H‐2 haplotypes, show that the immune CTL were highly specific for RL♂ 1 target cells. Only with the P815 mastocytoma cells was a weak cross‐reactivity detected by both direct tests and competition experiments. Allogeneic (H‐2 k ) AKR lymphoma cells which share the X1 antigen with RL♂ 1 do not react, possibly due to an H‐2 restriction of the CTL activity. The CTL‐reacting antigen cannot be definitely identified, since several specificities, including the serologically defined X1 antigen, are possibly involved simultaneously. The Hh antigens which could have accounted for the F 1 anti‐parent reaction, appear irrelevant.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.1830080909