Open AccessImmunity against mouse thymus‐leukemia antigen (TL) protects against development of lymphomas induced by a chemical carcinogen, N ‐butyl‐ N ‐nitrosourea
Author(s) -
Tsujimura Kunio,
Obata Yuichi,
Matsudaira Yasue,
Ozeki Satoshi,
Taguchi Osamu,
Nishida Keiko,
Okanami Yuko,
Akatsuka Yoshiki,
Kuzushima Kiyotaka,
Takahashi Toshitada
Publication year - 2004
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2004.tb02202.x
Subject(s) - leukemia , antigen , biology , lymphoma , immunity , carcinogen , transgene , genetically modified mouse , immunology , humoral immunity , immune system , microbiology and biotechnology , cancer research , gene , genetics
Mouse thymus‐leukemia antigens (TL) are aberrantly expressed on T lymphomas in C57BL/6 (B6) and C3H/He (C3H) mice, while they are not expressed on normal T lymphocytes in these strains. When N ‐butyl‐ N ‐nitrosourea (NBU), a chemical carcinogen, was administered orally to B6 and C3H strains, lymphoma development was slower than in T3 b ‐TL gene‐transduced counterpart strains expressing TL ubiquitously as self‐antigens, suggesting that anti‐TL immunity may play a protective role. In addition, the development of lymphomas was slightly slower in C3H than in B6, which seems to be in accordance with the results of skin graft experiments indicating that both cellular and humoral immunities against TL were stronger in C3H than B6 mice. The interesting finding that B lymphomas derived from a T3 b ‐TL transgenic strain (C3H background) expressing a very high level of TL were rejected in C3H, but not in H‐2K b transgenic mice (C3H background), raises the possibility that TL‐specific effector T cell populations are eliminated and/or anergized to a certain extent by interacting with H‐2K b molecules.