ライフサイエンスコーパス: granulocytic

1 develop and why the MDSC response is heavily granulocytic.

2 notypes, 71% were eosinophilic and 25% mixed granulocytic.

3 mains facilitate phagocytosis of bacteria by granulocytic amoebocytes; the function of the CBD is not

4 Human granulocytic anaplasmosis (HGA) is a tick-borne disease

5 Human granulocytic anaplasmosis (HGA) is caused by the obligat

6 Lyme disease, human granulocytic anaplasmosis (HGA), and babesiosis are emer

7 hagocytophilum, the etiologic agent of human granulocytic anaplasmosis (HGA), has genes predicted to

8 gocytophilum is the etiologic agent of human granulocytic anaplasmosis (HGA), one of the major tick-b

9 hagocytophilum, the causative agent of human granulocytic anaplasmosis (HGA), shares the same enzooti

10 are presumptively diagnosed as having human granulocytic anaplasmosis (HGA).

11 naplasma phagocytophilum, the cause of human granulocytic anaplasmosis (HGA).

12 naplasma phagocytophilum, the cause of human granulocytic anaplasmosis (HGA).

13 te intracellular bacterium that causes human granulocytic anaplasmosis (HGA).

14 m that infects granulocytes and causes human granulocytic anaplasmosis (HGA).

15 The occurrence of canine granulocytic anaplasmosis in western Washington State su

16 Human granulocytic anaplasmosis is caused by the obligate intr

17 No granulocytic anaplasmosis vaccine exists.

18 Anaplasma phagocytophilum causes granulocytic anaplasmosis, a debilitating infection that

19 odes scapularis transmits the agent of human granulocytic anaplasmosis, among other pathogens.

20 proteins associated with the agent of human granulocytic anaplasmosis, an emerging disease, and the

21 tracellular bacterium and the agent of human granulocytic anaplasmosis, an emerging tick-borne diseas

22 pper Midwest and transmit the agent of human granulocytic anaplasmosis, Anaplasma phagocytophilum, am

23 of pathogens causing human babesiosis, human granulocytic anaplasmosis, and tick-borne encephalitis.

24 ors pathogens that cause Lyme disease, human granulocytic anaplasmosis, babesiosis and other diseases

25 ry intracellular bacterium that causes human granulocytic anaplasmosis, consists of alternate infecti

26 hagocytophilum, the etiologic agent of human granulocytic anaplasmosis, has a large paralog cluster (

27 ry intracellular bacterium that causes human granulocytic anaplasmosis, has significantly less coding

28 naplasma phagocytophilum, the agent of human granulocytic anaplasmosis, in Ixodes scapularis tick sal

29 ologic agent of the tick-borne disease human granulocytic anaplasmosis, is an obligate intracellular

30 hagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intracellular

31 ), the agent of the tick-borne disease human granulocytic anaplasmosis, is an obligate intracellular

32 hagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intracellular

33 hagocytophilum, the etiologic agent of human granulocytic anaplasmosis, is an obligatory intracellula

34 naplasma phagocytophilum, the agent of human granulocytic anaplasmosis, is an unusual obligate intrac

35 illness caused by A. phagocytophilum, human granulocytic anaplasmosis, occurs irrespective of pathog

36 ry intracellular bacterium that causes human granulocytic anaplasmosis, replicates in the membrane-bo

37 naplasma phagocytophilum, the agent of human granulocytic anaplasmosis, survives within PMNs in part

38 te intracellular bacterium that causes human granulocytic anaplasmosis.

39 hagocytophilum, the causative agent of human granulocytic anaplasmosis.

40 cause the emerging infectious disease human granulocytic anaplasmosis.

41 ts neutrophils to cause the emerging disease granulocytic anaplasmosis.

42 emerging and potentially fatal disease human granulocytic anaplasmosis.

43 ium that infects granulocytes to cause human granulocytic anaplasmosis.

44 gocytophilum is the etiologic agent of human granulocytic anaplasmosis.

45 ion, the causative agent of human and animal granulocytic anaplasmosis.

46 ry intracellular bacterium that causes human granulocytic anaplasmosis.

47 by Ixodes scapularis ticks and causing human granulocytic anaplasmosis.

48 naplasma phagocytophilum, the agent of human granulocytic anaplasmosis.

49 s were comprised of CD11b(+)Ly6-G(+)Ly6-C(+) granulocytic and CD11b(+)Ly6-G(-)Ly6-C(+) monocytic subt

50 in normal CD34(+) progenitors modifies their granulocytic and erythroid differentiation.

51 nsent for chemotherapy, and concordance with granulocytic and erythroid growth factor administration

52 sts of two major subsets of Ly6G(+)Ly6C(low) granulocytic and Ly6G(-)Ly6C(high) monocytic cells.

53 ession profiling of mouse tumor-infiltrating granulocytic and monocytic (MO-MDSC) subsets compared wi

54 Forced MN1 expression impaired both granulocytic and monocytic differentiation in vitro in p

55 ependent myelomonocytic precursor capable of granulocytic and monocytic differentiation.

56 s, increased numbers of colony-forming units granulocytic and monocytic in cultures of human or mouse

57 f IRF8 exhibit uncontrolled expansion of the granulocytic and monocytic lineages that progress into a

58 promote survival and differentiation of the granulocytic and monocytic lineages.

59 ranulocytic MDSCs, peptibodies depleted both granulocytic and monocytic MDSC subsets.

60 in myeloid cells, including macrophages and granulocytic and monocytic myeloid-derived suppressor ce

61 b(+) population of immature cells containing granulocytic and monocytic progenitors, which expand und

62 acrophage activation is attenuated in severe granulocytic asthma highlighting defective innate immuni

63 inophilic asthma, neutrophilic asthma, mixed granulocytic asthma, and paucigranulocytic asthma (PGA).

64 and a monocytic bias in comparison with the granulocytic bias in Npm1(cA/+);Nras(G12D/+) mutants.

65 The high levels of CD73 expression in granulocytic CD11b(+)Gr-1(high) cells correlated with hi

66 eptors promote preferential expansion of the granulocytic CD11b(+)Gr1(high) subset of MDSCs in vitro.

67 Instead, we found a significant expansion of granulocytic (CD11b(+)Ly6G(+)Ly6C(low)) and monocytic (C

68 tic, CD11b(+) Ly6C(hi) Ly6G(-) cells but not granulocytic, CD11b(+) Ly6C(int) Ly6G(+) cells purified

69 mmatory phenotypes according to their sputum granulocytic cell count.Measurements and Main Results: I

70 ed to adopt the erythroid cell fate into the granulocytic cell fate.

71 Of the expanded monocytic and granulocytic cell populations of MDSCs, the monocytic su

72 elated with elevated CD8+ T cell and reduced granulocytic cell proportions.

73 osed on the basis of neoplastic expansion of granulocytic cells and exclusion of genetic drivers that

74 rentiation of erythroid, megakaryocytic, and granulocytic cells as well as primary erythroid progenit

75 ression, and ameliorates the accumulation of granulocytic cells caused by AML1-ETO.

76 his was preceded by an overrepresentation of granulocytic cells in the bone marrow and a greatly incr

77 he retention of hematopoietic stem cells and granulocytic cells in the bone marrow.

78 ) Ly-6C(hi) monocytic and CD11b(+) Ly-6G(hi) granulocytic cells locally.

79 The selective sensitivity of G913X Elane granulocytic cells to ER stress provides new and strong

80 d numbers of T cells and the accumulation of granulocytic cells with an immune phenotype resembling g

81 known to descend from immature monocytic and granulocytic cells, respectively, which are produced in

82 A 2-fold increase in monocytic compared with granulocytic colonies was observed in IL-3/IL-6/SCF or G

83 called Mirn223) mutant mice have an expanded granulocytic compartment resulting from a cell-autonomou

84 lification of early neutrophil precursors in granulocytic compartments, and CD62L- and CD49d-dependen

85 rs mediate T cell suppression, whereas their granulocytic counterparts lack suppressive function.

86 expression of transcription factors driving granulocytic differentiation (Cebpe, Gfi1, and Klf5), an

87 and Notch1 together play a critical role in granulocytic differentiation and AML, and particularly i

88 which are potential effectors of its role in granulocytic differentiation and function.

89 Cebpe(-/-) mice have incomplete granulocytic differentiation and increased sensitivity t

90 t constitutive expression of SALL4 inhibited granulocytic differentiation and permitted expansion of

91 A1 is a new WT1 target gene involved in both granulocytic differentiation and resistance to cell deat

92 emia (APL) is characterized by a blockade of granulocytic differentiation at the promyelocyte stage.

93 Granulocytic differentiation from normal and leukaemic p

94 cific genes that are important regulators of granulocytic differentiation have been identified includ

95 achievable doses markedly enhanced terminal granulocytic differentiation in AML cell lines, primary

96 ants that mimic acetylation failed to induce granulocytic differentiation in C/EBPalpha-dependent ass

97 es in zebrafish primitive erythropoiesis and granulocytic differentiation in cultured human cells.

98 Gfi-1 was up-regulated during G-CSF-induced granulocytic differentiation in myeloid 32D cells.

99 Inhibition of Sbds results in a defect in granulocytic differentiation in vitro and impairs myeloi

100 - or MyD88-deficient HSPCs with PGE2 rescued granulocytic differentiation in vivo.

101 In nonleukaemic cells, granulocytic differentiation is accompanied by reversal

102 In acute promyelocytic leukemia, granulocytic differentiation is arrested at the promyelo

103 of Jak3 transcription during G-CSF- induced granulocytic differentiation is mediated by the combined

104 s induction during retinoic acid (RA)-driven granulocytic differentiation is through RA receptor and

105 -colony stimulating factor (G-CSF)- mediated granulocytic differentiation of 32Dcl3 cells.

106 ppressed colony formation but did not induce granulocytic differentiation of BCR/ABL-expressing cells

107 zomib reversed the defective G-CSF-triggered granulocytic differentiation of CD34(+) cells from CN pa

108 t genes in vitro and disrupts G-CSF-mediated granulocytic differentiation of fresh human BM-derived C

109 portin, inhibited PCNA relocalization during granulocytic differentiation of HL-60 and NB4 promyelocy

110 but blocked all-trans-retinoic acid induced granulocytic differentiation of HL60 cells.

111 We also showed that during granulocytic differentiation of KCL22 cells, the C/EBPde

112 pt expressed and up-regulated during induced granulocytic differentiation of NB4 promyelocytic leukem

113 Retinoic acid (RA) promotes granulocytic differentiation of normal hematopoietic cel

114 ctopic overexpression of Jak3 can accelerate granulocytic differentiation of normal mouse bone marrow

115 ecule that is upregulated during the induced granulocytic differentiation of promyelocytic leukemic c

116 ll lines, PRAME protein expression inhibited granulocytic differentiation only in cell lines that dif

117 y reveal RASSF1A as a pivotal element in the granulocytic differentiation program induced by ATRA in

118 In addition, AR can restore G-CSF-dependent granulocytic differentiation upon transduction into ARKO

119 ttenuation of RASSF1A inhibited ATRA-induced granulocytic differentiation via regulation of the cell-

120 inhibited granulocytic differentiation while granulocytic differentiation was normal with the control

121 Both patients' serum inhibited granulocytic differentiation while granulocytic differen

122 E mutation diminishes enzymatic activity and granulocytic differentiation without significantly affec

123 CEACAM1 expression correlated with granulocytic differentiation, and Ceacam1(-/-) mice deve

124 r-binding protein-alpha (C/EBP-alpha), block granulocytic differentiation, and to induce AML in vivo.

125 pha) in p210BCR/ABL-expressing cells induces granulocytic differentiation, inhibits proliferation, an

126 /ABL)-expressing hematopoietic cells induces granulocytic differentiation, inhibits proliferation, an

127 mRNAs, that are indispensible regulators of granulocytic differentiation, is altered by SBDS mutatio

128 in alpha (C/EBPalpha), a master regulator of granulocytic differentiation, is severely impaired in le

129 , where all-trans retinoic acid (RA) induces granulocytic differentiation, we developed two emergent

130 F/LEF signaling in human CD34+ cells reduced granulocytic differentiation, whereas its activation enh

131 n of A1 in 32D cl3 cells induces spontaneous granulocytic differentiation, with both morphologic and

132 nuclear-to-cytoplasmic relocalization during granulocytic differentiation.

133 phatidic acid-led activation of Fes kinase-->granulocytic differentiation.

134 (5b, 5c, and 6a-c) were highly efficient in granulocytic differentiation.

135 viral infection, favoring monocytic over the granulocytic differentiation.

136 in human CEBPA-silenced AML samples restored granulocytic differentiation.

137 in response (UPR), and ultimately a block in granulocytic differentiation.

138 and impairs all-trans retinoic acid-induced granulocytic differentiation.

139 essor that is critically required for normal granulocytic differentiation.

140 cific expression, and is up-regulated during granulocytic differentiation.

141 ion independent of interleukin-3, and blocks granulocytic differentiation.

142 ory loop involving miR-223 and C/EBPa during granulocytic differentiation.

143 RNA interference impaired C/EBPalpha-induced granulocytic differentiation.

144 s down-regulated with G-CSF-induced terminal granulocytic differentiation.

145 l inhibition of either FLT3 or MEK1 leads to granulocytic differentiation.

146 expression of Cebpe and required for normal granulocytic differentiation.

147 e colony-stimulating factor (G-CSF)-mediated granulocytic differentiation.

148 ranulopoiesis that act at distinct stages of granulocytic differentiation.

149 PE) is an essential transcription factor for granulocytic differentiation.

150 ts target genes and caused a severe block in granulocytic differentiation.

151 of Trem1 and regulates its expression during granulocytic differentiation.

152 e accumulation of immature cells and reduced granulocytic differentiation.

153 ves, while enforced expression of MYC blocks granulocytic differentiation.

154 The causative agent of human granulocytic ehrlichiosis was recently reclassified as A

155 uman anaplasmosis (previously known as human granulocytic ehrlichiosis).

156 counts of CD15+CD16+ neutrophils, decreased granulocytic expression of integrin CD11b, and Th2-relat

157 CD14(neg)CD15(pos) low-density granulocytes/granulocytic (G)-MDSCs were more specifically expanded i

158 selectively target CD11b(+)Ly6G(+)Ly6C(low) granulocytic (G)-MDSCs, sparing CD11b(+)Ly6G(-)Ly6C(high

159 demonstrate here that monocytic (mMDSC) and granulocytic (gMDSC) subsets of myeloid-derived suppress

160 ccurred at the expense of differentiation to granulocytic Gr1(+)Ly6B(+) cells.

161 hils appear to be independently modulated as granulocytic hyperplasia does not result in neutrophilia

162 c mice showed erythroid, megakaryocytic, and granulocytic hyperplasia in the bone marrow and spleen,

163 ocytosis, hepatosplenomegaly and bone marrow granulocytic hyperplasia without evidence of dysplasia,

164 CD11c1/CD1231 plasmacytoid DCs, and striking granulocytic hyperplasia.

165 ckout (KO) mice exhibit completely penetrant granulocytic hyperplasia.

166 These mice demonstrated accumulation of granulocytic IMCs in the skin upon topical application o

167 Th1 and Th2 responses and an unconventional granulocytic infiltrate and thrombosis of the arteries.

168 The widespread granulocytic infiltration and intra-alveolar edema obser

169 erized by overproduction of granulocytes and granulocytic infiltration of the spleen and liver, which

170 female mice, was also accompanied by greater granulocytic infiltration, antral hyperplasia, and dimin

171 as involving distinct T(H) polarization and granulocytic infiltration.

172 ed proinflammatory response with more severe granulocytic inflammation and higher gene expression for

173 rently classified based on quantification of granulocytic inflammation and provided additional insigh

174 the pathogen's environment, we inferred that granulocytic inflammation generates a nutrient-replete n

175 a type 2/type 17 cytokine profile and mixed granulocytic inflammation in the airways.

176 g pathologic corticosteroid-refractory mixed granulocytic inflammation, but on the other hand underpi

177 asthma with neutrophil-predominant or mixed granulocytic inflammation.

178 is plays a central role in the resolution of granulocytic inflammation.

179 , and 2 as highly atopic with relatively low granulocytic inflammation.

180 cs exhibit corticosteroid-unresponsive mixed granulocytic inflammation.

181 sociated with signatures of eosinophilic and granulocytic inflammatory signals, whereas optimal contr

182 duced microvascular thrombosis, and enhanced granulocytic influx in C-domain-immunized mice.

183 Eosinophils are granulocytic leukocytes implicated in numerous aspects o

184 l function in the host defense properties of granulocytic leukocytes, mucosal surfaces, skin and othe

185 mble monocytic-like (CD11b(+)Ly6C(high)) and granulocytic-like (CD11b(+)Gr1(high)) MDSCs.

186 find that SHP2 shRNA knockdown in the 32Dcl3 granulocytic line reduces ERK activation, diminishes CEB

187 ncogene that subverts differentiation in the granulocytic lineage by associating with C/EBPalpha and

188 ating factor (G-CSF)-induced mobilization of granulocytic lineage cells from the bone marrow to the p

189 is involved in G-CSF-induced mobilization of granulocytic lineage cells from the bone marrow to the p

190 nt but also probably promotes the release of granulocytic lineage cells from the bone marrow to the p

191 nitor cells leading to severe defects in the granulocytic lineage, without affecting any other Cebpa-

192 y, with skewed cell differentiation favoring granulocytic lineage.

193 Specifically, cells of the monocytic and granulocytic lineages increased nearly 60% and 80%, resp

194 ell differentiation skewing toward monocytic/granulocytic lineages.

195 them into the erythroid, megakaryocytic, and granulocytic lineages.

196 sive proliferation of cells of monocytic and granulocytic lineages.

197 ed early myeloid progenitor cells toward the granulocytic/macrophage lineage while reducing the numbe

198 xpression of the monocytic marker, Ly6C, and granulocytic marker, Ly6G.

199 SHP2 knockdown, exogenous C/EBPalpha rescues granulocytic markers, and exogenous RUNX1 rescues C/EBPa

200 trans retinoic acid (ATRA) treatment induces granulocytic maturation and complete remission of leukem

201 s also required, albeit at lower levels, for granulocytic maturation.

202 r tissue with a preferential accumulation of granulocytic MDSC (grMDSCs) over monocytic MDSC (moMDSCs

203 Granulocytic MDSC have increased level of reactive oxyge

204 At all stages of infection, granulocytic MDSC suppressed CD4+ and CD8+ T cell prolif

205 r MDSC subsets, including monocytic MDSC and granulocytic MDSC, have been described to date.

206 of surprising magnitude, the majority being granulocytic MDSC.

207 We further demonstrated that the granulocytic-MDSC (G-MDSC) subset was responsible for th

208 to macrophages and re-routed M-MDSC, but not granulocytic-MDSC (PMN-MDSC), into cells that elicited d

209 Granulocytic MDSCs (gMDSCs) expanded transiently in acut

210 In this study, we demonstrate that granulocytic MDSCs (GR-MDSCs) accumulate in human placen

211 In this article, we demonstrate that granulocytic MDSCs accumulate in CF patients chronically

212 Mechanistically, expanded granulocytic MDSCs cause gammadelta lymphocytes in TLR5-

213 ong with numbers of CD11b(+)Ly6G(hi)Ly6C(lo) granulocytic MDSCs in both the bone marrow and the TME.

214 denosine by CD73 expressed at high levels on granulocytic MDSCs may promote their expansion and facil

215 Granulocytic MDSCs showed a ~>=3-fold increase in maximu

216 ly suppressed antitumor immune responses but granulocytic MDSCs surprisingly enhanced the clearance o

217 s of mice with PGIA contains a population of granulocytic MDSCs that potently suppress DC maturation

218 We further demonstrated that the ability of granulocytic MDSCs to suppress CD3/CD28-induced T cell p

219 ling axis culminating in the mobilization of granulocytic MDSCs to the breast cancer lung metastatic

220 ol Gr-1-specific antibody primarily depleted granulocytic MDSCs, peptibodies depleted both granulocyt

221 e, recombinant G-CSF or adoptive transfer of granulocytic-MDSCs isolated from 4T1 tumor-bearing mice,

222 inflammatory microenvironment constituted by granulocytic-MDSCs.

223 n the cytoplasmic fraction of differentiated granulocytic, megakaryocytic, or erythroid cells obtaine

224 se of myelofibrosis, and is characterized by granulocytic/megakaryocytic proliferation and lack of re

225 at it was dispensable for the development of granulocytic, monocytic, and megakaryocytic cells.

226 c progenitor cells that produce lymphoid and granulocytic-monocytic (myeloid) lineages is unclear.

227 nd initiates megakaryocytic-erythroid versus granulocytic-monocytic lineage decision-making.

228 rentiation into megakaryocytic-erythroid and granulocytic-monocytic lineages.

229 rs, including common myeloid progenitors and granulocytic-monocytic precursors to the NK-cell lineage

230 Furthermore, we show that Cebpa-deficient granulocytic-monocytic progenitors were equally resistan

231 to influence the binary cell fate choices of granulocytic-monocytic progenitors(GMPs) during viral in

232 d Runx1 DNA-binding assays demonstrated that granulocytic/monocytic (G/M) commitment is marked by Run

233 ferentiation of myeloid lineages and reduced granulocytic/monocytic populations.

234 rant Ras/ERK signaling leads to expansion of granulocytic/monocytic precursors, which are highly resp

235 ed mouse bone marrow cells, and bipotential (granulocytic/monocytic) human acute myeloid leukemia cel

236 roducing long-term rEC-hMPP-derived myeloid (granulocytic/monocytic, erythroid, megakaryocytic) and l

237 equired for the development of monocytic and granulocytic myeloid cells from early progenitors, and N

238 ic cells with an immune phenotype resembling granulocytic myeloid-dependent suppressor cells (gMDSCs)

239 LDN/granulocytic myeloid-derived suppressor cell frequency i

240 elective, inhibitory effect of phenformin on granulocytic myeloid-derived suppressor cell-driven immu

241 ogression due to a compensatory emergence of granulocytic myeloid-derived suppressor cells (G-MDSCs)

242 In this article, we demonstrate that granulocytic myeloid-derived suppressor cells (G-MDSCs)

243 Granulocytic myeloid-derived suppressor cells (G-MDSCs)

244 tiated, T regulatory cells (Treg), Th17, and granulocytic myeloid-derived suppressor cells (gMDSC) we

245 These cell subsets include monocytic and granulocytic myeloid-derived suppressor cells (M- and G-

246 equired for the G-CSF-driven mobilization of granulocytic myeloid-derived suppressor cells (MDSC) to

247 factors produced by tumors, neutrophils, and granulocytic myeloid-derived suppressor cells (MDSCs) fr

248 ctively recruited CD11b(+)Gr-1(high)Ly-6C(+) granulocytic myeloid-derived suppressor cells (MDSCs) to

249 de that ultimately led to the recruitment of granulocytic myeloid-derived suppressor cells (PMN-MDSCs

250 en splenic and tumor polymorphonuclear cells/granulocytic myeloid-derived suppressor cells are due to

251 report that phenformin selectively inhibits granulocytic myeloid-derived suppressor cells in spleens

252 nd inhibits the expansion of neutrophils and granulocytic myeloid-derived suppressor cells in the tum

253 essive chemokine profiles and high levels of granulocytic myeloid-derived suppressor cells resulted i

254 ulation of immunosuppressive neutrophils (or granulocytic myeloid-derived suppressor cells), is resis

255 and IDO), number of M2-type macrophages and granulocytic myeloid-derived suppressor cells, and protu

256 ces production of reactive oxygen species in granulocytic myeloid-derived suppressor cells, whereas t

257 +) cells reveals a phenotype consistent with granulocytic myeloid-derived suppressor cells.

258 frequency of low-density neutrophils (LDNs)/granulocytic myeloid-derived suppressor cells.

259 Granulocytic (neutrophil, eosinophil, and basophil) mark

260 olic aconitase activity in erythroid but not granulocytic or megakaryocytic progenitors.

261 ed sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic dimi

262 proposed to serve a charge-balancing role in granulocytic phagocytes such as neutrophils and eosinoph

263 ients with eosinophilic as compared to mixed granulocytic phenotype (61.58 vs 37.31 pg/ml, P < 0.05).

264 s APL, normal progenitor, and differentiated granulocytic phenotypes as different robust states from

265 DSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to

266 subdivided into monocytic (mononuclear) and granulocytic (polymorphonuclear) cells using the Ly6C an

267 Finally, a similar IL-4- and IL-13-producing granulocytic population was identified in peripheral blo

268 okine production in a previously undescribed granulocytic population, termed type 2 myeloid (T2M) cel

269 lic leukocytosis and the release of immature granulocytic populations that accumulate in circulation

270 Granulocytic precursors from G193X Elane mice, though wi

271 protein expression were detected in primary granulocytic precursors from SCN patients.

272 el, expression of mutant NE in primary human granulocytic precursors increased expression of CHOP (DD

273 regulates the G-CSF-induced proliferation of granulocytic precursors, Lyn regulates the production of

274 protein expression in both murine and human granulocytic precursors.

275 rotein response, and ultimately apoptosis of granulocytic precursors.

276 response (UPR), and ultimately apoptosis of granulocytic precursors.

277 catenin signaling pathway in fine tuning the granulocytic production, opening venues for clinical int

278 mpt to characterize VOCs according to sputum granulocytic profile in a large population of patients w

279 a(lo)CD45(+) phenotype that were enriched in granulocytic progenitors (G-CFCs).

280 Similar inhibition of differentiation of granulocytic progenitors from a control marrow was obser

281 012 and January 2013, cultures of autologous granulocytic progenitors from bone marrow aspirate were

282 riggered granulopoiesis, is downregulated in granulocytic progenitors of severe congenital neutropeni

283 to a significant reduction in the number of granulocytic progenitors, CFU-granulocyte, obtained with

284 and more sensitive to 5-fluorouracil-induced granulocytic regeneration.

285 id not develop a proinflammatory cytokine or granulocytic response to hMPV infection.

286 he NOMV entered the lung and caused an acute granulocytic response.

287 6, and SCF to induce myelopoiesis, levels of granulocytic RNAs are reduced and monocyte-specific RNAs

288 MS (also known as granulocytic sarcoma or chloroma) is a rare EM tumor of

289 AML of relatively short latency and frequent granulocytic sarcoma was noted.

290 This granulocytic signature was accompanied by monocyte and l

291 hematopoiesis in bone marrow resulting in a granulocytic skew toward that of neutrophils and eosinop

292 e insights facilitated the genetic rescue of granulocytic specification but not post-commitment defec

293 els demonstrated a preferential expansion of granulocytic subset of MDSC.

294 The loss of the granulocytic subset via conditional MCL-1 deletion did n

295 onocytic suppressor-cell subset, but not the granulocytic subset, requires continuous c-FLIP expressi

296 omated clustering to unbiasedly identify all granulocytic subsets in the tumor microenvironment: baso

297 These studies point towards the granulocytic subtype as a potential cellular target of i

298 were enriched for the neutrophilic and mixed granulocytic subtypes.

299 ity of C/EBPalpha to drive the expression of granulocytic target genes in vitro and disrupts G-CSF-me

300 Thus, IRF8 does not regulate granulocytic vs monocytic fate in GMPs, but instead acts