ライフサイエンスコーパス: granulocyte

1 es, dendritic cells, tissue macrophages, and granulocytes.

2 and a significant expansion of monocytes and granulocytes.

3 ation of bone marrow-derived macrophages and granulocytes.

4 monocytes, macrophages, dendritic cells, and granulocytes.

5 meningeal macrophages, dendritic cells, and granulocytes.

6 , which, in turn, locally differentiate into granulocytes.

7 of infiltrating macrophages and neutrophilic granulocytes.

8 es than in CD34+ progenitors, monocytes, and granulocytes.

9 osure, outdoor release increased circulating granulocytes.

10 ypically compared with healthy adult control granulocytes.

11 ce were sufficient in increasing circulating granulocytes.

12 by hyperproduction of IL-1beta by neutrophil granulocytes.

13 hibit defects in terminal differentiation of granulocytes, a phenotype reminiscent of SGD.

14 nal negative phenotypic correlations between granulocyte abundance and white matter integrity.

15 In basophils of allergic subjects, tricolor granulocyte activation test using grass pollen demonstra

16 essment of viability/apoptosis, and tricolor granulocyte activation test were used.

17 a monoclonal antibody to eliminate residual granulocyte activity.

18 cilitate development of protocols for robust granulocyte and lymphoid cell production from hPSCs, for

19 nal in vitro identification as an inducer of granulocyte and macrophage development from progenitor c

20 Correlations between granulocyte and monocyte clonalities were greatest, foll

21 Granulocytes and B cells were also diminished in the bon

22 Manipulation of the cross-talk between granulocytes and endothelial cells may lead to new thera

23 The role of monocytes/macrophages, granulocytes and IL-1 signaling was investigated using d

24 Myeloperoxidase is expressed exclusively in granulocytes and immature myeloid cells and transforms t

25 in monocytes and macrophages and absent from granulocytes and lymphocytes.

26 ion of inflammatory cells, mainly neutrophil granulocytes and macrophages, into the organ.

27 or all) reduced the upregulation of CD11b on granulocytes and monocytes by 59 and 40%, respectively (

28 We found that granulocytes and monocytes rapidly replaced macrophages

29 g of Ly-6C/Ly-6G-specific VHH immunotoxin to granulocytes and monocytes, granulocytes were significan

30 Granulocytes and pro-inflammatory Ly6C(high) monocytes i

31 Clinical parameters, activation of blood granulocytes and sputum characteristics were assessed in

32 tions of C/EBPepsilon fail to develop normal granulocytes and suffer from repeated infections.

33 Finally, we identify subsets of granulocytes and T lymphocytes present in all wounds pav

34 lineages, including monocytes, macrophages, granulocytes, and dendritic and B and T cells.

35 The role of monocytes/macrophages, granulocytes, and interleukin 1 signaling was investigat

36 s increase in circulating white blood cells, granulocytes, and interleukin 17A (IL-17A).

37 ure of macrophage subtypes, dendritic cells, granulocytes, and lymphocytes.

38 ed immune effector cells, such as monocytes, granulocytes, and lymphocytes.

39 s, blood Ly6Chigh inflammatory monocytes and granulocytes, and sustained blood antimicrobial response

40 ptor in monocytes, the Fcepsilon receptor in granulocytes, and the RANK receptor in osteoclasts.

41 -regulatory cells; expansion of HLA-DR+CD56+ granulocytes; and reductions in type 3 innate lymphoid c

42 Phenotypic markers of circulating granulocytes are strong discriminators between infected

43 Gene expression analyses indicated that granulocytes are the main source of the cytokine TNFalph

44 erythrocytes, megakaryocytes, basophils, and granulocytes, but not macrophages.

45 novel, lipopolysaccharide (LPS)-responsive, granulocyte cell subset.

46 hment of PD-1(+)CD4(+) T cells only within a granulocyte CN positively correlated with survival in a

47 l transplantation, with a five-day course of granulocyte colony stimulating factor (G-CSF) as the mos

48 Eighteen molecules (interleukine (IL)-1beta, granulocyte colony stimulating factor (G.CSF), IL-13, IL

49 PEGylated recombinant human granulocyte colony stimulating factor (pegfilgrastim) is

50 eraction chromatography of recombinant human granulocyte colony stimulating factor is demonstrated.

51 demonstrate that activating mutations in the granulocyte colony stimulating factor receptor (CSF3R),

52 of up to two 28-day cycles); or intravenous granulocyte colony-stimulating factor (300 mug/m(2) per

53 3 ligand, interleukin-3, interleukin-6, and granulocyte colony-stimulating factor (5 GFs) either alo

54 with CSF3R truncation mutations; therapeutic granulocyte colony-stimulating factor (G-CSF) administra

55 to the treatment when forced into cycle via granulocyte colony-stimulating factor (G-CSF) administra

56 the stabilization of the therapeutic protein granulocyte colony-stimulating factor (G-CSF) against st

57 ersely, the myeloproliferation was driven by granulocyte colony-stimulating factor (G-CSF) and admini

58 Rgamma) produced severely reduced amounts of granulocyte colony-stimulating factor (G-CSF) and of nit

59 We assessed the efficacy and safety of granulocyte colony-stimulating factor (G-CSF) in steroid

60 Granulocyte colony-stimulating factor (G-CSF) is used cl

61 ocyte chemoattractive protein 1 (MCP-1), and granulocyte colony-stimulating factor (G-CSF) levels in

62 opoietic counterpart, 2 designs bound to the granulocyte colony-stimulating factor (G-CSF) receptor a

63 ed downregulation of the Csf3r gene, reduced granulocyte colony-stimulating factor (G-CSF) receptor l

64 elopoiesis prevented HSPC mobilization after granulocyte colony-stimulating factor (G-CSF) stimulatio

65 BM) to the blood circulation by the cytokine granulocyte colony-stimulating factor (G-CSF) through co

66 LCs expressed significantly higher levels of granulocyte colony-stimulating factor (G-CSF), interleuk

67 ts with WHIM syndrome are often treated with granulocyte colony-stimulating factor (G-CSF), which can

68 Nociceptor neurons drive granulocyte colony-stimulating factor (G-CSF)-induced HS

69 magnitude to a standard multi-day regimen of granulocyte colony-stimulating factor (G-CSF).

70 stered with Flt3 ligand (FL) (days 1-10) and granulocyte colony-stimulating factor (GCSF) (days 4-10)

71 GSD-Ib patients with incomplete response to granulocyte colony-stimulating factor (GCSF) treatment d

72 89) were randomized to 1) ATG and pegylated granulocyte colony-stimulating factor (GCSF), 2) ATG alo

73 nterleukin (IL)-4, IL-6, IL-8, IL-10, IL-15, granulocyte colony-stimulating factor (GCSF), MCP-1, tum

74 l severity (e.g. decreased responsiveness to granulocyte colony-stimulating factor and increased leuk

75 and many were prevented by interleukin-1 or granulocyte colony-stimulating factor blockade, revealin

76 models: (i) three different ligands based on granulocyte colony-stimulating factor GCSF homo-dimeric

77 Treatment with a high dose of granulocyte colony-stimulating factor increases neutroph

78 companied by mutations in CSF3R encoding the granulocyte colony-stimulating factor receptor (G-CSFR)

79 s and monocytes is primarily governed by the granulocyte colony-stimulating factor receptor family (C

80 cytokine receptors (erythropoietin receptor, granulocyte colony-stimulating factor receptor, and MPL)

81 dvent of hematopoietic cytokines (especially granulocyte colony-stimulating factor) in shortening the

82 sly every 3 weeks, plus prednisone daily and granulocyte colony-stimulating factor) or the other andr

83 y every 3 weeks, 10 mg daily prednisone, and granulocyte colony-stimulating factor) versus abirateron

84 d increased BAL fluid IL-1alpha, IL-6, IL-8, granulocyte colony-stimulating factor, and GM-CSF levels

85 luid myeloperoxidase, IL-8, IL-1alpha, IL-6, granulocyte colony-stimulating factor, and GM-CSF levels

86 ") CLAG-M (cladribine, high-dose cytarabine, granulocyte colony-stimulating factor, and mitoxantrone)

87 , soluble vascular cell adhesion molecule-1, granulocyte colony-stimulating factor, and soluble Fas.

88 ta show that hematopoietic stress, including granulocyte colony-stimulating factor, do not increase t

89 d plasma levels of cytokines (interleukin 6, granulocyte colony-stimulating factor, interleukin 1 rec

90 are (either fludarabine plus cytarabine plus granulocyte colony-stimulating factor, mitoxantrone plus

91 In NK cell-deficient mice, granulocyte colony-stimulating factor-expanded neutrophi

92 increasing use of mismatched, unrelated, and granulocyte colony-stimulating factor-mobilized peripher

93 We also show that granulocyte colony-stimulating factors (GCSF and GM-CSF)

94 usion, tumor necrosis factor inhibitors, and granulocyte colony-stimulating factors.

95 ies have found that the neuroactive cytokine granulocyte-colony stimulating factor (G-CSF) alters coc

96 he neuroprotective effects of the cytokines, granulocyte-colony stimulating factor (G-CSF) and stem c

97 Previous work from our group has identified granulocyte-colony stimulating factor (G-CSF) as a neuro

98 Using a granulocyte-colony stimulating factor (G-CSF) receptor k

99 Following VSG, circulating granulocyte-colony stimulating factor (G-CSF) was increa

100 her key inflammatory factors including IL-8, granulocyte-colony stimulating factor (G-CSF), IL-33, IL

101 transfer of transplant (tx), tumor (tm), and granulocyte-colony stimulating factor (g-csf)-expanded M

102 marrow adipose tissue, in part via increased granulocyte-colony stimulating factor (G-CSF).

103 aly in adulthood due to the up-regulation of granulocyte-colony stimulating factor (G-CSF); these eff

104 tarabine 2,000 mg/m(2)/dose on days 1-5; and granulocyte-colony stimulating factor 5 ug/kg/dose, days

105 otein-1, monocyte chemotactic protein-3, and granulocyte-colony stimulating factor during the acute p

106 he hematopoietic BM, restored the effects of granulocyte-colony stimulation factor (G-CSF), and parti

107 onse to Schistocephalus infection, and their granulocytes constitutively generate threefold more reac

108 Overlaying granulocyte counts onto the 10 clusters as metadata furt

109 endritic cell differentiation while limiting granulocyte development.

110 host defense, yet gaps in understanding how granulocytes differentiate from hematopoietic stem cells

111 lon is a critical transcriptional factor for granulocyte differentiation and function.

112 emergence of CSF3 lead to reorganisation of granulocyte distribution between amphibian and early rep

113 s known about the activation status of these granulocytes during helminth infection.

114 oneal saline stored a large number of mature granulocytes expressing a high level of Gr1 (Gr1(hi) cel

115 ity of hemocytes, with different subtypes of granulocytes expressing distinct and evolutionarily cons

116 G-MDSCs, made of immature and mature granulocytes expressing high levels of degranulation mar

117 Granulocytes from patients deficient in G6PC3 or G6PT ac

118 Interestingly, Trem1, a gene critical to granulocyte function, was identified as a direct C/EBPep

119 ut sepsis and CD14(neg)CD15(pos) low-density granulocytes/granulocytic (G)-MDSCs were more specifical

120 y human hematopoietic stem cells into mature granulocytes, highlighting the utility of our approach t

121 In addition, immature granulocyte (IG) count, plasma cell-free DNA (cfDNA), an

122 le model using the activation state of blood granulocytes, (ii) compare its diagnostic value with spu

123 e of CTSC reduced infiltration of neutrophil granulocytes impaired their capacity for cleaving E-cadh

124 wounds, identifying significant increases in granulocytes in chronic wounds, and we show that patient

125 Our data suggest an inhibition of granulocytes in forming these species in CO92 Deltapgm-i

126 in depletion efficiency of monocytes versus granulocytes in mice.

127 long with an increase in the ratio of Gr1(+) granulocytes in peripheral white blood cells following b

128 postvaccination and found significantly more granulocytes in PIV-vaccinated mice than in PIIV-vaccina

129 differentiation of myeloid progenitors into granulocytes in steady-state and emergency granulopoiesi

130 stitute the largest population of phagocytic granulocytes in the blood of mammals.

131 row granulocyte reserve with an elevation of granulocytes in the circulation.

132 te responses that lead to an accumulation of granulocytes in the lungs.

133 Persistently elevated eosinophil granulocytes in the peripheral blood in children is chal

134 yte precursors (GMPs) and could develop into granulocytes in the presence of granulocyte-macrophage c

135 n addition to stimulation of the receptor on granulocytes in the regulation of HSPC localization and

136 , and a shift to inflammatory monocytes from granulocytes in their inflamed lungs.

137 r experiments, wild type, but not Tnfa(-/-), granulocytes induced vascular recovery, and wild-type gr

138 1R inhibitor with a CXCR2 antagonist blocked granulocyte infiltration of tumors and showed strong ant

139 Th17 responses and increased recruitment of granulocytes into the neuroretina.

140 n but by reducing infiltration of neutrophil granulocytes into the pancreas.

141 molog 1 (Trib1) is an important regulator of granulocytes; knockout mice lack eosinophils and have in

142 CD66b(+) CB low-density granulocytes (LDG) and CB normal-density granulocytes we

143 a subset of neutrophils known as low-density granulocytes (LDGs) have been implicated in the pathogen

144 characterized by the presence of low-density granulocytes (LDGs) with a heightened capacity for spont

145 genic neutrophil subset known as low-density granulocytes (LDGs).

146 reduced NADPH oxidase function was found in granulocytes, leading to impaired NET formation.

147 ific CD4(+) T cells, increases the number of granulocyte-like myeloid-derived suppressor cells (and t

148 CSF-3, originally defined as a regulator of granulocyte lineage development via its cell surface rec

149 o instruct the lineage choice of uncommitted granulocyte M (GM) progenitors toward an M fate.

150 g factor (M-CSF; inflammation resolving) and granulocyte-M-CSF (GM-CSF; proinflammatory) may contribu

151 signature genes such as RORgammat, CCR6, and granulocyte macrophage colony-stimulating factor (GM-CSF

152 genitors after coculture with breast cancer: granulocyte macrophage colony-stimulating factor (GM-CSF

153 rent elevation of serum IFNgamma IL-10, GzB, granulocyte macrophage colony-stimulating factor, macrop

154 ared with all other treatments except CTLA-4/granulocyte macrophage colony-stimulating factor.

155 n clonal expansion of phenotypically defined granulocyte macrophage progenitors (GMPs) and acquisitio

156 ed in fusogenic cytokine (interleukin-4 plus granulocyte macrophage-colony stimulating factor)-induce

157 sue, inflammation increased the secretion of granulocyte macrophage-colony stimulating factor, IL-12,

158 s increased intracellular calcium levels and granulocyte macrophage-colony-stimulating factor, tumor

159 the BM and spleen that are hypersensitive to granulocyte macrophage-CSF due to hyperactive RAS/ERK si

160 nd the release of high immunogenic levels of granulocyte-macrophage colony stimulating factor (GM-CSF

161 s study, we have analyzed the involvement of granulocyte-macrophage colony stimulating factor (GM-CSF

162 Recently, granulocyte-macrophage colony stimulating factor (GM-CSF

163 (interleukin-3 receptor [IL-3R], IL-5R, and granulocyte-macrophage colony stimulating factor recepto

164 to PROSTVAC (Arm V; n = 432), PROSTVAC plus granulocyte-macrophage colony-stimulating factor (Arm VG

165 Granulocyte-macrophage colony-stimulating factor (GM-CSF

166 Granulocyte-macrophage colony-stimulating factor (GM-CSF

167 ected, macroporous alginate gels loaded with granulocyte-macrophage colony-stimulating factor (GM-CSF

168 ctional DCs in the presence of the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF

169 n the inflammatory response, as decreases in granulocyte-macrophage colony-stimulating factor (GM-CSF

170 rug targets, including neurotrophins and the granulocyte-macrophage colony-stimulating factor (GM-CSF

171 ry PAP is characterized by the disruption of granulocyte-macrophage colony-stimulating factor (GM-CSF

172 P co-administered intradermally with 200 mug granulocyte-macrophage colony-stimulating factor (GM-CSF

173 Therefore, we investigated neutralizing granulocyte-macrophage colony-stimulating factor (GM-CSF

174 The cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF

175 he presence of FGL2 in tumor cells inhibited granulocyte-macrophage colony-stimulating factor (GM-CSF

176 ve been extensively studied, others, such as granulocyte-macrophage colony-stimulating factor (GM-CSF

177 uction of proinflammatory mediators, such as granulocyte-macrophage colony-stimulating factor (GM-CSF

178 Granulocyte-macrophage colony-stimulating factor (GM-CSF

179 IFN-beta, and interleukin-4 (IL-4), but not granulocyte-macrophage colony-stimulating factor (GM-CSF

180 Granulocyte-macrophage colony-stimulating factor (GM-CSF

181 microbiota enhances respiratory defenses via granulocyte-macrophage colony-stimulating factor (GM-CSF

182 develop into granulocytes in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF

183 We hypothesized that targeting granulocyte-macrophage colony-stimulating factor (GM-CSF

184 nes/cytokines such as CCL-3 (MIP-1alpha) and granulocyte-macrophage colony-stimulating factor (GM-CSF

185 Granulocyte-macrophage colony-stimulating factor (GM-CSF

186 releasing interleukin (IL)-1beta that drives granulocyte-macrophage colony-stimulating factor (GM-CSF

187 1 induces the alveolar epithelium to produce granulocyte-macrophage colony-stimulating factor (GM-CSF

188 omaterial vaccine that delivers the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF

189 tory cytokines IL-17A, IFN-gamma, IL-22, and granulocyte-macrophage colony-stimulating factor (GM-CSF

190 metry following treatment with IL-3, IL-5 or granulocyte-macrophage colony-stimulating factor (GM-CSF

191 r et al find that donor T cells that secrete granulocyte-macrophage colony-stimulating factor (GM-CSF

192 c-MYC) and exposure to interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF

193 ing a cytokine-profiling assay, we show that granulocyte-macrophage colony-stimulating factor (GMCSF)

194 of irinotecan, temozolomide, dintuximab, and granulocyte-macrophage colony-stimulating factor (I/T/DI

195 hemokine (C-C motif) ligand 5 (P < 0.01) and granulocyte-macrophage colony-stimulating factor (P < 0.

196 Using recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-C

197 on of proinflammatory (interleukin-6 [IL-6], granulocyte-macrophage colony-stimulating factor [GM-CSF

198 1 and type-17 T cells secrete cytokines (eg, granulocyte-macrophage colony-stimulating factor and int

199 with MS, characterized by the expression of granulocyte-macrophage colony-stimulating factor and the

200 (+) DCs acquired high langerin and CD1a with granulocyte-macrophage colony-stimulating factor and tra

201 id-poly-L-lysine carboxymethylcellulose) and granulocyte-macrophage colony-stimulating factor as adju

202 ardial AT and performed B-cell depletion and granulocyte-macrophage colony-stimulating factor blockad

203 ter U-IRI results in sustained expression of granulocyte-macrophage colony-stimulating factor by rena

204 Granulocyte-macrophage colony-stimulating factor is a po

205 itol 3-kinase (PI3K) effector Akt induced by granulocyte-macrophage colony-stimulating factor or inte

206 7, interferon-gamma, tissue necrosis factor, granulocyte-macrophage colony-stimulating factor) and cy

207 ignificant cytokine responses (Th1, Th2, and granulocyte-macrophage colony-stimulating factor).

208 terferon gamma, tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor, and gr

209 of cytokines produced by T-helper 17 cells (granulocyte-macrophage colony-stimulating factor, interl

210 the folding of a complex lasso glycoprotein, granulocyte-macrophage colony-stimulating factor, modeli

211 on gamma, tumor necrosis factor (TNF) alpha, granulocyte-macrophage colony-stimulating factor, monocy

212 ors, such as chemokine (C-C motif) ligand 9, granulocyte-macrophage colony-stimulating factor, solubl

213 sion of FATP2 in PMN-MDSCs was controlled by granulocyte-macrophage colony-stimulating factor, throug

214 l clusters and 3-fold upregulated numbers of granulocyte-macrophage colony-stimulating factor-produci

215 Granulocyte-macrophage colony-stimulating factor-recepto

216 Granulocyte-macrophage colony-stimulating factor-recepto

217 eron gamma, tumor necrosis factor alpha, and granulocyte-macrophage colony-stimulating factor.

218 n disease pathogenesis and possibly also for granulocyte-macrophage colony-stimulating factor.

219 ients with PAP due to autoantibodies against granulocyte-macrophage colony-stimulating factor; geneti

220 Tumor-secreted TGF-beta and granulocyte-macrophage CSF (GM-CSF) enhanced the KDR/ID2

221 egakaryocyte-erythroid progenitor (MEP), and granulocyte-macrophage progenitor (GMP) cells, accompani

222 ly from both primitive (CD34+CD38-) and late granulocyte-macrophage progenitor (GMP) cells.

223 We traced distinct trajectories through the granulocyte-macrophage progenitor (GMP) compartment show

224 ol I transcription reduces both the leukemic granulocyte-macrophage progenitor and leukemia-initiatin

225 hil/macrophage lineage outputs from a common granulocyte-macrophage progenitor are still not complete

226 -primed multi-potential progenitors (LMPPs), granulocyte-macrophage progenitors (GMPs) and multi-lymp

227 that the cell cycle rate heterogeneity among granulocyte-macrophage progenitors (GMPs) determines the

228 uncover a unique spatiotemporal mechanism of granulocyte-macrophage progenitors (GMPs) employed in em

229 (CMPs), common lymphoid progenitors (CLPs), granulocyte-macrophage progenitors (GMPs), megakaryocyte

230 ng-term haematopoietic stem cells (HSCs) and granulocyte-macrophage progenitors compared with wild-ty

231 eloid progenitors but significantly lower in granulocyte-macrophage progenitors.

232 nophil progenitors (EoPs), downstream of the granulocyte/macrophage progenitor (GMP).

233 ructure and minimal infiltration by CD11b(+) granulocytes/macrophages as compared with SA-engineered

234 responses involving eosinophil and basophil granulocytes, mast cells and humoral factors such as IgE

235 ading to impaired progenitor maintenance and granulocyte maturation.

236 yeloid-lineage progenitors were derived from granulocyte monocyte precursors (GMPs) and could develop

237 umor-MDSC was induced by cancer cell-derived granulocyte-monocyte colony-stimulating factor (GM-CSF)

238 lavage eosinophils had more surface IL-3 and granulocyte-monocyte colony-stimulating factor receptors

239 elopoiesis and differentiation skewed toward granulocyte-monocyte progenitors (GMP) during joint and

240 Granulocyte-monocyte progenitors (GMPs) and monocyte-den

241 Granulocyte-monocyte progenitors (GMPs) have been previo

242 esis was left-shifted with selective loss of granulocyte-monocyte progenitors.

243 Clonogenic assay for CFU- granulocyte-monocyte suggested that HMGB1 may be require

244 and cell cycle, but increased cell death and granulocyte/monocyte differentiation, two main HOXA9 fun

245 d levels of proinflammatory cytokines, overt granulocyte/monocyte progenitor cell apoptosis, and fail

246 ssions, we find no detectable alpha7nAChR in granulocytes, monocytes and alveolar macrophages, and lo

247 type-related regulatory networks extended to granulocytes, monocytes, and macrophages.

248 stical computation, to quantify the yield of granulocytes, monocytes, lymphocytes and three subsets o

249 Here, we studied 5 cell lineages (granulocytes, monocytes, T cells, B cells, and natural k

250 by enhancing local inflammation, notably via granulocytes, monocytes/macrophages, and CD1a(int)-expre

251 e activation and proliferation of neutrophil granulocytes (neutrophils) in the ileum of mice developi

252 show that sustained fungal exposure impacts granulocyte numbers.

253 ing a mechanism whereby MPO mutations affect granulocyte numbers.

254 gation, TF microparticle induction, or TF on granulocytes or eosinophils.

255 tion that is manifested by higher numbers of granulocytes, plasmablasts, and inflammatory Ly6C(hi) CC

256 ng pathogens by polymorphonuclear neutrophil granulocytes (PMNs), followed by PMN apoptosis and effer

257 lineages and find evidence of proliferating granulocyte populations.

258 deletion, we found that Trib1 regulates both granulocyte precursor lineage commitment and mature eosi

259 adult stages with bone marrow production of granulocyte precursors and positive selection of mutants

260 Adoptive transfer of BM, but not peripheral, granulocytes prevented the death of mice transplanted wi

261 se in monocyte progenitors and a decrease in granulocyte progenitors among GMP cells.

262 HSC)-enriched LSK population but not myeloid-granulocyte progenitors.

263 eatures, including recruitment/activation of granulocytes, proliferation of fibrocytes/smooth muscle

264 by delivering TNFalpha to endothelial cells, granulocytes promote blood vessel growth and hematopoiet

265 nflammatory cytokine production, but reduced granulocyte recruitment by aMDM.

266 osstalk and triggered a profound increase in granulocyte recruitment to tumors.

267 duced microglial proliferation, and impaired granulocyte recruitment with an earlier spread of pneumo

268 cells, resulting in reduction of the marrow granulocyte reserve with an elevation of granulocytes in

269 Interestingly, this lack of intestinal granulocyte response in aged mice during severe C. diffi

270 y uninfected population initiated a stronger granulocyte response to Schistocephalus infection, and t

271 ependently contributing to the regulation of granulocyte responses and pathology during Toxoplasma go

272 While affected granulocytes show reduced glucose utilization, the under

273 In this study, we observe that granulocyte signatures in the MM TME contribute to a mor

274 Mice with a deletion of the granulocyte specific miR-223 gene showed a similarly imp

275 ells caused HDAC2-mediated downregulation of granulocyte-specific chemokine expression in CAF, which

276 urrent peripheral blood pattern of acquired, granulocyte-specific telomere shortening.

277 understanding of the role of human neonatal granulocyte subpopulations and calgranulin C (S100A12).

278 In the current study, we identify a unique granulocyte subset, with characteristics of an immature

279 s the frequency and functional phenotypes of granulocyte subsets with emergence of CRTH2 as a disease

280 s; and (3) telomere shortening determined in granulocytes suggested ~20 years of added proliferative

281 tions of neurons/glia for the brain data and granulocytes/T cells/B cells/monocytes for the blood dat

282 Eosinophils are a subset of granulocytes that can be involved in the pathogenesis of

283 C-PHIV had shorter granulocyte TL compared to uninfected peers, regardless

284 PHIV and those with reduced FVC have shorter granulocyte TL, possibly the result of increased immune

285 Packed blood cell (granulocyte) TL from 621 children were compared cross-se

286 Interestingly, we found these infiltrating granulocytes to be SSC(high) CD11b(+) CD125(+) Siglec-F(

287 Propensity of isolated polymorhonuclear granulocytes to form neutrophil extracellular traps (NET

288 ples, to assess the recruitment of ILC2s and granulocytes to the upper airways of subjects with atopy

289 are major sources of chemokines that recruit granulocytes to tumors.

290 l clusters, and inhibition of CXCR2-mediated granulocyte trafficking to the central nervous system re

291 characterize the mutational landscape of the granulocyte transcriptome using RNA sequencing data and

292 hil counts, aspirin-induced changes in blood granulocyte transcripts did not differ between groups.

293 e levels, platelet-leukocyte aggregates, and granulocyte transcripts were assessed.Measurements and M

294 tes induced vascular recovery, and wild-type granulocyte transfer did not prevent death or promote va

295 Granulocytes were consistently increased, dysplastic, an

296 ity granulocytes (LDG) and CB normal-density granulocytes were isolated and functionally and phenotyp

297 H immunotoxin to granulocytes and monocytes, granulocytes were significantly more sensitive than mono

298 TME components, in particular monocytes and granulocytes, which are often ignored in microenvironmen

299 DNI) is the fraction of circulating immature granulocytes, which reflects severe bacterial infections

300 Eosinophils, tissue-dwelling granulocytes with several homeostatic roles, have a surp