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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)

Item Type:Article
Title: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)
Creators Name:Kammertoens, T. and Qin, Z. and Briesemeister, D. and Bendelac, A. and Blankenstein, T.
Abstract:Mice deficient either in subtypes of immune cells, cytokines or lytic pathways have been subjected to chemical carcinogenesis by methylcholanthrene (MCA) 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 immuno-competence. 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. While deficiency of T-cells, NKT-cells, perforin, Fasligand, 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.
Keywords:Chemical Carcinogenesis, Immune-Deficient Mice, Methylcholanthrene, Immunosurveillance, Animals, Mice
Source:International Journal of Cancer
ISSN:0020-7136
Publisher:Wiley (U.S.A.)
Volume:131
Number:7
Page Range:1499-1508
Date:1 October 2012
Official Publication:https://doi.org/10.1002/ijc.27411
PubMed:View item in PubMed

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