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Cancer Cell. 2010 Feb 17;17(2):121-34. doi: 10.1016/j.ccr.2009.12.019. Epub 2010 Feb 4.

FcRgamma activation regulates inflammation-associated squamous carcinogenesis.

Author information

1
Department of Pathology, University of California, San Francisco, 94143, USA.

Abstract

Chronically activated leukocytes recruited to premalignant tissues functionally contribute to cancer development; however, mechanisms underlying pro- versus anti-tumor programming of neoplastic tissues by immune cells remain obscure. Using the K14-HPV16 mouse model of squamous carcinogenesis, we report that B cells and humoral immunity foster cancer development by activating Fcgamma receptors (FcgammaRs) on resident and recruited myeloid cells. Stromal accumulation of autoantibodies in premalignant skin, through their interaction with activating FcgammaRs, regulate recruitment, composition, and bioeffector functions of leukocytes in neoplastic tissue, which in turn promote neoplastic progression and subsequent carcinoma development. These findings support a model in which B cells, humoral immunity, and activating FcgammaRs are required for establishing chronic inflammatory programs that promote de novo carcinogenesis.

PMID:
20138013
PMCID:
PMC3082507
DOI:
10.1016/j.ccr.2009.12.019
[Indexed for MEDLINE]
Free PMC Article

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