RESUMO
Chemotherapy resist is the problem for clinic,and some researches find that chemotherapy with anthracycline and oxaliplatin not only induces the tumor cell apoptosis,but also the celt immunogenic cell death (ICD) by inducing the tumor cell apoptosis and releasing three kinds of signals:exposure of calreticulin on the cell surface to stimulate the dendritic cell (DC) to engulf,and the secretion of adenosine triphosphate to recruit DC to enter into tumor bed,and the release of the high mobility group B1 to promote DC to steadily bind with dying tumor cell to induce specific T cell antitumor immune response.It is with great meaning to promote the chemotherapy protocol by studying the ICD induced by chemotherapy.
RESUMO
Objective To explore the role of T cell-mediated immunity in the pathogenesis of venous thromboembolism ( VTE ) by analyzing the differential expression of T cell immune-related gene mRNAs peripheral blood mononuclear cells (PBMCs) between VTE patients and controls with GeneChip Human Genome. Methods Human eDNA microarray analysis was employed in PBMCs from 20 VTE patients and 20 hypertensive controls,and random variant model (RVM) corrected t-test was used for statistical analysis of differential gene expression.Results Six mRNA stripes including CD247,CD3D,CD3G,Granzyme A (GzmA),Granzyme B (GzmB) and Zeta-chain-associated protein kinase 70 (ZAP70)were found to be associated with T cell-mediated immunity.Significant down-regulation of these six mRNAs was found in the VTE group compared with the controls ( 15.3050 ± 0.6346 vs 15.8053 ± 0.5567,13.7878 ±0.7731 vs 14.3820 ±0.4857,13.3299 ± 0.9104 vs 14.1246 ± 0.6011,14.8893 ± 0.8675 vs 15.5305 ±0.4624,15.9113 ±0.8123 vs 16.4553 ±0.5055,14.3652 ±0.7717 vs 14.3652 ±0.7717;all P values ＜ 0.05 ).Conclusions T cells' function including antigen recognition,signal transduction and cytotoxicity was impaired in VTE patients.T cell-mediated immunity dysfunction probably plays an important role in the pathogenesis of VTE.