FcRγ Activation Regulates Inflammation-Associated Squamous Carcinogenesis

被引：451

作者：

Andreu, Pauline ^{[1
]}

Johansson, Magnus ^{[1
]}

Affara, Nesrine I. ^{[1
]}

Pucci, Ferdinando ^{[3
,4
]}

Tan, Tingting ^{[1
]}

Junankar, Simon ^{[1
]}

Korets, Lidiya ^{[1
]}

Lam, Julia ^{[1
]}

Tawfik, David ^{[1
]}

DeNardo, David G. ^{[1
]}

Naldini, Luigi ^{[3
,4
]}

de Visser, Karin E. ^{[5
]}

De Palma, Michele ^{[3
,4
]}

Coussens, Lisa M. ^{[1
,2
]}

机构：

[1] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA

[3] San Raffaele Telethon Inst Gene Therapy, Angiogenesis & Tumor Targeting Res Unit, I-20132 Milan, Italy

[4] Univ Vita Salute San Raffaele, San Raffaele Inst, I-20132 Milan, Italy

[5] Netherlands Canc Inst, Div Mol Biol, NL-1066 CX Amsterdam, Netherlands

来源：

CANCER CELL | 2010年 / 17卷 / 02期

基金：

美国国家卫生研究院; 瑞典研究理事会;

关键词：

K14-HPV16 TRANSGENIC MICE; MAST-CELLS; TIE2-EXPRESSING MONOCYTES; HUMORAL IMMUNITY; PRIMARY TUMORS; CANCER; MACROPHAGES; GROWTH; ANGIOGENESIS; RECEPTORS;

D O I：

10.1016/j.ccr.2009.12.019

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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 Bcells and humoral immunity foster cancer development by activating Fc gamma receptors (Fc gamma Rs) on resident and recruited myeloid cells. Stromal accumulation of autoantibodies in premalignant skin, through their interaction with activating Fc gamma Rs, 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 Fc gamma Rs are required for establishing chronic inflammatory programs that promote de novo carcinogenesis.

引用

页码：121 / 134

页数：14

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