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De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent

de Visser, Karin E., Korets, Lidiya V., Coussens, Lisa M.·2005·Cancer Cell
DOI 10.1016/j.ccr.2005.04.014
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Abstract

Chronic inflammation predisposes tissue to cancer development; however, regulatory mechanisms underlying recruitment of innate leukocytes toward developing neoplasms are obscure. We report that genetic elimination of mature T and B lymphocytes in a transgenic mouse model of inflammation-associated de novo epithelial carcinogenesis, e.g., K14-HPV16 mice, limits neoplastic progression to development of epithelial hyperplasias that fail to recruit innate immune cells. Adoptive transfer of B lymphocytes or serum from HPV16 mice into T and B cell-deficient/HPV16 mice restores innate immune cell infiltration into premalignant tissue and reinstates necessary parameters for full malignancy, e.g., chronic inflammation, angiogenic vasculature, hyperproliferative epidermis. These findings support a model in which B lymphocytes are required for establishing chronic inflammatory states that promote de novo carcinogenesis.

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Metadata

Authors
de Visser, K. E., Korets, L. V., & Coussens, L. M.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2005-05
Volume
7
Issue
5
Pages
411-423
ISSN
1535-6108
DOI
10.1016/j.ccr.2005.04.014
Cited by
715
References
4
Language
en
Licence

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