RESUMO
Metabolic reprogramming plays a very important role in the immunoregulatory process, and T cells, as the indispensable part in the immune response, realize the change of function and state through metabolic reprogramming. And endothelial cells exhibit similar metabolic reprogramming. This review explores the interaction between endothelial cells and T cells to reveal the mechanism of the former as non-professional antigen presenting cells to recruit and activate the latter and the specific mechanism of cytokines produced by the latter in inflammatory response to regulate the function and state of the former, aiming to find the potential therapeutic targets for chronic inflammation and provide new ideas for the treatment.
Assuntos
Células Endoteliais , Linfócitos T , Humanos , Imunidade , InflamaçãoRESUMO
Objective To investigate the effects of nucleotide binding oligomerization domain-like receptor family caspase recruitment domain containing 3 (NLRC3) on the proliferation, migration and invasion of human colon cancer HCT116 and LoVo cells. Methods NLRC3 was knocked down in HCT116 and LoVo cells by NLRC3-specific siRNA (si-NLRC3). NLRC3 mRNA and protein expression was detected by real-time quantitative PCR and Western blotting. The proliferation ability of cancer cells was detected by CCK-8 assay; the clone formation ability was detected by clone formation assay; the invasion ability was detected by TranswellTM assay; the migration ability was detected by cell scratch healing assay. Results The transfection of si-NLRC3 down-regulated the expression of NLRC3 in HCT116 and LoVo cells. After NLRC3 knockdown, the proliferation and invasion ability of colon cancer cells were significantly strengthened and the cell migration was not significantly changed. Conclusion Knockdown of NLRC3 in HCT116 and LoVo cells can enhance cell proliferation and invasion ability, but has no effects on cancer cell migration.
