| First Author | Kammertoens T | Year | 2012 |
| Journal | Int J Cancer | Volume | 131 |
| Issue | 7 | Pages | 1499-508 |
| PubMed ID | 22212899 | Mgi Jnum | J:186111 |
| Mgi Id | MGI:5431041 | Doi | 10.1002/ijc.27411 |
| Citation | Kammertoens T, et al. (2012) 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-alpha, perforin). Int J Cancer 131(7):1499-508 |
| abstractText | 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-alpha-receptor failed to reveal significant differences in tumor development, the presence of B-cells and IL-4 enhanced tumor development under similar experimental conditions. |
