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B‐cells and IL‐4 promote methylcholanthrene‐induced carcinogenesis but there is no evidence for a role of T/NKT‐cells and their effector molecules (Fas‐ligand, TNF‐α, perforin)
Author(s) -
Kammertoens Thomas,
Qin Zhihai,
Briesemeister Dana,
Bendelac Albert,
Blankenstein Thomas
Publication year - 2012
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.27411
Subject(s) - perforin , carcinogenesis , biology , immune system , methylcholanthrene , immunocompetence , tumor necrosis factor alpha , immunology , lytic cycle , effector , genetics , cancer , carcinogen , cd8 , virus
Mice deficient either in subtypes of immune cells, cytokines or lytic pathways have been subjected to chemical carcinogenesis by methylcholanthrene to evaluate whether these components of the immune system affect tumor development. Inbred mice of the same genotype but from different sources differed in tumor development in magnitude comparable to that previously attributed to differences in immunocompetence. This suggested that genetic drift between separate inbred colonies of mice and/or environmental factors ( e.g., transport of the animals) influenced carcinogenesis. Therefore, littermates were used as control in subsequent experiments. Although deficiency of T‐cells, NKT‐cells, perforin, Fas‐ligand, TNF‐α‐receptor failed to reveal significant differences in tumor development, the presence of B‐cells and IL‐4 enhanced tumor development under similar experimental conditions.