摘要

Peripheral T-cell lymphoma is the generic term of a group of heterogeneous disease in non-Hodgkin's lymphoma. To investigate the quantity of CD14(+)HLA-DR-/low MDSC and T cell subsets in peripheral blood of peripheral T cell lymphoma (PTCL) patients, and explore the biological functions of CD14(+)HLA-DR-/low MDSC in peripheral T-cell lymphoma. Flow cytometry was used to determine CD14(+)HLA-DR-/low MDSC and T cell subsets in peripheral blood of 33 peripheral T-cell lymphoma patients and 23 healthy cases; CD3 + T cells, CD14(+)HLA-DR-/low MDSC cells and HLA-DR+ cells were selected with magnetic activated cell sorting; Biotin-labeled micro magnetic beads (CD2 /CD3 /CD28) were used to stimulate amplification of CD3 + T cells, which were co-cultured and analyzed by flow cytometry for the effect of different concentrations of CD14(+)HLA-DR-/low MDSC on the proliferative activity of autologous CD3+ T cells. 1. CD14(+)HLA-DR-/low cells /CD14(+) monocytes and CD4(+) CD25(+) regulatory T cells Treg /CD4(+) Tlymphocytes were 3.28% (0.40% -17.74%) and 8.81% (0.76% -78.11 %) respectively, higher than the healthy control group with statistically significant difference (P < 0.05);. 2. CD4(+) CD25(+) Treg /CD4(+) Tlymphocyte and CD14(+)HLA-DR-/CD14(+) monocytes in nucleated cells of lymphoma patients were 8.81% (0.76%-78.11%) and 3.28% (0.40% -17.74%) respectively, which was in positive correlation (correlation coefficient r = 0.510), with statistically significant difference (P = 0.002); 3. When the ratio of CD14(+)HLA-DR-/low and T cells was 1: 1, the proliferation inhibition of MDSC on autologous T cell is the strongest; after adding nor-NOHA, an ARG1 inhibitor, proliferation of T cells was recovered to 75.09 +/- 5.18 %, IDO inhibitor 1-MT made the proliferation rate of T cells recovered to 84.05 +/- 2.93%, and the proliferation rate of T cells was recovered to 97.80 +/- 2.20% after combination of the IDO inhibitor and ARG1 inhibitor. CD14(+)HLA-DR-/low MDSC inhibit the proliferation of T lymphocytes, which may be related ARG1 and IDO.