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1 MDSC burden correlates with poorer clinical outcomes, cr
2 MDSC depletion may enhance T cell responses to lentivira
3 MDSC from melanoma tumor models decreased the levels of
4 MDSC generated from CCR2 mice failed to be mobilized and
5 MDSC migration was dependent on expression of CCR2, wher
6 MDSC miR-126a(+) exosomes further induce IL13(+) Th2 cel
7 MDSC-induced 'metastatic gene signature' derived from mu
8 MDSCs consist of two major subsets, monocytic and polymo
9 MDSCs expand during the later phases of sepsis in mice,
10 MDSCs may therefore play a role in locally maintaining i
11 MDSCs use NO to nitrate both the T-cell receptor and STA
12 MDSCs were phenotyped for cell surface receptor expressi
13 MDSCs were suppressive of autologous T-cell responses as
16 chanisms that lead to induction of activated MDSCs and IL-13(+) Th2 cells have not yet been identifie
21 expression levels strongly correlate with an MDSC gene signature, and high expression of YAP or MDSC-
23 t flow measurements were taken using DMA and MDSC, which were accompanied by FTIR, WAXD and ESEM.
25 characterized by decreased TAMs (CD206+) and MDSCs (Gr1+ CD11b+), increased dendritic cells (CD86+) a
26 er, the mechanistic details of how Tregs and MDSCs are recruited in various tumors are not yet well u
30 th persistent increased percentages of blood MDSCs had increased nosocomial infections, prolonged int
32 mulating factor (GM-CSF), mainly produced by MDSCs, was identified as a key factor to mediate these e
34 a model, we found an accumulation of CCR5(+) MDSCs in melanoma lesions associated with both increased
38 2 and MIF and an increased number of CD33(+) MDSCs were detected in BC tissues, and these increases w
40 y exhibited myeloid-derived suppressor cell (MDSC) markers and acquired the ability to inhibit T cell
41 +) CD34(-) [myeloid-derived suppressor cell (MDSC)-like fibrocytes] cells in stable COPD (n = 41) and
42 n of proliferative responses required T cell-MDSC contact and was mediated by inducible nitric oxide
43 equency of myeloid derived suppressor cells (MDSC) and are at increased risk for cardiovascular disea
47 ulation of myeloid-derived suppressor cells (MDSC) in melanoma microenvironment is supported by chemo
48 oration of myeloid-derived suppressor cells (MDSC) in the tumor microenvironment, initially reduced b
51 2-positive myeloid-derived suppressor cells (MDSC) to form a premetastatic niche that ultimately prom
52 orted that myeloid-derived suppressor cells (MDSC), which are a heterogeneous population of immunosup
55 pansion of myeloid-derived suppressor cells (MDSC); however, little is known regarding the subpopulat
56 d cells as myeloid-derived suppressor cells (MDSCs) accumulated, which was associated with the transf
59 ediated by myeloid-derived suppressor cells (MDSCs) and showed that MDSCs expanded in melanoma patien
63 Myeloid progenitor-derived suppressor cells (MDSCs) arise from myeloid progenitors and suppress both
66 ulation of myeloid-derived suppressor cells (MDSCs) has been observed in solid tumors and is correlat
67 increased myeloid-derived suppressor cells (MDSCs) induce detrimental immunosuppression, but little
68 n of donor myeloid-derived suppressor cells (MDSCs) mediated by ILC2 production of IL-13, improved GI
72 responses (myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and programmed death
73 ulation of myeloid-derived suppressor cells (MDSCs), which actively suppressed antitumor immune respo
81 (+)IFNgamma(+) cells in response to CMVpp65; MDSC depletion further augmented CD4(+)CX3CR1(+)IFNgamma
83 recently showed that IRF8 inversely controls MDSC burden in tumor models, particularly the PMN-MDSC s
84 tment reduces the virus-induced PD-L1(+) DC, MDSC, TAM and Treg, as well as co-inhibitory molecules-d
86 cular mechanism by which cancer cells direct MDSC homing to primary tumor and suggests that targeting
92 ingly, these CD45(+)CD33(+)CD11b(+)HLA-DR(-) MDSCs exhibited increased CXCR2 expression compared with
93 strated that CD45(+)CD33(+)CD11b(+)HLA-DR(-) MDSCs from fresh BC tissues displayed high levels of sup
94 /EBPalpha resulted in significantly enhanced MDSC proliferation and expansion, as well as an increase
97 Here, we identified a new subset of MDSC (Eo-MDSC) in S. aureus-infected mice that phenotypically res
99 sing in response to CMV infection can escape MDSC-mediated suppression, and defined TIGIT antagonists
103 el showed that collagen type 1 intensity for MDSC-like fibrocytes was positively associated with lung
104 ce of the CCR5/CCR5 ligand axis not only for MDSC recruitment but also for further activation of thei
106 s) low-density granulocytes/granulocytic (G)-MDSCs were more specifically expanded in patients with s
107 et CD11b(+)Ly6G(+)Ly6C(low) granulocytic (G)-MDSCs, sparing CD11b(+)Ly6G(-)Ly6C(high) M-MDSCs, with r
110 c myeloid-derived suppressor cells (M- and G-MDSCs) defined by their ability to suppress T-cell respo
116 , we demonstrate that granulocytic MDSCs (GR-MDSCs) accumulate in human placenta of healthy pregnanci
120 At all stages of infection, granulocytic MDSC suppressed CD4+ and CD8+ T cell proliferation in re
121 this study, we demonstrate that granulocytic MDSCs (GR-MDSCs) accumulate in human placenta of healthy
122 lpha conditional null mice displayed greater MDSC infiltration, increased vascularization and acceler
126 ion of MDSC expanded in presence of HIV (HIV MDSC), but decreased with culture of HIV MDSC with autol
130 -27 regulated the expression of B7-H4 on HIV MDSC, and controlled CMV-specific T cell activity by lim
131 also provide comprehensive insights into how MDSCs are recruited to other organs where they contribut
132 rt that BTK is expressed by murine and human MDSCs, and that ibrutinib is able to inhibit BTK phospho
133 We hypothesized that after sepsis in humans, MDSCs will be persistently increased, functionally immun
137 2/MIF-CXCR2 axis as an important mediator in MDSC recruitment and as predictors and potential therape
138 de of chemokine (C-X3-C motif) receptor 1 in MDSCs by chemokine (C-X3-C motif) receptor 1 neutralizin
139 ed Dickkopf-1 (Dkk1) targets beta-catenin in MDSCs, thus exerting immune suppressive effects during t
142 expression in activating iNOS expression in MDSCs when they are generated under pathologic condition
146 pha) expression was significantly reduced in MDSCs from tumor-bearing mice compared to non-tumor-bear
148 ysis was conducted to determine if increased MDSC appearance was associated with in-hospital and long
149 fied a mechanism by which tumor cells induce MDSC accumulation and expansion in the bladder cancer (B
150 howed that MDSC miR-126a rescues DOX-induced MDSC death in a S100A8/A9-dependent manner and promotes
151 work suggests treatment interruption-induced MDSC may especially undermine the effectiveness of such
152 ed that bladder cancer cell line J82 induced MDSC migration via CXCL2/MIF-CXCR2 signaling in vitro.
153 nistic studies demonstrated that J82-induced MDSC trafficking and CXCR2 expression were associated wi
159 riched at the nos2 promoter in tumor-induced MDSCs, and inhibition or silencing of SETD1B diminished
160 although IRF8 was silenced in tumor-induced MDSCs, iNOS expression was significantly elevated in tum
161 was significantly elevated in tumor-induced MDSCs, suggesting that the expression of iNOS is regulat
164 mportantly, premetastatic liver-infiltrating MDSCs induced tumor cell survival without involvement of
165 Targeted therapy against mCRPC-infiltrating MDSCs, using multikinase inhibitors such as cabozantinib
168 e testing, we demonstrate that monocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs can be detected
169 re a unique mechanism by which monocytic (M)-MDSCs are spared, allowing them to polarize towards M1 m
172 on is immunosuppressive due to (monocytic) M-MDSC infiltration, which results in tumor radioresistanc
175 xis as a targetable pathway to curtail the M-MDSC compartment and improve bladder cancer treatment.
182 )-MDSCs, sparing CD11b(+)Ly6G(-)Ly6C(high) M-MDSCs, with reduced tumor burden in 4T1-Neu tumor-bearin
185 f G-MDSCs, arginase 1, and S100A12 but not M-MDSCs were associated with subsequent occurrence of noso
186 and correlated with the level of recruited M-MDSCs, which highly expressed IL-13 receptor alpha1.
192 previous research demonstrating psoriatic Mo-MDSC are unable to suppress autologous and heterologous
194 tly contributes to tissue infiltration by MO-MDSCs and monocytes, thereby contributing to the pathoge
195 nocytic myeloid-derived suppressor cells (MO-MDSCs) within the hepatic compartment suppress inflammat
196 o demonstrated that psoriatic and control Mo-MDSCs both induce regulatory T-cell conversion from naiv
197 to HSEC monolayers, proportionally fewer MO-MDSCs underwent transendothelial migration, indicating t
199 compared the transmigratory potential of MO-MDSCs and monocytes after adhesion to hepatic endothelia
200 owever, little is known about the role of Mo-MDSCs and their functional relationship to T-cell suppre
201 urrently not known whether recruitment of MO-MDSCs from blood via hepatic sinusoidal endothelium (HSE
202 ticle, we found reduced levels of CD13 on MO-MDSCs, which has recently been reported to control cell
203 e regulatory T cells induced by psoriatic Mo-MDSCs displayed decreased suppressive functionality.
206 Two major MDSC subsets, including monocytic MDSC and granulocytic MDSC, have been described to date.
215 t BRAFi-resistant melanomas, the addition of MDSC depletion/blockade (anti-Gr-1 + CCR2 antagonist) pr
217 rch efforts have also increased awareness of MDSC in non-malignant inflammatory diseases, including a
218 ted with anti-Jagged, whereas coinjection of MDSC-like cells from anti-Jagged-treated mice with cance
220 e to CMVpp65 were enhanced with depletion of MDSC expanded in presence of HIV (HIV MDSC), but decreas
223 Here we demonstrate functional inhibition of MDSC with IPI-145, an inhibitor of PI3Kdelta and PI3Kgam
228 ration, survival, and suppressive potency of MDSC, and that a feedback homeostatic mechanism maintain
229 e CD11b(+) Ly6G(+) Ly6C(++) subpopulation of MDSC induced by P. gingivalis infection was able to diff
230 ced the expansion of three subpopulations of MDSC (Ly6G(++) Ly6C(+), Ly6G(+) Ly6C(++), and Ly6G(+) Ly
232 the effect of the induced subpopulations of MDSC on the proliferative response of OVA-specific CD4(+
234 kin-1 receptor antagonist and suppression of MDSC-promoting cytokines secreted by prostate cancer cel
235 le for CCR5 in recruitment and activation of MDSCs, suggesting a novel strategy for melanoma treatmen
236 the accumulation and tolerogenic activity of MDSCs in tumors, and inhibited the expression of immunos
237 litis and survival (P < .001), conversion of MDSCs to PD ligand-expressing MDCs, and increased donor
238 out of Yap or antibody-mediated depletion of MDSCs promoted macrophage reprogramming, reactivation of
240 by which tumor cells evoke the expansion of MDSCs in acute myeloid leukemia (AML) has not been well
243 xpansion and the tumor-promoting function of MDSCs, we discovered CCAAT/enhancer binding protein alph
246 n and decreased the number and percentage of MDSCs and Tregs in the TME, but also induced a shift in
248 ients with AML exhibit increased presence of MDSCs in their peripheral blood, in comparison with norm
249 resulting in the selective proliferation of MDSCs in comparison with functionally competent antigen-
252 > B6 lethal GVHD model, adoptive transfer of MDSCs from TLI/ATS/CTX-conditioned recipients is associa
253 d anti-Jagged1/2-blocking antibody CTX014 on MDSC-mediated T-cell suppression in tumor-bearing mice.
254 ene signature, and high expression of YAP or MDSC-related genes predicts decreased survival in PDAC p
255 ocytic (M)-MDSCs and polymorphonuclear (PMN)-MDSCs can be detected using several of the markers used
260 hesus M-MDSCs lacked expression of CD33, PMN-MDSCs were identified as CD33(+) low-density neutrophils
261 ved GPs had an increased ability to form PMN-MDSCs; 3) tumor-derived GPs shared gene expression patte
262 ese findings support the hypothesis that PMN-MDSCs result from selective expansion of IRF8(lo) GPs, a
263 produce CXCL1, which recruits CXCR2-positive MDSCs to form a premetastatic niche to promote liver met
265 nction of this switch during sepsis promotes MDSC expansion that adversely impacts sepsis outcome.
267 w report that the recovery of both recipient MDSCs (P < .01) and MDCs (P < .01) is significantly incr
269 t for the use of anti-Jagged1/2 to reprogram MDSC-mediated T-cell suppression in tumors, with implica
275 cific PI3Kdelta/gamma inhibitors to suppress MDSC to enhance responses to immune checkpoint blockade.
276 EVs that induces proliferation in the target MDSC population via downstream effects on cell cycle pro
277 to primary tumor and suggests that targeting MDSC recruitment represents an attractive therapeutic ap
281 Mouse models of prostate cancer show that MDSCs (CD11b(+)Gr1(+)) promote tumour initiation and pro
282 ved suppressor cells (MDSCs) and showed that MDSCs expanded in melanoma patients express dendritic ce
285 promote breast tumor lung metastasis through MDSC miR-126a(+) exosomal-mediated induction of IL-13(+)
286 mpanied by upregulation of genes relevant to MDSCs such as arginase-1, IDO1, PDL1, and IL-10 at the i
289 4/green fluorescent protein (GFP)-transduced MDSCs formed significantly less bone in COX-2 knock-out
290 Furthermore, we showed that FTY720 triggers MDSCs to release GM-CSF via S1P receptor 3 (S1pr3) throu
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