| Literature DB >> 20138013 |
Pauline Andreu1, Magnus Johansson, Nesrine I Affara, Ferdinando Pucci, Tingting Tan, Simon Junankar, Lidiya Korets, Julia Lam, David Tawfik, David G DeNardo, Luigi Naldini, Karin E de Visser, Michele De Palma, Lisa M Coussens.
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. 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID： 20138013 PMCID： PMC3082507 DOI： 10.1016/j.ccr.2009.12.019
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743