FcRγ Activation Regulates Inflammation-Associated Squamous Carcinogenesis
Copyright policy )FcRγ Activation Regulates Inflammation-Associated Squamous Carcinogenesis
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.
- University of California System United States
- Division of Molecular Biology The Netherlands Cancer Institute Netherlands
- UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- University of California, San Francisco United States
- UCSF Helen Diller Family Comprehensive Cancer Center United States
Cancer Research, B-Lymphocytes, CD11b Antigen, Neovascularization, Pathologic, Receptors, IgG, Mice, Transgenic, CELLCYCLE, Cell Biology, Models, Biological, Immunity, Humoral, Mice, Oncology, CELLIMMUNO, Carcinoma, Squamous Cell, Animals, Myeloid Cells, Mast Cells, Neoplasms, Glandular and Epithelial, MOLIMMUNO
Cancer Research, B-Lymphocytes, CD11b Antigen, Neovascularization, Pathologic, Receptors, IgG, Mice, Transgenic, CELLCYCLE, Cell Biology, Models, Biological, Immunity, Humoral, Mice, Oncology, CELLIMMUNO, Carcinoma, Squamous Cell, Animals, Myeloid Cells, Mast Cells, Neoplasms, Glandular and Epithelial, MOLIMMUNO
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