TMPE

AcronymDefinition
TMPETraffic Manager: President Edition (game)
TMPETraffic Manager: President Edition (Cities Skylines game)
TMPETeleservice Marches Publics Europeens (French: European Public Teleservice Markets)
References in periodicals archive ?
We found that lower degranulation capabilities correlated with a decrease of the percentage of [perforin.sup.+] NK cells in iPE and ptPE (Supplemental Figure 4) as compared to autologous PB-NK, which became significant in iPE, tmPE ([CD56.sup.dim] subset), and ptPE ([CD56.sup.bright] subset) (Figures 5(c)-5(e)).
This experimental schedule was performed both on autologous PE-derived NKs, as well as by polarizing age-matched healthy control-derived NK cells, with iPE, ptPE, and tmPE liquids.
Our data show that NK cells derived from iPE and tmPE produce the proangiogenic cytokine VEGF, in a statistically significant manner, as compared to healthy donor PBNK cells (Figure 7).
We found that PE-NK cells display a higher amount of intracellular VEGF as compared to autologous and healthy PB-NK cells (Figure 7) that became statistically significant from those isolated from tmPE fluids.
Although patient PB-NK and PE-NK cells are not fully anergic as they respond to stimulation by IL-2 in the culture medium, however, addition of TGF[beta] or iPE or tmPE fluids resulted in a strong inhibition of this crucial effector function of NK cells, even in healthy donor NK cells, suggesting a predominant role for the PE tumor microenvironment in the establishment of an alternative NK cell activation status.
Flow cytometric analysis on NK cells in samples from healthy individuals (hPB), peripheral blood (iPB) and pleural effusion (iPE) from patients with inflammatory disease, peripheral blood (ptPB) and pleural effusion (ptPE) from patients with primary tumor, and peripheral blood (tmPB) and pleural effusion (tmPE) from patients with tumor metastasis showed no difference in CD9 expression levels in terms of positive cell percentage (A) and mean fluorescence intensity (MFI) (B).
Flow cytometric analysis showed the percentage of NK cells in all samples from healthy controls (hPB), peripheral blood (iPB) and pleural effusion (iPE) from patients with inflammatory disease, peripheral blood (ptPB) and pleural effusion (ptPE) from patients with primary tumor, and peripheral blood (tmPB) and pleural effusion (tmPE) from patients with tumor metastasis.
Flow cytometric analysis demonstrated that in NK cells from patients with pleural effusions, CD49a expression was increased in the [CD56.sup.bright] subset from pleural effusion (significantly in ptPE and in tmPE) as compared to PB-NK cell samples (a, b).
Flow cytometric analysis on NK cell subsets from healthy individuals (hPB), peripheral blood (iPB) and pleural effusion (iPE) from patients with inflammatory disease, peripheral blood (ptPB) and pleural effusion (ptPE) from patients with primary tumor and peripheral blood (tmPB), and pleural effusion (tmPE) from patients with tumor metastasis revealed a decrease percentage of mature NK cells correlated to the downregulation of CD57 marker in PE samples as compared with PB and healthy donors.
Flow cytometric analysis on NK cell subsets of healthy individuals (hPB), peripheral blood (iPB) and pleural effusion (iPE) from patients with inflammatory disease, peripheral blood (ptPB) and pleural effusion (ptPE) from patients with primary tumor, and peripheral blood (tmPB) and pleural effusion (tmPE) from patients with tumor metastasis revealed upregulation of CD69, an activating and decidual NK marker, in PE samples compared to autologous and healthy control PB-NK cells (a, b).