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1 Tumor growth promotes the expansion of myeloid suppressor cells.
2 s combined with a reduction in tumor-induced myeloid suppressor cells.
3 s the development, survival, and function of myeloid suppressor cells.
4 ating lymphocytes and reducing the number of myeloid suppressor cells.
5 vation of macrophages to function similar to myeloid suppressor cells.
6 ave M1 macrophages and retain high levels of myeloid suppressor cells after surgery; in addition, the
7 revealed CD11b(+)/Gr-1(+) as a heterogeneous myeloid suppressor cell also expressing low levels of MH
9 phil-to-lymphocyte ratios and percentages of myeloid suppressor cells but increased numbers of cytoki
10 mation expands a heterogeneous population of myeloid suppressor cells capable of inhibiting T cell fu
13 differentiation and accumulation of immature myeloid suppressor cells (ImC) is one of the major mecha
15 eads to a rapid and significant expansion of myeloid suppressor cells in peripheral lymphoid tissues.
16 ffect, we found that a dramatic expansion of myeloid suppressor cells in SHIP(-/-) mice impairs primi
17 creased percentage of regulatory T cells and myeloid suppressor cells in the pancreatic tumor and tum
18 s in the immune microenvironment, decreasing myeloid suppressor cells, increasing CD8+ T cells, and s
20 uitment of immunosuppressive CD11b(+)Gr-1(+) myeloid suppressor cells into the tumor microenvironment
21 ween natural killer (NK) cell activation and myeloid suppressor cell (MSC) expansion in tumor-bearing
26 population of immature myeloid cells, termed myeloid suppressor cells (MSCs), that have potent immuno
27 umors have elevated levels of Gr1(+)CD11b(+) myeloid suppressor cells (MSCs), which inhibit T cell ac
28 TGF-beta, explains previous observations on myeloid suppressor cells or TGF-beta and provides insigh
30 ion through effects on tumor vascularity and myeloid suppressor cell populations, in uveal melanoma t
31 goal of this study was to determine whether myeloid suppressor cells producing high arginase existed
34 e this threshold, GM-CSF induced Gr1+/CD11b+ myeloid suppressor cells that substantially impaired ant
36 ma microenvironment of arginase, a marker of myeloid suppressor cells, which is critical for their T-
37 eased infiltrating T lymphocytes and reduced myeloid suppressor cells, which were more apoptotic.
39 well as decreased levels of T regulatory and myeloid suppressor cells within the tumor microenvironme