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Nat Cancer ; 5(7): 1045-1062, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38831058

RESUMO

Tumor progression is accompanied by fibrosis, a condition of excessive extracellular matrix accumulation, which is associated with diminished antitumor immune infiltration. Here we demonstrate that tumor-associated macrophages (TAMs) respond to the stiffened fibrotic tumor microenvironment (TME) by initiating a collagen biosynthesis program directed by transforming growth factor-ß. A collateral effect of this programming is an untenable metabolic milieu for productive CD8+ T cell antitumor responses, as collagen-synthesizing macrophages consume environmental arginine, synthesize proline and secrete ornithine that compromises CD8+ T cell function in female breast cancer. Thus, a stiff and fibrotic TME may impede antitumor immunity not only by direct physical exclusion of CD8+ T cells but also through secondary effects of a mechano-metabolic programming of TAMs, which creates an inhospitable metabolic milieu for CD8+ T cells to respond to anticancer immunotherapies.


Assuntos
Neoplasias da Mama , Linfócitos T CD8-Positivos , Colágeno , Microambiente Tumoral , Macrófagos Associados a Tumor , Microambiente Tumoral/imunologia , Linfócitos T CD8-Positivos/imunologia , Linfócitos T CD8-Positivos/metabolismo , Feminino , Neoplasias da Mama/imunologia , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Colágeno/metabolismo , Animais , Macrófagos Associados a Tumor/imunologia , Macrófagos Associados a Tumor/metabolismo , Humanos , Camundongos , Fator de Crescimento Transformador beta/metabolismo , Macrófagos/imunologia , Macrófagos/metabolismo , Reprogramação Metabólica
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