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Publication : Enhanced formation of azoxymethane-induced colorectal adenocarcinoma in gammadelta T lymphocyte-deficient mice.

First Author  Matsuda S Year  2001
Journal  Jpn J Cancer Res Volume  92
Issue  8 Pages  880-5
PubMed ID  11509121 Mgi Jnum  J:70900
Mgi Id  MGI:2148439 Doi  10.1111/j.1349-7006.2001.tb01176.x
Citation  Matsuda S, et al. (2001) Enhanced Formation of Azoxymethane-induced Colorectal Adenocarcinoma in gammadelta T Lymphocyte-deficient Mice. Jpn J Cancer Res 92(8):880-5
abstractText  T cell receptor (TCR) gammadelta-positive T lymphocytes, which are localized mostly within the intraepithelial space of intestinal epithelium, have been suggested to play a role in maintaining the normal configuration of intestinal epithelium. However, the role of TCRgammadelta-positive T lymphocytes in the formation and progression of colorectal adenocarcinoma that originates from colorectal epithelial cells remains to be elucidated. In this study, TCRalphabeta and TCRgammadelta-positive T lymphocyte-deficient mice (homozygous TCRa and TCRd-gene knockout mice) and the background wild-type mice were administered azoxymethane, and the formation of macroscopic tumors and microscopic aberrant crypt foci in colorectal mucosa were compared among the three types of mice. Well-differentiated adenocarcinoma appeared 5 months after 5 administrations of azoxymethane (10 mg / kg weight) only in a few TCRd -gene knockout mice and the frequency of the carcinoma-bearing mice was increased at 7 and 9 months after the administration. Aberrant crypt foci were also detected in the colorectal mucosa of TCRd -gene knockout mice to a greater extent than in colorectal mucosa of TCRa-gene knockout mice 1 month after the azoxymethane administration. These results suggest that TCRgammadelta-positive T lymphocytes, which are present mainly in the intraepithelial space, play a role in suppression of the formation and progression of colorectal adenocarcinoma in mice.
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