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H‐2D b gene transfer into highly metastatic D122 cells results in tumor rejection in allogeneic recipients, but does not affect metastasis in syngeneic recipients. Implications for mechanisms of allorejection
Author(s) -
Plaksin Daniel,
Gelber Cochava,
Eisenbach Lea
Publication year - 1992
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.2910520517
Subject(s) - ctl* , transfection , biology , antigen , population , immunology , major histocompatibility complex , cancer research , lewis lung carcinoma , gene , clone (java method) , histocompatibility , metastasis , microbiology and biotechnology , cancer , medicine , human leukocyte antigen , genetics , cd8 , environmental health
Highly metastatic, weakly immunogenic Lewis lung carcinoma clones express very low levels of H‐2K b and moderate levels of H‐2D b class‐1 major histocompatibility complex antigens. These cells metastasize spontaneously in mice with C57BL/6 genetic background possessing the H‐2D b locus, and grow as local tumors across allogeneic barriers. Transfection of the H‐2D b genes into the highly metastatic clone D122 did not alter the growth or metastatic capacity of these cells in syngeneic mice. However, these cells were rejected in allogeneic mice. Transfection of the H‐2K d or H‐2K k genes into D122 elicited a CTL population that cross‐reacted with cells bearing native H‐2D b antigens. These data suggest that overlapping allo‐CTL populations are induced by a native alloantigen and by alloantigen peptides presented through self class‐l molecules. © 1992 Wiley‐Liss, Inc.