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J Immunol ; 193(6): 2994-3002, 2014 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-25122922

RESUMO

Natural products are a major source for cancer drug development. NK cells are a critical component of innate immunity with the capacity to destroy cancer cells, cancer-initiating cells, and clear viral infections. However, few reports describe a natural product that stimulates NK cell IFN-γ production and unravel a mechanism of action. In this study, through screening, we found that a natural product, phyllanthusmin C (PL-C), alone enhanced IFN-γ production by human NK cells. PL-C also synergized with IL-12, even at the low cytokine concentration of 0.1 ng/ml, and stimulated IFN-γ production in both human CD56(bright) and CD56(dim) NK cell subsets. Mechanistically, TLR1 and/or TLR6 mediated PL-C's activation of the NF-κB p65 subunit that in turn bound to the proximal promoter of IFNG and subsequently resulted in increased IFN-γ production in NK cells. However, IL-12 and IL-15Rs and their related STAT signaling pathways were not responsible for the enhanced IFN-γ secretion by PL-C. PL-C induced little or no T cell IFN-γ production or NK cell cytotoxicity. Collectively, we identify a natural product with the capacity to selectively enhance human NK cell IFN-γ production. Given the role of IFN-γ in immune surveillance, additional studies to understand the role of this natural product in prevention of cancer or infection in select populations are warranted.


Assuntos
Benzodioxóis/farmacologia , Glicosídeos/farmacologia , Interferon gama/biossíntese , Células Matadoras Naturais/imunologia , Fator de Transcrição RelA/imunologia , Antígeno CD56/biossíntese , Antígeno CD56/genética , Células Cultivadas , Células HEK293 , Humanos , Interleucina-12/farmacologia , Interleucina-15/farmacologia , Ativação Linfocitária/imunologia , Interferência de RNA , RNA Interferente Pequeno , Receptores de Interleucina-15 , Transdução de Sinais/imunologia , Receptor 1 Toll-Like/genética , Receptor 1 Toll-Like/imunologia , Receptor 6 Toll-Like/imunologia , Fator de Transcrição RelA/biossíntese , Regulação para Cima
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