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The role of gp 70 in the target antigen recognized by murine leukemia virus immune cytotoxic T‐lymphocytes
Author(s) -
Watson Andrew,
Bach Fritz H.
Publication year - 1980
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910260414
Subject(s) - tunicamycin , antigen , microbiology and biotechnology , cytotoxic t cell , biology , immune system , murine leukemia virus , virology , friend virus , virus , immunology , biochemistry , in vitro , apoptosis , unfolded protein response
The role of the murine leukemia virus (MLV) envelope glycoprotein, gp 70 , in the formation of the target antigen recognized by in vivo generated MLV‐immune cytotoxic T‐lymphocytes (FMR‐MLV immune T) was studied. Treatment of the Rauscher MLV‐transformed C57BL/6 target cell, RBL‐5, for 4 h with the protein glycosylation inhibitor tunicamycin, was found to render the cells resistant to lysis by FMR‐MLV immune T c while lysis of the tunicamycin‐treated RBL‐5 cells by allogeneic H‐2 b immune T c was not decreased. This failure of FMR‐MLV‐immune T c to lyse tunicamycintreated RBL‐5 cells correlated with an inhibitory effect of tunicamycin on the synthesis of gp70, resulting from impaired glycosylation of the gp70 precursor, gpPr90. Yet, examination of the tunicamycin‐treated RBL‐5 cell surface by lactoperoxidase 125 I iodination and immunoprecipitation techniques, revealed (I) that neither unglycosylated gp70 nor gpPr90 antigens were detectable and (2) that the gp70 antigens from tunicamycin‐treated and untreated RBL‐5 cells were identical in their (I) migration pattern in SDS polyacrylamide gel electrophoresis (SDS PAGE) (2) isoelectric focusing profiles on a pH 3.5 ‐ pH 10 gradient and (3) external, lactoperoxidase accessible, 125 I peptides. Further, tunicamycin‐treated RBL‐5 cells retained 33% ‐ 50% of their Rauscher MLV gp70 expression, as determined by quantitative absorption of a goat anti‐Rauscher MLV gp70 serum. When this latter result was interpreted with reference to the study by Lesley et al. (1974), who observed a linear relationship between the amount of alloantigen expressed and susceptibility to immune T c killing, it was concluded that this quantitative change in gp70 expression could not adequately account for the failure of FMR‐MLV immune T c to lyse tunicamycin‐treated RBL‐5 cells. It is therefore proposed that an MLV‐induced antigen other than gp70 may be recognized on RBL‐5 cells by FMR‐MLV immune T c .