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Expression of alien histocompatibility antigens on SJL/J tumors detected by cell-mediated and serological analyses

โœ Scribed by Benjamin Bonavida; Janet M. Roman


Publisher
Springer-Verlag
Year
1981
Tongue
English
Weight
744 KB
Volume
11
Category
Article
ISSN
0340-7004

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โœฆ Synopsis


Reticulum cell sarcoma (RCS) cells of SJL/J (H-2 s) mice have been shown to express antigens that are cross-reactive with allogeneic cells of the H-2 d and H-2 b haplotypes by cell-mediated cytotoxicity, antibody-mediated cytotoxicity, immunofluorescence, and quantitative absorption assays. These alien antigens have been detected on both spontaneous and in vivo-and in vitro-passaged RCS cells to varying degrees.

The in vitro cell lines were able to stimulate a syngeneic cytotoxic T cell response detected in a 4-h 51Cr release assay. The cytotoxic cells reacted with in vitro RCS tumor targets but not with in vivo or spontaneous RCS tumors. Furthermore, the cytotoxic cells lysed H-2 d and to a lesser extent 1-1-2 b target cells, but not H-2 k, H-2 p, or H-2 r cells. The cross-reactivity was also observed with SJL/J anti-BALB/c cytotoxic cells, which can lyse in vitro RCS targets effectively. The in vivo tumors were not stimulatory in cytotoxic responses and did not serve as targets.

H-2 d specificities were also detected in cultured RCS tumor cells by cytotoxic antibody. Both allogeneic SJL/J anti-BALB/c, C57B1/6 anti-BALB/c sera reacted with RCS tumor cells and not normal SJL/J cells. Furthermore, monospecific D a sera were also cytotoxic against RCS lines. The cytotoxic activity could be absorbed by BALB/c cells and RCS cells but not with normal SJL/J cells. The H-2 ~t specificities were also detected on the in vivo lines by indirect immunofluorescence. The majority (= 60%) of spontaneously arising tumors expressed either H-2 a or H-2 b allospecificities in the immunofiuorescence assays. Although these antigens may not be inappropriate for the SJL/J strain, their differential expression on tumor cells may be significant in the etiology of the tumor.


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