ライフサイエンスコーパス: G-CSF

1 G-CSF and GM-CSF are used widely to promote the producti

2 G-CSF and M-CSF are two lineage-specific cytokines that

3 G-CSF did not improve mRS (ordinal regression), odds rat

4 G-CSF has diverse biological effects on a broad range of

5 G-CSF is a hemopoietic growth factor that has a role in

6 G-CSF is an essential cytokine that regulates proliferat

7 G-CSF is efficient and well tolerated but is not require

8 G-CSF or CSF-3, originally defined as a regulator of gra

9 G-CSF receptor deficiency and CXCL1 blockade suppressed

10 G-CSF was found to play a key role in MDSC mobilization

11 G-CSF, 10 mug/kg/day subcutaneously, was started Day 1 a

12 G-CSF- and G-CSF receptor-deficient mice are profoundly

13 ammatory mediators such as IL-1beta, Cxcl-1, G-CSF, and IL-6 are increased.

14 10 RCTs comprising 196 stroke patients (116 G-CSF, 80 placebo), mean age 67.1 (SD 12.9), 92% ischaem

15 ition of neutrophil production via the IL-17/G-CSF axis, and rhythmic modulation of the haematopoieti

16 recruitment by neutralization of IL-1alpha, G-CSF, or neutrophil depletion itself promoted resolutio

17 Thus, we identified an excessive IL-1alpha/G-CSF response as a major driver of enhanced sterile inf

18 nt bone marrow niche signals (SCF, IL-1beta, G-CSF, TGFbeta and CXCL4) and activation of an inducible

19 These findings thus define a G-CSF effect on MPO chemical biology that endows unsuspe

20 In addition, G-CSF treatment reduced the levels of four of five measu

21 that high-dose cyclophosphamide given after G-CSF-mobilized blood cell transplantation would reduce

22 s negatively impacted HSC mobilization after G-CSF with or without chemotherapy but had no effect on

23 ts suggest that CD8(+) DCs, pDCs, IL-12, and G-CSF play important roles in priming effective antitumo

24 cific depletion of ILCs prevented IL-17- and G-CSF-dependent granulocytosis and resistance to sepsis.

25 nerated higher levels of IL-6, IL-1beta, and G-CSF following ex vivo LPS challenge.

26 the galectin-3-induced secretion of IL-6 and G-CSF cytokines from the endothelial cells.

27 intestine and increased circulatory IL-6 and G-CSF, along with a hematopoietic shift toward granulocy

28 ytokines (IL-12p40, IL-1beta, TNF-alpha, and G-CSF) and chemokines (CXCL2, CCL5) were significantly e

29 G-CSF- and G-CSF receptor-deficient mice are profoundly protected i

30 n, and also increased keratinocyte CXCL1 and G-CSF production.

31 IL-3 also influences IFN-gamma, CXCL9, and G-CSF production in response to infection.

32 ing G-CSF treatment reduces excitability and G-CSF-induced visceral pain in vivo.

33 markers (IL-6, nCD64, IL-1ra, PCT, MCP1, and G-CSF) yielded the same predictive power as collecting a

34 d thereby inhibits STAT3 phosphorylation and G-CSF receptor signaling.

35 sults suggest that the combination of RT and G-CSF should be further evaluated in preclinical and cli

36 ch as hematopoietic cell transplantation and G-CSF- or inflammation-induced stress myelopoiesis.

37 Anti-G-CSF receptor rapidly halted the progression of establi

38 The eyes of G-CSF-deficient and anti-G-CSF monoclonal antibody-treated WT mice had minimal ne

39 G-CSF-STAT3 signaling loop with either anti-G-CSF antibody or STAT3 inhibitor depleted the CSC subpo

40 rom an inflammatory phenotype following anti-G-CSF receptor therapy in collagen Ab-induced arthritis.

41 reduced in G-CSF-deficient mice and in anti-G-CSF monoclonal antibody-treated, wild-type (WT) mice.

42 ollowing administration of neutralizing anti-G-CSF antiserum.

43 ls in the blood and arthritic joints of anti-G-CSF receptor-treated mice showed alterations in cell a

44 e, blocking neutrophil trafficking with anti-G-CSF receptor suppressed local production of proinflamm

45 e U.S. Food and Drug Administration approved G-CSF (filgrastim) for the treatment of congenital and a

46 As G-CSF treatment also induces HSC proliferation, we sough

47 Primary prophylaxis (PP) was defined as G-CSF administration within 5 days of beginning chemothe

48 randomised controlled trials (RCT) assessing G-CSF in patients with hyperacute, acute, subacute or ch

49 e randomized to ATG and pegylated G-CSF (ATG+G-CSF) (N = 17) or placebo (N = 8).

50 ptide was not significantly different in ATG+G-CSF (0.49 nmol/L/min) versus placebo (0.29 nmol/L/min)

51 gulatory T cells (Treg) were elevated in ATG+G-CSF subjects at 6, 12, and 18 but not 24 months.

52 A phase II study of ATG+G-CSF in patients with new-onset type 1 diabetes is ongo

53 pe 1 diabetes is ongoing and may support ATG+G-CSF as a prevention strategy in high-risk subjects.

54 Subjects treated with ATG+G-CSF demonstrated reduced CD4(+) T cells and CD4(+)/CD8

55 ATG/G-CSF therapy was associated with relative preservation

56 Combination ATG/G-CSF treatment tended to preserve beta cell function in

57 A1c was lower in ATG/G-CSF-treated subjects at the 6-month study visit.

58 further investigate the actions of blocking G-CSF/G-CSF receptor signaling in inflammatory disease,

59 Both G-CSF and SCF had pronounced effects on frataxin levels

60 A new G-CSF-driven (methylated BSA/G-CSF) arthritis model was established enabling us to de

61 but had no effect on mobilization induced by G-CSF with plerixafor.

62 Mobilization induced by G-CSF, AMD3100 or ischemia was evaluated by flow cytomet

63 ing molecular mechanism of MTA1 induction by G-CSF was proved to be through induction of c-Fos and it

64 In db/db mice, mobilization by G-CSF or AMD3100 was either increased or unaffected (P <

65 graftment efficiency than those mobilized by G-CSF.

66 sue (TNF-alpha, IFN-gamma, IL-6, CCL2, CCL3, G-CSF, osteopontin).

67 This drug combination (AraC+CHK1i+G-CSF) will open the doors for a more efficient treatmen

68 igand" (MPO-EL), is expressed on circulating G-CSF-mobilized leukocytes and is naturally expressed on

69 matory cytokines, including granulocyte CSF (G-CSF) and chemokines.

70 lobulin (ATG) and pegylated granulocyte CSF (G-CSF) would preserve beta cell function in patients wit

71 It was more efficient than granulocyte CSF (G-CSF), a common treatment of severe neutropenia, which

72 anulocyte colony-stimulating factor (G-CSF), G-CSF, Plerixafor, or Plerixafor+G-CSF were transduced w

73 acrophage colony-stimulating factor (GM-CSF)/G-CSF in vitro, inhibited GVHD-induced death and attenua

74 f central nervous system ECs produce GM-CSF, G-CSF, IL-6, Cxcl1, and Cxcl2.

75 on, through increased plasma levels of CSF3 (G-CSF; beta = 0.29; P = 0.002), and an increased inflamm

76 These data suggest that G-CSFR/G-CSF targeting may be a safe therapeutic strategy for a

77 ncreases in STAT3 activating serum cytokines G-CSF and IL-6.

78 -6 and IL-1beta), and chemotactic cytokines (G-CSF, CXCL12, CXCL1, and CX3CL1).

79 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significant

80 the two groups, whereas in historical data, G-CSF was less effective in patients with diabetes.

81 Taken together, our results define G-CSF as a CSC-activating factor in neuroblastoma, sugge

82 nts, we demonstrate that bone marrow-derived G-CSF-responsive cells home to the injured brain and are

83 Similarly, high-dose G-CSF (or downstream signaling through AKT/BCL2) rescues

84 ersistent pancytopenia despite moderate-dose G-CSF treatment.

85 the increased demand for neutrophils during G-CSF-induced emergency granulopoiesis in humans.

86 ing CX3CR1 or nitric oxide production during G-CSF treatment reduces excitability and G-CSF-induced v

87 emokine CXCL1, cytokine IL-6, and endogenous G-CSF proteins.

88 IL-1beta, IL-6, IL-10, IL-12 (p70), eotaxin, G-CSF, GM-CSF, macrophage chemoattractant protein-1, mac

89 Exogenous G-CSF enhances tumor growth and metastasis in human xeno

90 okine granulocyte-colony-stimulating factor (G-CSF or Csf-3) as a key mediator of visceral sensitizat

91 e via granulocyte colony-stimulating factor (G-CSF) administration.

92 otein granulocyte colony-stimulating factor (G-CSF) against storage at 4 degrees C and shipping tempe

93 izing granulocyte colony-stimulating factor (G-CSF) and chemokine receptor-mediated signals.

94 with granulocyte colony-stimulating factor (G-CSF) and dexamethasone.

95 cy of granulocyte colony-stimulating factor (G-CSF) and haemopoietic stem-cell infusions in patients

96 ts of granulocyte colony-stimulating factor (G-CSF) and of nitric oxide (NO) upon challenge with cory

97 ines, granulocyte-colony stimulating factor (G-CSF) and stem cell factor (SCF) in a humanized murine

98 on of granulocyte colony-stimulating factor (G-CSF) and the ELR(+) CXC chemokine CXCL1.

99 ts of granulocyte colony-stimulating factor (G-CSF) and underlying mechanisms in a gerbil model of gl

100 on of granulocyte colony-stimulating factor (G-CSF) by hypoxic breast cancer cells and tumors in an o

101 agent granulocyte colony-stimulating factor (G-CSF) caused rapid redistribution of HSCs across the sk

102 , and granulocyte colony-stimulating factor (G-CSF) concentrations correlated strongly to vaccine eff

103 rived granulocyte-colony stimulating factor (G-CSF) directs expansion and differentiation of hematopo

104 thout granulocyte colony-stimulating factor (G-CSF) during follow-up was 0.5 x 10(9)/L.

105 on of granulocyte colony-stimulating factor (G-CSF) enhanced RT-mediated antitumor activity by activa

106 using granulocyte colony-stimulating factor (G-CSF) for hematopoietic stem cell (HSC) mobilization ha

107 Granulocyte colony-stimulating factor (G-CSF) has been shown to increase survival in patients w

108 that granulocyte-colony stimulating factor (G-CSF) in patients with glycogenosis-related pancytopeni

109 Granulocyte colony-stimulating factor (G-CSF) is a regulator of neutrophil production, function

110 Human granulocyte colony-stimulating factor (G-CSF) is an endogenous glycoprotein involved in hematop

111 okine granulocyte-colony stimulating factor (G-CSF) is commonly used therapeutically to augment neutr

112 Granulocyte colony-stimulating factor (G-CSF) is used clinically to treat leukopenia and to enf

113 Granulocyte colony-stimulating factor (G-CSF) is widely used clinically to prevent neutropenia

114 , and granulocyte colony-stimulating factor (G-CSF) levels in the amniotic fluid of ZIKV-positive pre

115 rast, granulocyte colony-stimulating factor (G-CSF) levels were significantly higher, and the percent

116 Granulocyte colony stimulating factor (G-CSF) may enhance recovery from stroke through neuropro

117 lated granulocyte colony-stimulating factor (G-CSF) preserves beta-cell function for at least 12 mont

118 human granulocyte-colony stimulating factor (G-CSF) prior to MS/MS and MS(3) analysis to specifically

119 after granulocyte colony-stimulating factor (G-CSF) prophylaxis in patients with breast cancer who re

120 ing a granulocyte-colony stimulating factor (G-CSF) receptor knockout mouse model in combination with

121 okine granulocyte colony-stimulating factor (G-CSF) through complex mechanisms.

122 ty of granulocyte colony-stimulating factor (G-CSF) to mobilize endogenous cells have attracted the m

123 , and granulocyte colony-stimulating factor (G-CSF) was chosen, due to its clinically proven neurogen

124 ATG), granulocyte-colony stimulating factor (G-CSF), a dipeptidyl peptidase IV inhibitor (DPP-4i), an

125 pha), granulocyte colony-stimulating factor (G-CSF), and interleukin 6 (IL-6).

126 a2m), granulocyte colony stimulating factor (G-CSF), and three monoclonal antibodies (mAbs).

127 yurea+granulocyte colony-stimulating factor (G-CSF), G-CSF, Plerixafor, or Plerixafor+G-CSF were tran

128 -78), granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor

129 -17A, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor

130 IL-8, granulocyte-colony stimulating factor (G-CSF), IL-33, IL-11, IL-1alpha, and IL-1beta.

131 beta, granulocyte colony-stimulating factor (G-CSF), interleukin-12/23 (IL-12/23), and IL-13 trended

132 mma), granulocyte colony-stimulating factor (G-CSF), monocyte chemoattractant protein 1 (MCP-1), macr

133 ce of granulocyte colony-stimulating factor (G-CSF), the key granulopoietic cytokine, after LPS chall

134 duced granulocyte colony-stimulating factor (G-CSF), which was required for extramedullary HSC accumu

135 upon granulocyte-colony stimulating factor (G-CSF)- mediated granulocytic differentiation of 32Dcl3

136 on of granulocyte colony-stimulating factor (G-CSF)-mobilized blood cells from HLA-matched related or

137 ssive granulocyte colony-stimulating factor (G-CSF)-regulated neutrophilic response and prolonged inf

138 on of granulocyte colony-stimulating factor (G-CSF)-treated donors (GDs) consists of mature CD66b(+)C

139 en of granulocyte colony-stimulating factor (G-CSF).

140 se to granulocyte colony-stimulating factor (G-CSF).

141 on of granulocyte colony-stimulating factor (G-CSF).

142 on of granulocyte-colony stimulating factor (G-CSF); these effects are reversed following administrat

143 with granulocyte colony-stimulating factor (G-CSF/Csf3) or by secretion of G-CSF from the tumor.

144 , and granulocyte colony-stimulating factor [G-CSF]) were higher in STI-positive macaques during STI

145 n resulted in monocyte development following G-CSF induction whereas inhibition of Erk1/2 signaling p

146 al latency that can be reactivated following G-CSF treatment.

147 ilization to refrigeration, but critical for G-CSF stabilization at elevated temperatures.

148 hat they are also consistent with a role for G-CSF as a switch that activates innate immune responses

149 Several studies point to a critical role for G-CSF as the main mediator of emergency granulopoiesis.

150 these data demonstrate an important role for G-CSF in invoking autophagy within hematopoietic and mye

151 These data reveal an integral role for G-CSF-driven neutrophil responses in ocular autoimmunity

152 fter transplantation with splenic cells from G-CSF-treated donors blocks suppression of aGVHD, sugges

153 XCR4 antagonist plerixafor, differently from G-CSF, is effective in mobilizing HSCs in patients with

154 understand which patients benefit most from G-CSF prophylaxis in this setting.

155 relies on incoming IL-10(+) neutrophils from G-CSF-treated donor spleen (G-Neutrophils).

156 was completely deficient in neutrophils from G-CSF-treated donors.

157 Furthermore, G-CSF-induced neutrophil and HSC mobilization is impaire

158 However, G-CSF is also produced in response to infection, and exc

159 esponded to treatment with recombinant human G-CSF.

160 utside of the bone marrow, and also identify G-CSF as a potential therapeutic target in the treatment

161 Importantly, G-CSF receptor blockade did not adversely affect viral c

162 ly, dorsal root ganglion neurons cultured in G-CSF failed to respond to G-CSF in vitro, and Csf3r gen

163 ne uveoretinitis was dramatically reduced in G-CSF-deficient mice and in anti-G-CSF monoclonal antibo

164 ous adverse events were more frequent the in G-CSF and stem-cell infusion group (12 [43%] patients) t

165 hese MSCs by various interventions including G-CSF administration diminished cancer cell homing.

166 tin receptor antagonist, PESLAN-1, increased G-CSF- or AMD3100-mobilization of WBCs and LSKs, compare

167 tained neutrophilia accompanied by increased G-CSF signaling and testicular vacuolation associated wi

168 CBD administration in mice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.

169 d715, derived from an SCN patient inhibited G-CSF-induced expression of NE in a dominant negative ma

170 first time, the efficacy of BMMC injection, G-CSF mobilization, and the combination of both with sta

171 INTERPRETATION: G-CSF with or without haemopoietic stem-cell infusion di

172 genitor cell potential from ex vivo-isolated G-CSF-mobilized human blood neutrophils.

173 ntify a novel hypoxia-induced CAIX-NF-kappaB-G-CSF cellular signaling axis culminating in the mobiliz

174 IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and TGF-alpha.

175 lly, we demonstrate that the receptor ligand G-CSF selectively activates STAT3 within neuroblastoma C

176 ase of IL-1alpha and IL-1 receptor -mediated G-CSF production.

177 gnificant difference in all-cause mortality (G-CSF 11.2%, placebo 7.6%, p = 0.4).

178 which potently antagonizes binding of murine G-CSF and thereby inhibits STAT3 phosphorylation and G-C

179 e developed a neutralizing mAb to the murine G-CSF receptor, which potently antagonizes binding of mu

180 n MDSC mobilization inasmuch as neutralizing G-CSF caused a significant decrease in MDSC.

181 A new G-CSF-driven (methylated BSA/G-CSF) arthritis model was

182 We also show that M-CSF, but not G-CSF, stimulated strong and sustained activation of Erk

183 mRNA expression induced by administration of G-CSF in vivo, as a model of emergency granulopoiesis in

184 Finally, administration of G-CSF-neutralizing antibody can prevent the establishmen

185 d be partially reversed by administration of G-CSF.

186 unveiling new perspectives on the biology of G-CSF and MPO, and on the role of E-selectin receptor/li

187 of rheumatoid arthritis, and Ab blockade of G-CSF also protects against disease.

188 compensated cirrhosis given a combination of G-CSF and darbopoietin alpha survived for 12 months more

189 However, the consequences of G-CSF stimulation on the transcriptome of neutrophils an

190 lected from healthy individuals after 5 d of G-CSF administration.

191 e therapeutic responses using lower doses of G-CSF combined with targeting to correct NE mislocalizat

192 nulopoiesis-specific mechanism downstream of G-CSF receptor signaling that leads to LEF-1 downregulat

193 we describe for the first time the effect of G-CSF receptor blockade in a therapeutic model of inflam

194 animals neutropenic, suggesting an effect of G-CSF receptor blockade on neutrophil homing to inflamma

195 These neuroprotective effects of G-CSF may be linked to inhibition of inflammation and po

196 es provide an explanation for the effects of G-CSF on T cell function and demonstrate that IL-10 is r

197 The eyes of G-CSF-deficient and anti-G-CSF monoclonal antibody-treat

198 A polyethylene glycol-modified form of G-CSF is approved for the treatment of neutropenias.

199 diabetes (>/=20 weeks) induced impairment of G-CSF- or AMD3100-mobilization (P < 0.01, n = 8).

200 y mice subjected to intrathecal injection of G-CSF exhibit pronounced visceral hypersensitivity, an e

201 cells restored induction of Egr1, but not of G-CSF.

202 t a validated short transduction protocol of G-CSF plus plerixafor-mobilized CD34(+) cells from FA-A

203 for functional importance and redundancy of G-CSF receptor-mediated signaling in human granulopoiesi

204 Herein, we investigated the role of G-CSF in a murine model of human uveitis-experimental au

205 -gamma in mast cells leading to secretion of G-CSF and consequent MDSC mobilization.

206 BMP4 reduces the expression and secretion of G-CSF by inhibiting NF-kappaB (Nfkb1) activity in human

207 ating factor (G-CSF/Csf3) or by secretion of G-CSF from the tumor.

208 it enabled the convergent total synthesis of G-CSF aglycone.

209 ehensive reevaluation of the clinical use of G-CSF in these patients to support white blood cell coun

210 00-mobilized LSK cells, and had no effect on G-CSF.

211 Cs are preferentially mobilized to the PB on G-CSF treatment.

212 topoiesis and EMH in response to bleeding or G-CSF treatment.

213 Overall, G-CSF did not improve stroke outcome in this individual

214 months) were randomized to ATG and pegylated G-CSF (ATG+G-CSF) (N = 17) or placebo (N = 8).

215 5 mg/kg intravenously) followed by pegylated G-CSF (6 mg subcutaneously every 2 weeks for 6 doses) an

216 s (ILCs) in the intestine, increasing plasma G-CSF levels and neutrophil numbers in a Toll-like recep

217 Plerixafor+G-CSF cells produced the highest beta-globin expression/

218 or (G-CSF), G-CSF, Plerixafor, or Plerixafor+G-CSF were transduced with the TNS9.3.55 beta-globin len

219 Overall, Plerixafor+G-CSF not only allows high CD34+ cell yields but also pr

220 d in all xenografted groups, with Plerixafor+G-CSF-mobilized cells achieving superior short-term engr

221 ion with G-CSF; 3) both (BMMC injection plus G-CSF); or 4) conventional treatment (control group).

222 ve developed a synthetic platform to prepare G-CSF aglycone with the goal of enabling access to nativ

223 Conclusion Primary G-CSF prophylaxis was associated with low-to-modest bene

224 ed that IL-33-stimulated macrophages produce G-CSF, which in turn, boosted MDSCs.

225 can prolong neutrophil survival by producing G-CSF and GM-CSF, delaying the mitochondrial outer membr

226 These results demonstrate that prolonged G-CSF may be responsible for both the development and ac

227 Significantly, we reveal that prolonged G-CSF stimulation is both necessary and sufficient for t

228 hrm1) signaling in the hypothalamus promotes G-CSF-elicited HSC mobilization via hormonal priming of

229 Fifty patients received G-CSF either sporadically (n = 24) or continuously (n =

230 ith untreated animals, animals that received G-CSF following radiation injury exhibited enhanced func

231 whereas it was not in patients who received G-CSF plus plerixafor.

232 poorer mobilization in patients who received G-CSF with/without chemotherapy, whereas it was not in p

233 Patients with diabetes who received G-CSF without plerixafor had a lower probability of reac

234 poorer mobilization in patients who received G-CSF.

235 IFN-lambda1, IP-10, TRAIL), cell recruiting (G-CSF, IL-1beta, IL-8, MCP-1, MCP-3, TNF-alpha), polariz

236 ity disrupted CEBPbeta induction and reduced G-CSF expression in CRTC2/3m stromal cells, our results

237 ppaB pathway in CAIX-depleted cells restored G-CSF secretion.

238 ghtened IL-4 activity, with IL-4 restricting G-CSF-induced neutrophil expansion and migration to tiss

239 l T-cell expressed and presumably secreted), G-CSF (granulocyte-colony-stimulating factor) and MMP2 (

240 ralization of the postburn increase in serum G-CSF largely blocked STAT3 activation in marrow cells,

241 kines in semen correlated with HIV shedding (G-CSF, tumor necrosis factor-alpha [TNF-alpha], interfer

242 nic inflammation, thereby identifying spinal G-CSF as a target for treating chronic abdominal pain.

243 ndomly assigned to groups given subcutaneous G-CSF (5 mug/kg/d) for 5 days and then every third day (

244 care (control), treatment with subcutaneous G-CSF (lenograstim) 15 mug/kg for 5 days, or treatment w

245 EC-intrinsic MYD88 signaling and subsequent G-CSF production by ECs is required for myeloid progenit

246 In turn, higher levels of systemic G-CSF increased peripheral neutrophilia, which amplified

247 icroglia express the G-CSF receptor and that G-CSF signaling mediates microglial activation following

248 o G-CSF treatment without dividing, and that G-CSF-mediated proliferation is restricted to cells with

249 We conclude that G-CSF treatment generates a population of activated and

250 Mechanistically, we demonstrate that G-CSF injection increases Cathepsin S activity in spinal

251 Our findings indicate that G-CSF reduces hippocampal neuronal cell death dose-depen

252 We have observed that G-CSF activates autophagy in neutrophils and HSCs from b

253 We showed previously that G-CSF treatment generates low-density splenic granulocyt

254 We report that G-CSF is specifically up-regulated in the thoracolumbar

255 of myelopoiesis, we previously reported that G-CSF also promotes the delivery of leukocytes to sites

256 We show that G-CSF controls the ocular neutrophil infiltrate by modul

257 In vitro biochemical studies show that G-CSF programs MPO-EL expression on human blood leukocyt

258 el dilution of dormant HSCs, suggesting that G-CSF does not stimulate dormant HSC proliferation.

259 w that resident spinal microglia express the G-CSF receptor and that G-CSF signaling mediates microgl

260 nds of MELD change over time (p=0.55 for the G-CSF group vs standard care and p=0.75 for the G-CSF pl

261 SF group vs standard care and p=0.75 for the G-CSF plus stem-cell infusion group vs standard care).

262 hat tumor-expressed CAIX is required for the G-CSF-driven mobilization of granulocytic myeloid-derive

263 fusion group (12 [43%] patients) than in the G-CSF (three [11%] patients) and standard care (three [1

264 d care group (variceal bleed) and two in the G-CSF and stem-cell infusion group (one myocardial infar

265 patients with a serious adverse event in the G-CSF group (29.6% versus 7.5%, p = 0.07) with no signif

266 rse events were ascites (two patients in the G-CSF group and two patients in the G-CSF plus stem-cell

267 andard care group, -0.5 (-1.7 to 0.5) in the G-CSF group, and -0.5 (-1.3 to 1.0) in the G-CSF plus st

268 ascites twice), sepsis (four patients in the G-CSF plus stem-cell infusion group), and encephalopathy

269 s in the G-CSF group and two patients in the G-CSF plus stem-cell infusion group, one of whom was adm

270 ), and encephalopathy (three patients in the G-CSF plus stem-cell infusion group, one of whom was adm

271 e G-CSF group, and -0.5 (-1.3 to 1.0) in the G-CSF plus stem-cell infusion group.

272 nduction of CEBPbeta, a key regulator of the G-CSF gene.

273 mutations in the extracellular domain of the G-CSF receptor (CSF3R) have been reported only in severe

274 a is known to be marked by expression of the G-CSF receptor (G-CSFR).

275 A dose increase of the G-CSF successfully normalized his leukocyte count.

276 ts, and suggest that direct targeting of the G-CSF-STAT3 signaling represents a novel therapeutic app

277 Our findings suggest that the G-CSF STAT3 axis constitutes a key protective mechanism

278 mly assigned to the standard care, 26 to the G-CSF group, and 28 to the G-CSF plus stem-cell infusion

279 d care, 26 to the G-CSF group, and 28 to the G-CSF plus stem-cell infusion group.

280 r stabilization of the important therapeutic G-CSF, as well as a general platform for the future disc

281 Blockade of this G-CSF-STAT3 signaling loop with either anti-G-CSF antibo

282 ultured with microglia BV-2 cells exposed to G-CSF, dorsal root ganglion (DRG) nociceptors become hyp

283 urons cultured in G-CSF failed to respond to G-CSF in vitro, and Csf3r gene expression could not be d

284 euron-microglia interaction that responds to G-CSF by engaging Cathepsin S-CX3CR1-inducible NOS signa

285 te that dormant HSCs mobilize in response to G-CSF treatment without dividing, and that G-CSF-mediate

286 within the BM HSC compartment in response to G-CSF treatment.

287 In response to G-CSF, STAT3 acts in a feed-forward loop to transcriptio

288 system to track HSC divisions in response to G-CSF.

289 ntribution or stem cell activity and, unlike G-CSF, did not impede recovery of HS/PCs, thrombocyte nu

290 proliferation, we sought to examine whether G-CSF-mediated repopulation defects are a result of incr

291 sults reveal an important mechanism by which G-CSF and M-CSF instruct neutrophil versus monocyte line

292 hippocampal dentate gyrus increased in with G-CSF treatment.

293 Treating S100a9(-/-) mice with G-CSF reversed their increased susceptibility to infecti

294 oronary BMMC injection; 2) mobilization with G-CSF; 3) both (BMMC injection plus G-CSF); or 4) conven

295 n effectively out-competes PB mobilized with G-CSF.

296 -1,2,3,6-tetrahydropyridine mouse model with G-CSF showed significant induction of MTA1 and TH with r

297 al autoimmune uveoretinitis was reduced with G-CSF deficiency.

298 In phase 1 dose expansion studies with G-CSF support, 23r has shown promising single agent acti

299 Treatment with G-CSF at 25-50 mug/kg significantly reduced neuronal los

300 tim) 15 mug/kg for 5 days, or treatment with G-CSF for 5 days followed by leukapheresis and intraveno