ライフサイエンスコーパス: MDSC

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

14 led to the induction of IL-13R(+)miR-126a(+) MDSCs (DOX-MDSC).

15 ing the blocking of induction of miR-126a(+) MDSCs.

16 chanisms that lead to induction of activated MDSCs and IL-13(+) Th2 cells have not yet been identifie

17 In addition, MDSC frequency correlated significantly with circulating

18 model by tracking the systemic administered MDSC from CD45.1 congenic mice.

19 Tracking the administered MDSC showed that they promptly migrated to the islet gra

20 Although MDSC are partially characterized in HIV and SIV infectio

21 expression levels strongly correlate with an MDSC gene signature, and high expression of YAP or MDSC-

22 er, the levels of inflammatory cytokines and MDSC were more pronounced post-cART.

23 t flow measurements were taken using DMA and MDSC, which were accompanied by FTIR, WAXD and ESEM.

24 then promotes the production of DOX-MDSC and MDSC miR-126a(+) exosomes via MDSC IL-13R.

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

27 arc and plays an essential role in arresting MDSC proliferation.

28 and conditional deletion of NFkB-p65 blocked MDSC function.

29 Blood MDSC-like fibrocytes, however, are increased and associa

30 th persistent increased percentages of blood MDSCs had increased nosocomial infections, prolonged int

31 Furthermore, T cells preconditioned by MDSC have diminished responses to subsequent antigen exp

32 mulating factor (GM-CSF), mainly produced by MDSCs, was identified as a key factor to mediate these e

33 Tumor-infiltrating CCR5(+) MDSCs displayed higher immunosuppressive activity than t

34 a model, we found an accumulation of CCR5(+) MDSCs in melanoma lesions associated with both increased

35 In melanoma patients, CCR5(+) MDSCs were enriched at the tumor site and correlated wit

36 unosuppressive pattern compared with CCR5(-) MDSCs.

37 and the number of tumor-infiltrating CD33(+) MDSCs (P<0.01).

38 2 and MIF and an increased number of CD33(+) MDSCs were detected in BC tissues, and these increases w

39 e (TAM) and myeloid-derived suppressor cell (MDSC) infiltration in tumors via chemokine axis.

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

44 Myeloid-derived suppressor cells (MDSC) are a heterogeneous population of immature myeloid

45 Myeloid-derived suppressor cells (MDSC) are a major obstacle to promising forms of cancer

46 eration of myeloid-derived suppressor cells (MDSC) from precursors in mouse bone marrow.

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

49 uitment of myeloid-derived suppressor cells (MDSC) into the tumor microenvironment.

50 Myeloid derived suppressor cells (MDSC) produce nitric oxide (NO) and inhibit dendritic ce

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

53 Myeloid-derived suppressor cells (MDSC), which expand during states of elevated circulatin

54 allmark of myeloid-derived suppressor cells (MDSC).

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

57 at include myeloid-derived suppressor cells (MDSCs) and IL-13(+) Th2 cells.

58 ization to myeloid-derived suppressor cells (MDSCs) and M2-like macrophages.

59 ediated by myeloid-derived suppressor cells (MDSCs) and showed that MDSCs expanded in melanoma patien

60 Myeloid-derived suppressor cells (MDSCs) are greatly expanded in cancer patients and tumor

61 Myeloid-derived suppressor cells (MDSCs) are known to play important roles in tumour immun

62 Myeloid-derived suppressor cells (MDSCs) are major regulators of T cell responses in sever

63 Myeloid progenitor-derived suppressor cells (MDSCs) arise from myeloid progenitors and suppress both

64 ulation of myeloid-derived suppressor cells (MDSCs) both in vitro and in vivo.

65 Myeloid-derived suppressor cells (MDSCs) described in cancer and inflammatory processes ma

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

69 Myeloid-derived suppressor cells (MDSCs) play a critical role in promoting immune toleranc

70 anulocytic myeloid-derived suppressor cells (MDSCs) to the liver of HLA-DR4 transgenic mice.

71 CD11c(neg) myeloid-derived suppressor cells (MDSCs) were enriched in GVHD target organs.

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

74 ons termed myeloid-derived suppressor cells (MDSCs).

75 ecrease of myeloid-derived suppressor cells (MDSCs).

76 Although ROS are toxic to most cells, MDSC survive despite their elevated content and release

77 aintains a steady-state level of circulating MDSC in tumor-bearing individuals.

78 After SS/SS in humans, circulating MDSCs are persistently increased, functionally immunosup

79 The abundance of circulating MDSCs correlates with prostate-specific antigen levels a

80 The frequency of circulating MDSCs rapidly and transiently increased 24 h after vacci

81 (+)IFNgamma(+) cells in response to CMVpp65; MDSC depletion further augmented CD4(+)CX3CR1(+)IFNgamma

82 n factor nuclear factor I-A (NFI-A) controls MDSC expansion during sepsis and impacts survival.

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

85 feration more than pancreatic cancer derived MDSC.

86 cular mechanism by which cancer cells direct MDSC homing to primary tumor and suggests that targeting

87 DOX-MDSC promote breast tumor lung metastasis through MDSC m

88 induction of IL-13R(+)miR-126a(+) MDSCs (DOX-MDSC).

89 h2 cells then promotes the production of DOX-MDSC and MDSC miR-126a(+) exosomes via MDSC IL-13R.

90 The induction of DOX-MDSC is regulated in a paracrine manner.

91 After SS/SS, CD33CD11bHLA-DR MDSCs were dramatically increased out to 28 days (P < 0.

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

95 Eo-MDSC exhibit eosinophilic cytoplasmic granules and expre

96 Furthermore, Eo-MDSC accumulated at the site of infection and exerted a

97 Here, we identified a new subset of MDSC (Eo-MDSC) in S. aureus-infected mice that phenotypically res

98 Increases in the number of Eo-MDSC by adoptive transfer caused a significant exacerbat

99 sing in response to CMV infection can escape MDSC-mediated suppression, and defined TIGIT antagonists

100 Expanded MDSC during SIV infection, especially during the post-cA

101 In summary, we identified expanded MDSC subsets in DLBCL, as well as new mechanisms of immu

102 As expected, MDSC isolated from peripheral blood mononuclear cells (P

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

105 We propose a role for MDSCs in mitigating excessive tissue injury during TSS.

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

108 G-MDSCs, made of immature and mature granulocytes expressi

109 M-MDSCs and G-MDSCs strongly contribute to T-cell dysfunction in patie

110 c myeloid-derived suppressor cells (M- and G-MDSCs) defined by their ability to suppress T-cell respo

111 sCLU was only found in M-MDSCs but not in G-MDSCs.

112 High initial levels of G-MDSCs, arginase 1, and S100A12 but not M-MDSCs were asso

113 More specifically, G-MDSCs producing arginase 1 are associated with a higher

114 The generated MDSC were expressed C-C chemokine receptor type 2 (CCR2)

115 Furthermore, GR-MDSCs isolated from placenta polarized CD4(+) T cells to

116 , we demonstrate that granulocytic MDSCs (GR-MDSCs) accumulate in human placenta of healthy pregnanci

117 9 AML led to an expansion of CD11b(+) Gr1(+) MDSCs in bone marrow and spleen.

118 s, including monocytic MDSC and granulocytic MDSC, have been described to date.

119 g magnitude, the majority being granulocytic MDSC.

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

123 Blood DC-HIL(+) MDSC levels in untreated patients were significantly hig

124 Thus, DC-HIL(+) MDSCs are expanded in psoriasis patients, and their mech

125 HIV MDSC overexpressed B7-H4 and silencing B7-H4 increased t

126 ion of MDSC expanded in presence of HIV (HIV MDSC), but decreased with culture of HIV MDSC with autol

127 We examined how HIV MDSC control CD4(+) T cell IFNgamma response to a CMVpp6

128 HIV MDSC), but decreased with culture of HIV MDSC with autologous PBMCs.

129 cells were also decreased in presence of HIV MDSC.

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

134 decreased infiltration of immunosuppressive MDSC.

135 As observed in cancer immunotherapy, MDSCs could be a novel component in multimodality immuno

136 Genes involved in MDSC suppressive functions, including S100A12, S100A9, M

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

140 ne suppression via targeting beta-catenin in MDSCs.

141 In addition, deletion of C/EBPalpha in MDSCs enhanced the pro-angiogenic, immune suppressive an

142 expression in activating iNOS expression in MDSCs when they are generated under pathologic condition

143 giogenic and immune suppressive functions in MDSCs.

144 Jagged1/2 was induced in MDSCs by tumor-derived factors via NFkB-p65 signaling, a

145 inase and nuclear factor kappa B pathways in MDSCs was MyD88 dependent.

146 pha) expression was significantly reduced in MDSCs from tumor-bearing mice compared to non-tumor-bear

147 2, CCR2, is required to facilitate increased MDSC presence and tumor growth.

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

154 ion of p38, ERK or p65 decreased J82-induced MDSC trafficking and CXCR2 expression.

155 ody results in blockade of radiation-induced MDSC infiltration.

156 S expression and regulation in tumor-induced MDSCs are unknown.

157 Furthermore, tumor-induced MDSCs exhibited diminished STAT1 and NF-kappaB Rel prote

158 Instead, tumor-induced MDSCs showed increased SETD1B expression as compared wit

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

162 diminished iNOS expression in tumor-induced MDSCs.

163 Post-SIV infection, MDSC were elevated in acute infection and persisted duri

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

166 Low MDSC frequency was observed prior to SIV infection.

167 red CCL2 production and diminished both lung MDSC presence and tumor growth.

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

170 CD14(pos)HLA-DR(low/neg) monocytic (M)-MDSCs were expanded in intensive care unit patients with

171 L-13 and NKp30 partially restores ILC2 and M-MDSC levels and results in increased survival.

172 on is immunosuppressive due to (monocytic) M-MDSC infiltration, which results in tumor radioresistanc

173 Interestingly, only M-MDSC number was correlated with the International Progno

174 Selective M-MDSC chemoresistence to curcumin and DTX was mediated by

175 xis as a targetable pathway to curtail the M-MDSC compartment and improve bladder cancer treatment.

176 M-MDSCs and G-MDSCs strongly contribute to T-cell dysfunct

177 M-MDSCs infiltrated the vaccine injection site, but not va

178 he levels of PGD2, NKp30, ILC2s, IL-13 and M-MDSCs are restored.

179 Importantly, both M-MDSCs and PMN-MDSCs showed suppression of T cell prolife

180 onocytic myeloid-derived suppressor cells (M-MDSCs) via IL-13 secretion.

181 onocytic myeloid-derived suppressor cells (M-MDSCs), and group 2 innate lymphoid cells (ILC2).

182 )-MDSCs, sparing CD11b(+)Ly6G(-)Ly6C(high) M-MDSCs, with reduced tumor burden in 4T1-Neu tumor-bearin

183 Knockdown of sCLU in M-MDSCs and RAW264.7 macrophages was found to reverse thei

184 Importantly, sCLU was only found in M-MDSCs but not in G-MDSCs.

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.

187 However, whereas rhesus M-MDSCs lacked expression of CD33, PMN-MDSCs were identifi

188 Two major MDSC subsets, including monocytic MDSC and granulocytic

189 tified as the critical driver of EV-mediated MDSC expansion.

190 onstrated that STAT1 nitration also mediates MDSC inhibitory effects on immune cells.

191 es to confirm a role for CD13 in impaired MO-MDSC transmigration.

192 previous research demonstrating psoriatic Mo-MDSC are unable to suppress autologous and heterologous

193 f the surface protein DC-HIL on psoriatic Mo-MDSC.

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

198 plays an important role, are impaired in MO-MDSCs.

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.

204 is how the local and distant stroma modulate MDSCs during tumor progression.

205 We monitored MDSC frequency and function in SIV-infected rhesus macaq

206 Two major MDSC subsets, including monocytic MDSC and granulocytic MDSC, have been described to date.

207 Moreover, monocytic MDSC have the plasticity to differentiate into OC, thus

208 h CCR4(+) Treg and CCR2(+)Ly-6C(+) monocytic MDSCs in this disease setting.

209 iled to maximally accrue Tregs and monocytic MDSCs.

210 Frequency of DC-HIL(+) monocytic MDSCs (CD14(+)HLA-DR(no/low)) in blood and skin was mark

211 expression and reduced numbers of monocytic MDSCs.

212 ogether with targeted agents that neutralize MDSCs yet preserve T-cell function.

213 Notably, MDSC restoration relied upon MAPK pathway reactivation a

214 After cART interruption, we observed MDSC expansion of surprising magnitude, the majority bei

215 t BRAFi-resistant melanomas, the addition of MDSC depletion/blockade (anti-Gr-1 + CCR2 antagonist) pr

216 A single systemic administration of MDSC markedly prolonged survival of islet allografts wit

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

219 light on the heterogeneity and complexity of MDSC during chronic infection.

220 e to CMVpp65 were enhanced with depletion of MDSC expanded in presence of HIV (HIV MDSC), but decreas

221 Depletion of MDSC-like cells restored tumor growth in mice treated wi

222 was comparable to GM-CSF in its induction of MDSC.

223 Here we demonstrate functional inhibition of MDSC with IPI-145, an inhibitor of PI3Kdelta and PI3Kgam

224 Plasma levels of MDSC mediators S100A8/A9, S100A12, and arginase 1 were s

225 Migration of MDSC was examined in an islet allograft transplant model

226 To characterize the phenotype of MDSC subpopulations induced by infection, cells were sor

227 Lastly, the plasticity of MDSC to differentiate into osteoclasts was assessed by s

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

231 tle is known regarding the subpopulations of MDSC expanded by P. gingivalis infection.

232 the effect of the induced subpopulations of MDSC on the proliferative response of OVA-specific CD4(+

233 Here, we identified a new subset of MDSC (Eo-MDSC) in S. aureus-infected mice that phenotypi

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

239 ry neural arc, resulting in the expansion of MDSCs and colorectal cancer.

240 by which tumor cells evoke the expansion of MDSCs in acute myeloid leukemia (AML) has not been well

241 We hypothesized that the expansion of MDSCs in AML is accomplished by tumor-derived extracellu

242 icited a cell contact-dependent expansion of MDSCs.

243 xpansion and the tumor-promoting function of MDSCs, we discovered CCAAT/enhancer binding protein alph

244 ive activity, origin, and clinical impact of MDSCs in patients with sepsis.

245 Chemotherapeutic intervention of MDSCs has gained ground as a strategy for cancer therapy

246 n and decreased the number and percentage of MDSCs and Tregs in the TME, but also induced a shift in

247 migration and immunosuppressive potential of MDSCs in tumor lesions.

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-

250 In contrast to restoration of MDSCs, levels of T regulatory cells remained reduced in

251 ssion, but little is known about the role of MDSCs after sepsis.

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

256 models, although the mechanisms favoring PMN-MDSC responses remain poorly understood.

257 of myeloid differentiation to influence PMN-MDSC production has remained unknown.

258 burden in tumor models, particularly the PMN-MDSC subset.

259 Importantly, both M-MDSCs and PMN-MDSCs showed suppression of T cell proliferation in vitr

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

264 We hypothesized that NO producing MDSC in tumor-bearing hosts would inhibit DC antigen pre

265 nction of this switch during sepsis promotes MDSC expansion that adversely impacts sepsis outcome.

266 Psoriatic MDSCs were functionally diverse among patients in their

267 w report that the recovery of both recipient MDSCs (P < .01) and MDCs (P < .01) is significantly incr

268 ligand 26 in cancer cells profoundly reduces MDSC recruitment, angiogenesis, and tumor growth.

269 t for the use of anti-Jagged1/2 to reprogram MDSC-mediated T-cell suppression in tumors, with implica

270 Additionally, septic MDSCs had suppressed HLA gene expression and up-regulate

271 Moreover, since MDSC are suppressors of T cell immune activity, we deter

272 SLFN4+ MDSCs were not observed in infected GLI1-deficient mice.

273 Thus spatiotemporal MDSC infiltration may have clinical implications in tumo

274 lizing antibody could substantially suppress MDSC recruitment and tumor growth.

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

278 The prevailing view is that MDSC-mediated immunosuppression is restricted to tissues

279 We also showed that MDSC miR-126a rescues DOX-induced MDSC death in a S100A8

280 Cytogenetic studies demonstrated that MDSCs in patients with AML may be derived from leukemic

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

283 Our findings provide insight into the MDSC exosomal-mediated chemoresistance mechanism, which

284 3 receptors and miR-126a expressed on/in the MDSCs.

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

287 Thus, the T cell-to-MDSC balance, associated with a skewing toward type 2 im

288 Notably, patients with a T cell-to-MDSC ratio of less than 1 showed dramatically lower recu

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

291 Unlike MDSCs, myeloid cells with conditional deletion of the Nf

292 f DOX-MDSC and MDSC miR-126a(+) exosomes via MDSC IL-13R.

293 y monitored for quality control purpose when MDSC are generated in vitro for immune therapy.

294 T cell proliferation was restored when MDSC were treated with inhibitors of inducible nitric ox

295 nosuppression is restricted to tissues where MDSC co-mingle with T cells.

296 Whether MDSCs increase and influence T cell responses in tempora

297 or combining immune checkpoint blockade with MDSC-targeted therapies in the treatment of mCRPC.

298 immune checkpoint blockade was combined with MDSC-targeted therapy.

299 inally, TRAIL and CCL2 are co-regulated with MDSC/M2 markers in lung adenocarcinoma patients.

300 When co-cultured with MDSCs from SS/SS patients, antigen-driven T-cell prolife