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Mucosal Immunol ; 7(4): 842-56, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-24280935

RESUMO

Chronic inflammation has been associated with increased risk for developing gastrointestinal cancer. Interleukin-23 (IL-23) receptor signaling has been correlated with inflammatory bowel disease pathogenesis, as well as promotion of tumor growth. However, little is known about the relative potential for IL-23-directed causality in gut tumorigenesis. We report that IL-23 transgene expression was sufficient to induce rapid (3-4 weeks) de novo development of intestinal adenomas with 100% incidence. Initiation of tumorigenesis was independent of exogenous carcinogens, Helicobacter colonization, or pre-existing tumor-suppressor gene mutations. Tumorigenesis was mediated by Thy1(+)IL-23R(+) innate lymphoid cells (ILC3), in part, through IL-17 responses as tumor development was inhibited in RAG(-/-) × IL-17(-/-) double knockout mice. Remarkably, IL-23 initiation of tumorigenesis by resident ILCs consistently occurred before recruitment of conspicuous inflammatory infiltrates. Our results reveal an explicit role for IL-23-mediated initiation of gut tumorigenesis and implicate a key role for IL-23R(+) ILC3 in the absence of overt cellular infiltrate recruitment.


Assuntos
Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/imunologia , Imunidade Inata , Interleucina-23/genética , Ativação Linfocitária/imunologia , Linfócitos/imunologia , Adenoma/genética , Adenoma/patologia , Animais , Carcinógenos , Proliferação de Células , Citocinas/metabolismo , Duodeno/metabolismo , Duodeno/patologia , Expressão Gênica , Interferon gama/metabolismo , Interleucina-17/metabolismo , Interleucina-23/metabolismo , Mucosa Intestinal/imunologia , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologia , Camundongos , Fenótipo , Receptores de Interleucina/metabolismo , Transdução de Sinais
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