ライフサイエンスコーパス: granulocytic

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

2 develop and why the MDSC response is heavily granulocytic.

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

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

5 among A. phagocytophilum strains from human granulocytic anaplasmosis (HGA) patients, ticks, and a h

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

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

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

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

14 are presumptively diagnosed as having 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 odes scapularis transmits the agent of human granulocytic anaplasmosis, among other pathogens.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 cause the emerging infectious disease human granulocytic anaplasmosis.

37 ts neutrophils to cause the emerging disease granulocytic anaplasmosis.

38 emerging and potentially fatal disease human granulocytic anaplasmosis.

39 ium that infects granulocytes to cause human granulocytic anaplasmosis.

40 gocytophilum is the etiologic agent of human granulocytic anaplasmosis.

41 naplasma phagocytophilum, the agent of human granulocytic anaplasmosis.

42 ry intracellular bacterium that causes human granulocytic anaplasmosis.

43 nt for some clinical manifestations in human granulocytic anaplasmosis.

44 te intracellular bacterium that causes human granulocytic anaplasmosis.

45 hagocytophilum, the causative agent of human granulocytic anaplasmosis.

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

47 e marrow cells revealed increased numbers of granulocytic and early erythroid progenitors in the Fli-

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

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

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

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

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

53 ependent myelomonocytic precursor capable of granulocytic and monocytic differentiation.

54 , we demonstrate that elevated eIF4E impedes granulocytic and monocytic differentiation.

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

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

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

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

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

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

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

62 levels are found to be lower in c-Kit-Gr-1+ granulocytic bone marrow (BM) cells than in c-Kit+ immat

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

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

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

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

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

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

69 taining the ultrastructural features of this granulocytic cell type.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 elC mutation in CEBPA, the gene encoding the granulocytic differentiation factor C/EBPalpha.

90 Granulocytic differentiation from normal and leukaemic p

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

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

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

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

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

96 EBPepsilon interacts with Rb and E2F1 during granulocytic differentiation in NB4 and U937 human myelo

97 (TNF alpha) and RA synergistically enhanced granulocytic differentiation in NB4 cells but not in NB4

98 he Fes(act)-expressing cells was followed by granulocytic differentiation in the absence of granulocy

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 RA signaling in granulocytic differentiation involves regulated expressi

102 In nonleukaemic cells, granulocytic differentiation is accompanied by reversal

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

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

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

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

107 e that APL pathogenesis and retinoid-induced granulocytic differentiation of APL cells involve genes

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

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

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

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

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

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

114 Granulocytic differentiation of myeloid NB4 cells was no

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

116 We show that not only does C/EBPbeta induce granulocytic differentiation of non-APL myeloid cell lin

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

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

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

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

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

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

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

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

125 Both patients' serum inhibited granulocytic differentiation while granulocytic differen

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

127 egulation of hematopoietic stem cell homing, granulocytic differentiation, and cell cycle, whereas do

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

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

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

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

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

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

134 stigate the mechanisms of C/EBPalpha-induced granulocytic differentiation, we generated C/EBPalpha mu

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

136 nuclear-to-cytoplasmic relocalization during granulocytic differentiation.

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

138 (5b, 5c, and 6a-c) were highly efficient in granulocytic differentiation.

139 viral infection, favoring monocytic over the granulocytic differentiation.

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

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

142 of Trem1 and regulates its expression during granulocytic differentiation.

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

144 essor that is critically required for normal granulocytic differentiation.

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

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

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

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

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

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

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

152 ranulopoiesis that act at distinct stages of granulocytic differentiation.

153 iption factor that is essential for terminal granulocytic differentiation.

154 suggesting that this kinase induced terminal granulocytic differentiation.

155 e demonstrate the importance of C/EBPbeta in granulocytic differentiation.

156 e important in C/EBPepsilon-induced terminal granulocytic differentiation.

157 ngly suggest their role in the regulation of granulocytic differentiation.

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

159 derstanding roles that Msp2 proteins play in granulocytic ehrlichia infection and evolution of the po

160 The agent of human granulocytic ehrlichiosis (Anaplasma phagocytophilum) is

161 o genotypes of A. phagocytophilum, the human granulocytic ehrlichiosis (HGE) agent and a variant (AP-

162 d Ehrlichia chaffeensis but not in the human granulocytic ehrlichiosis agent.

163 anism Anaplasma phagocytophilum causes human granulocytic ehrlichiosis and specifically infects and m

164 Human granulocytic ehrlichiosis is an emerging infectious dise

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

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

167 nd causes human anaplasmosis (formerly human granulocytic ehrlichiosis).

168 ens that cause bovine anaplasmosis and human granulocytic ehrlichiosis, respectively.

169 hagocytophilum, the causative agent of human granulocytic ehrlichiosis, results in downregulation of

170 gen, Anaplasma phagocytophilum, the agent of granulocytic ehrlichiosis.

171 sma phagocytophilum causes the disease human granulocytic ehrlichiosis.

172 ously unknown physiologic roles for Fli-1 in granulocytic, erythroid, and NK cell proliferation and d

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

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

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

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

177 We report a class of granulocytic hemocytes that may be directly involved in

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

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

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

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

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

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

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

185 The widespread granulocytic infiltration and intra-alveolar edema obser

186 SR-A null mice display an increased initial granulocytic infiltration because of overproduction of t

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

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

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

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

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

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

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

194 asthma with neutrophil-predominant or mixed granulocytic inflammation.

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

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

197 Eosinophils are granulocytic leukocytes implicated in numerous aspects o

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

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

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

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

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

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

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

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

206 beit mostly in the more mature stages of the granulocytic lineage.

207 g factor receptor, expressed on cells of the granulocytic lineage.

208 y, with skewed cell differentiation favoring granulocytic lineage.

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

210 ell differentiation skewing toward monocytic/granulocytic lineages.

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

212 sive proliferation of cells of monocytic and granulocytic lineages.

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

214 C/EBPalphap30-ER/GR cells expressed several granulocytic markers in G-CSF and demonstrated nuclear m

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

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

217 ave been shown to lead to the induction of a granulocytic maturation program accompanied by the expre

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

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

220 Granulocytic MDSC have increased level of reactive oxyge

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

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

223 of surprising magnitude, the majority being granulocytic MDSC.

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

225 Granulocytic MDSCs (gMDSCs) expanded transiently in acut

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 d cells, resulting in a massive expansion of granulocytic neutrophils and macrophages at the expense

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

267 ced differentiation of HL-60 cells along the granulocytic pathway within 48 h.

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

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

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

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

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

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

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

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

276 Granulocytic precursors from G193X Elane mice, though wi

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

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

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

280 rotein response, and ultimately apoptosis of granulocytic precursors.

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

282 protein expression in both murine and human granulocytic precursors.

283 This suppression was due to an increase in granulocytic progenitors and a diminution of monocytic p

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

285 012 and January 2013, cultures of autologous granulocytic progenitors from bone marrow aspirate were

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

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

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

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

290 ansiently specialize the BM to support acute granulocytic responses and consequently promote extramed

291 6, and SCF to induce myelopoiesis, levels of granulocytic RNAs are reduced and monocyte-specific RNAs

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

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

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

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

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

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

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