ライフサイエンスコーパス: GM-CSF

1 GM-CSF (250 mug/m2/d) or placebo were administered subcu

2 GM-CSF alone did not improve 6-minute walk more than att

3 GM-CSF and GPR65 may thus serve as targets for therapeut

4 GM-CSF has been portrayed as a critical cytokine in the

5 GM-CSF is a pleiotropic cytokine that promotes the diffe

6 GM-CSF is rapidly produced by cardiac fibroblasts after

7 GM-CSF levels were increased in NPs compared with those

8 GM-CSF neutralization in diet-induced obese mice signifi

9 GM-CSF production also required amphiregulin, p38 MAPK s

10 GM-CSF production in CD4 T cells occurs both independent

11 GM-CSF regulated cholesterol clearance in macrophages in

12 GM-CSF substantially augments glycolytic flux in vitro (

13 GM-CSF was identified as an upstream modulator.

14 GM-CSF(+)CD4(+) cells, isolated using a triple cytokine

15 ificantly greater expression level of IL-12, GM-CSF, and interferon-gamma (IFN-gamma) than either sin

16 Both GM-CSF(+) and IL-17A(+)GM-CSF(+) double-producing CD4 T cells express increased

17 arthritis, and increased numbers of IL-17A(+)GM-CSF(+) double-producing CD4, CD8, gammadelta and NK c

18 ) and Ki67(+), included producers of IL-17A, GM-CSF, and IFN-gamma, and were most of the CD4(+) T cel

19 or low (IL-15, TNF-alpha, IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10, IL-7, IL-1alpha, and IL-5) sub

20 mulation, cosecreting IL-17A, IL-17F, IL-22, GM-CSF, and IFN-gamma.

21 Together these data identify the IL-23R/GM-CSF axis within ILC3 as a key control point in the ac

22 s well as TNF-alpha plus IFN-gamma, or IL-3, GM-CSF, and IL-5 alone significantly diminished the proa

23 lavage fluid from Rasgrp1-deficient mice; 4) GM-CSF-specific IgG is capable of neutralizing GM-CSF bi

24 ells, but rather promoted the expansion of a GM-CSF(+) Th17 cell subset, thereby enhancing its enceph

25 nes that express surfactant proteins, ABCA3, GM-CSF, podoplanin, and caveolin mRNA after 7 days, temp

26 nfections observed in patients with acquired GM-CSF deficiency.

27 In addition, GM-CSF, which is critical for the differentiation and pr

28 reatment of a second patient with adjunctive GM-CSF bolsters the clinical relevance of these findings

29 2-deoxyglucose was assessed before and after GM-CSF exposure.

30 e blocked by a neutralizing antibody against GM-CSF.

31 man lung cancer, the expression of TTF-1 and GM-CSF exhibits a statistically significant and positive

32 ibronectin and cytokines TNFalpha, ANG-1 and GM-CSF.

33 P-1 (monocyte chemoattractant protein-1) and GM-CSF genes, and that this signature is associated with

34 T to Th2 cytokines, such as IL-4, IL-13, and GM-CSF, stimulates ATM proliferation, whereas Th1 cytoki

35 E and were characterized as IL-17 (IL-17 and GM-CSF double-positive) CD4 cells.

36 a1KO Mvarphi, which in turn induce IL-17 and GM-CSF production in CD4 cells.

37 expression of the IL-23 receptor, IL-17, and GM-CSF.

38 ammation and reduced frequency of IL-17- and GM-CSF-producing CD4(+) T cells.

39 quently, 1,25D suppressed IL-22, IL-17F, and GM-CSF production from tonsillar and gut ILC3s.

40 r IL-5 share a common ss-chain with IL-3 and GM-CSF receptors.

41 ce secreted higher levels of IL-4, IL-5, and GM-CSF.

42 ipid(s) triggered the production of IL-8 and GM-CSF in respiratory epithelial cells through a TLR2-,

43 s generated in the presence of IFN-alpha and GM-CSF (IFN-DC) and loaded with apoptotic lymphoma cells

44 CCL1 and GM-CSF genes are also poised in human memory CD8 T cells

45 mal T-cell expressed and excreted)/CCL5, and GM-CSF production by CD8 and CD4 T cells following treat

46 me, fungal DppIVA cleaved C-C chemokines and GM-CSF.

47 atory and metabolic profiles, both M-CSF and GM-CSF generated comparable levels of glucose uptake in

48 g neutrophil survival by producing G-CSF and GM-CSF, delaying the mitochondrial outer membrane permea

49 C57BL/6 mice capable of producing GM-CSF and GM-CSF-deficient mice infected with a moderately virulen

50 ne atherosclerotic plaques by both M-CSF and GM-CSF.

51 f beta-hexosaminidase, prostaglandin D2, and GM-CSF and changes in reactive oxygen species levels wer

52 lts link HDM, IL-17A, amphiregulin, EGFR and GM-CSF in a mechanistic pathway in AEC and demonstrate t

53 , granulocyte colony-stimulating factor, and GM-CSF levels.

54 , granulocyte colony-stimulating factor, and GM-CSF levels.

55 cytokine expression and release in fMLF- and GM-CSF-activated neutrophils, whereas the PI3K pathway i

56 t CD4(+) T cells restored both IFN-gamma and GM-CSF production.

57 the frequency of pathogenic IFN-gamma(+) and GM-CSF(+) Th17 cells in the CNS.

58 olished production of IL-17A, IFN-gamma, and GM-CSF despite only partially reduced Ca(2+) influx.

59 T-cell receptor-induced IL-2, IFN-gamma, and GM-CSF expression.

60 release of thymic stromal lymphopoietin and GM-CSF from tracheal epithelial cells.

61 uced in the L2-IL5(OXA) EoE mouse model, and GM-CSF production was assessed by mRNA and protein analy

62 educed Flt3(+)CD11c(-)MHCII(+) monocytes and GM-CSF-dependent FcgammaRIII(+)PD-L2(+)CD209a(+) moDCs b

63 esistance to lung infection through Nod2 and GM-CSF.

64 fector molecules in CAR T cells-perforin and GM-CSF.

65 F and MMP9 release from WAT progenitors, and GM-CSF knockdown in breast cancer cells neutralized the

66 mation and angiogenesis, mediated by TNF and GM-CSF, respectively.

67 n particular, systemic increases in VEGF and GM-CSF levels were notable and were validated by a conve

68 us immune evasion superfamily, to antagonize GM-CSF (granulocyte macrophage colony-stimulating factor

69 Anti-GM-CSF neutralization in L2-IL5(OXA) EoE mice resulted i

70 ar rupture, a complication mitigated by anti-GM-CSF therapy.

71 Injections of anti-GM-CSF reduced angiogenesis and numbers of CD31+ blood v

72 L2-IL5(OXA) EoE mice were treated with anti-GM-CSF neutralizing antibody or isotype control and asse

73 s model is insufficient to cause cells to be GM-CSF hypersensitive.

74 a process that can be inhibited by blocking GM-CSF, and mobilization precedes inflammatory foci else

75 Both GM-CSF(+) and IL-17A(+)GM-CSF(+) double-producing CD4 T

76 activation states of macrophages induced by GM-CSF and M-CSF in either cell culture or atherosclerot

77 cultured CD103(neg)CD11c(+) cells induced by GM-CSF readily supported exponential growth of L. monocy

78 ls or administration of exosomes produced by GM-CSF-expanded bone marrow cells.

79 osphorylation and attenuated C5, CCL1, CCL2, GM-CSF, IL-1alpha, IL-1beta and ICAM-1 inflammatory cyto

80 ecursor for FcgammaRIII(+)PD-L2(+)CD209a(+), GM-CSF-dependent moDCs but was distal from the DC lineag

81 treatment stimulating endogenous stem cells (GM-CSF) have been investigated for their potential in pr

82 Combined GM-CSF neutralization and MMP9 inhibition synergisticall

83 In contrast, GM-CSF deficiency resulted in increased accumulation of

84 xercise alone) (n = 53), attention control + GM-CSF (GM-CSF alone) (n = 53), attention control + plac

85 alone) (n = 53), attention control + GM-CSF (GM-CSF alone) (n = 53), attention control + placebo (n =

86 lating factor (M-CSF) and granulocyte-M-CSF (GM-CSF) and its implications for fluorine 18 ((18)F) flu

87 flammation resolving) and granulocyte-M-CSF (GM-CSF; proinflammatory) may contribute to the inconsist

88 ted TGF-beta and granulocyte-macrophage CSF (GM-CSF) enhanced the KDR/ID2 signaling axis in BMDCs.

89 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly incr

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

91 cell expression of the inflammatory cytokine GM-CSF, concomitant with pancreatic infiltration of infl

92 educed levels of the rAM maturation cytokine GM-CSF.

93 levels of several proinflammatory cytokines (GM-CSF, IFN-gamma, IL-1beta, IL-6, and IL-8) across stim

94 4(-/-) ) eosinophils treated with cytokines (GM-CSF, IL-4, IL-33) were adoptively transferred into eo

95 onal knockout (KO) Th17 cells have decreased GM-CSF mRNA in comparison with wild-type (WT) Th17 cells

96 further demonstrate that MAIT cell-dependent GM-CSF production stimulated monocyte differentiation in

97 Breast cancer-derived GM-CSF induced GM-CSF and MMP9 release from WAT progenit

98 In the heart, fibroblast-derived GM-CSF alerts its neighboring myeloid cells to attract n

99 f the ES cell- and adult progenitor-derived, GM-CSF-instructed, nonconventional DC subsets.

100 lled in clinical trials evaluating the E75 + GM-CSF and GP2 + GM-CSF vaccines, there have been no rec

101 equently, hearts of mice deficient in either GM-CSF or its receptor recruit fewer leukocytes and func

102 nct response to acetate treatment, elevating GM-CSF, IL-1alpha, and IL-1beta cytokine expression.

103 Our findings establish the CARD9/RASGRF1/ERK/GM-CSF axis as critical to the pathophysiology of sCNSc.

104 Significantly increased levels of esophageal GM-CSF expression was detected in the L2-IL5(OXA) mouse

105 ps: supervised exercise + GM-CSF (exercise + GM-CSF) (n = 53), supervised exercise + placebo (exercis

106 016, to 1 of 4 groups: supervised exercise + GM-CSF (exercise + GM-CSF) (n = 53), supervised exercise

107 At 12-week follow-up, exercise + GM-CSF did not significantly improve 6-minute walk dista

108 al virotherapy with an HSV vector expressing GM-CSF has been recently approved by the Food and Drug A

109 locyte-macrophage colony-stimulating factor (GM-CSF or Csf-2) is a pro-inflammatory mediator implicat

110 locyte-macrophage colony-stimulating factor (GM-CSF) (oAd) and DCs for sustained release of both ther

111 locyte macrophage colony-stimulating factor (GM-CSF) and matrix metallopeptidase 9 (MMP9).

112 locyte macrophage colony-stimulating factor (GM-CSF) axis in colitis.

113 locyte-macrophage colony-stimulating factor (GM-CSF) by central nervous system (CNS)-infiltrating T h

114 locyte-macrophage colony-stimulating factor (GM-CSF) can enhance the immunogenicity of rabies vaccine

115 locyte macrophage colony-stimulating factor (GM-CSF) can function as a key proinflammatory cytokine.

116 locyte macrophage colony-stimulating factor (GM-CSF) drive dendritic cell differentiation, whereas GM

117 locyte-macrophage colony-stimulating factor (GM-CSF) for improving walking ability in people with low

118 locyte macrophage colony-stimulating factor (GM-CSF) has progression-promoting potentials in certain

119 locyte/macrophage colony-stimulating factor (GM-CSF) in orchestrating these events.

120 locyte-macrophage colony-stimulating factor (GM-CSF) is a pleiotropic cytokine that plays a critical

121 locyte-macrophage colony-stimulating factor (GM-CSF) is EGFR dependent in keratinocytes.

122 locyte-macrophage colony-stimulating factor (GM-CSF) level in the EDM-TTF-1(+) conferred the antiangi

123 locyte-macrophage colony-stimulating factor (GM-CSF) or tumor necrosis factor (TNF), or immunoglobuli

124 locyte-macrophage colony-stimulating factor (GM-CSF) plus blockade of the M2 cytokines macrophage col

125 locyte-macrophage colony-stimulating factor (GM-CSF) produced by T helper 17 (Th17) cells plays an es

126 locyte macrophage colony-stimulating factor (GM-CSF) resembled in vivo inflammatory macrophages, whil

127 locyte-macrophage colony-stimulating factor (GM-CSF) signaling in SFB-colonized mice prevented GMP ex

128 locyte/macrophage-colony stimulating factor (GM-CSF) signaling normally maintains surfactant homeosta

129 locyte-macrophage colony-stimulating factor (GM-CSF) signaling, which stimulates pathogen killing and

130 locyte/macrophage colony-stimulating factor (GM-CSF) that acts locally and distally to generate and r

131 locyte macrophage colony stimulating factor (GM-CSF) was presented in the supplementary documents to

132 locyte-macrophage colony-stimulating factor (GM-CSF), a clinically used cytokine, increases macrophag

133 locyte macrophage-colony-stimulating factor (GM-CSF), a unifying characteristic in the disease.

134 locyte macrophage colony stimulating factor (GM-CSF), IL-8, IL-18, monocyte chemotactic protein-1 (CC

135 locyte macrophage colony stimulating factor (GM-CSF), interleukin 6 (IL-6) among others, and stabiliz

136 locyte-macrophage colony-stimulating factor (GM-CSF), mainly produced by MDSCs, was identified as a k

137 locyte macrophage colony-stimulating factor (GM-CSF), transforming growth factor beta (TGFbeta), and

138 locyte macrophage-colony stimulating factor (GM-CSF), which recruits and maintains intestinal inflamm

139 locyte-macrophage colony-stimulating factor (GM-CSF).

140 locyte-macrophage colony-stimulating factor (GM-CSF).

141 nulocyte monocyte colony stimulating factor (GM-CSF).

142 locyte-macrophage colony-stimulating factor (GM-CSF; an agonist cytokine linked with eosinophil survi

143 locyte-macrophage colony-stimulating factor [GM-CSF], IL-4, and MIP-1alpha) responses of the treated

144 locyte-macrophage colony-stimulating factor [GM-CSF], macrophage colony-stimulating factor [MCSF], in

145 Finally, GM-CSF-deficient mice exhibited a defect in monocyte dif

146 Our findings describe a novel role for GM-CSF as an essential initiating cytokine in cardiac in

147 d to identify alveolar-like macrophages from GM-CSF-treated bone marrow cultures, which provides a us

148 Furthermore, GM-CSF stimulation renders colon cancer cells more resis

149 trials evaluating the E75 + GM-CSF and GP2 + GM-CSF vaccines, there have been no recurrences in patie

150 These results identify the EGFR-->GM-CSF axis as a target for therapeutic development.

151 sed mice with transgenic expression of human GM-CSF, interleukin-3, and stem cell factor in a NOD/SCI

152 We identified GM-CSF and TGF-beta1 as key cytokines to generate langer

153 These findings identify GM-CSF as central to the protective immune response that

154 These results identify GM-CSF as both a key contributor to the pathogenesis of

155 a consistent cellular phenotype of impaired GM-CSF responses.

156 tokine in cardiac inflammation and implicate GM-CSF as a potential target for therapeutic interventio

157 Patients with acquired deficiency in GM-CSF are susceptible to infections with Cryptococcus n

158 C57BL/6 mice deficient in GM-CSF are resistant to EAE induced by immunization with

159 nalyses showed a trend toward improved OS in GM-CSF-treated patients with resected visceral metastase

160 creased multiple plasma cytokines, including GM-CSF, IFN-alpha2, IL-12p70, IP-10 and VEGF, during bot

161 ype 1 diabetes was associated with increased GM-CSF, IL-4, and IL-13 cytokine secretion among Ag-stim

162 FR inhibition reduced HDM and IL-17A induced GM-CSF production in a dose-dependent manner in cultured

163 Breast cancer-derived GM-CSF induced GM-CSF and MMP9 release from WAT progenitors, and GM-CSF

164 ood and cultured with the known OSM inducers GM-CSF and follistatin-like 1, and OSM levels were measu

165 High-dose metformin inhibited GM-CSF and MMP9 release from WAT progenitors in in vitro

166 Despite abundant lung GM-CSF and intact GM-CSF receptor signaling, PPAR-gamma was not sufficient

167 Monocytes integrated GM-CSF and IL-4 stimulation combinatorically and tempora

168 In vivo, in mice and in rabbits, intravenous GM-CSF administration resulted in a 70% and 73% increase

169 s LBNSE or the GM-CSF-expressing RABV (LBNSE-GM-CSF).

170 Despite abundant lung GM-CSF and intact GM-CSF receptor signaling, PPAR-gamma

171 Mechanistically, GM-CSF acts upon the local macrophage compartment, drivi

172 Mechanistically, GM-CSF upregulated IRF4 expression by enhancing JMJD3 de

173 for example, miR-466i functioned to mediate GM-CSF and IL-17 mRNA decay, which was confirmed by in v

174 nfection, and production of immune mediators GM-CSF, IFN-gamma and MCP-1, while suppressing an excess

175 lipoprotein-driven atherosclerosis in mice, GM-CSF promotes advanced plaque progression by increasin

176 e rindopepimut (500 mug admixed with 150 mug GM-CSF) or control (100 mug keyhole limpet haemocyanin)

177 nimals, and 3) high doses of codelivered MVA/GM-CSF inhibit mucosal Ab responses and the protection e

178 a Ankara (MVA) expressing rhesus GM-CSF (MVA/GM-CSF) on the immunogenicity and protection elicited by

179 High doses of MVA/GM-CSF did not affect the levels of systemic envelope (E

180 no or the lowest dose (1 x 10(5) PFU) of MVA/GM-CSF resisted all 12 challenges.

181 (aPAP) whereby IgG autoantibodies neutralize GM-CSF.

182 -CSF-specific IgG is capable of neutralizing GM-CSF bioactivity; and 5) Rasgrp1-deficient mice also l

183 variants that expressed human, mouse, or no GM-CSF produced equivalent amounts of killing.

184 transfer of IRF8-deficient T cells, but not GM-CSF-deficient T cells, increased MDSC accumulation in

185 ice induced G-CSF, CXCL1, and M-CSF, but not GM-CSF.

186 Abrogation of GM-CSF receptor signaling in adoptive transfer recipient

187 rotein (MOG)35-55 The mechanism of action of GM-CSF in EAE is poorly understood.

188 This action of GM-CSF is mediated by its interleukin-23-inducing activi

189 d the proinflammatory and algesic actions of GM-CSF.

190 Intratracheal administration of GM-CSF induced final rAM maturation in post-AAI mice and

191 The combination of GM-CSF plus the MIF inhibitor 4-iodo-6-phenyl-pyrimidine

192 factant degradation; 3) the concentration of GM-CSF-specific IgG is elevated in both serum and bronch

193 in cells at physiological concentrations of GM-CSF.

194 ealand White rabbits to assess the effect of GM-CSF on (18)F-FDG uptake in normal versus inflamed art

195 However, little is known about the effect of GM-CSF on cancer cells.

196 Walking exercise may augment the effects of GM-CSF in PAD, since exercise-induced ischemia enhances

197 EB1 are critical to mediate these effects of GM-CSF.

198 Lack of expansion of GM-CSF-producing Th17 cells led to ameliorated disease i

199 ells also included an elevated expression of GM-CSF and absence of IL-10 expression, indicating a pro

200 Moreover, the co-expression of GM-CSF and its receptors as well as phosphorylated ERK1/

201 Expression of GM-CSF and the ectodomain of FcgammaIIIA receptor led to

202 -17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+)

203 en of CRC patients, high-level expression of GM-CSF positively correlates with local metastases in ly

204 entifies a progression-promoting function of GM-CSF in colon cancer by inducing EMT.

205 ce, consequently inhibiting the induction of GM-CSF-producing pathogenic Th cells.

206 erlying the cognate receptor interactions of GM-CSF and IL-2, without sharing any structural similari

207 y disease, EGFR inhibition reduced levels of GM-CSF and TNF-alpha, as well as airway hyperreactivity,

208 from IKKbetaca mice had increased levels of GM-CSF.

209 IgG-mediated neutralization of GM-CSF thereby inhibits alveolar macrophage homeostasis

210 Here we show increased numbers of GM-CSF-producing CD4 and CD8 lymphocytes in the blood an

211 ratinocytes led to 11-fold overexpression of GM-CSF and 200-fold overexpression of TNF.

212 our CT analysis highlights the potential of GM-CSF treatment.

213 roduction is only induced in the presence of GM-CSF and IL-33 via the p38-MK2/3 signaling module.

214 Defective production of GM-CSF leads to insufficient post-AAI rAM maturation in

215 17) show that the dysregulated production of GM-CSF rather than IL-17 induces spontaneous immunopatho

216 ion in vitro, and that in vivo production of GM-CSF was delayed in the lungs of MR1(-/-) mice.

217 s have measured in vitro innate responses of GM-CSF dendritic cells (DCs) that are functionally disti

218 However, the role of GM-CSF in advanced atherosclerotic plaque progression, t

219 Further studies should explore the role of GM-CSF stimulation to enhance the detection of inflammat

220 of KIR2DS4 on uNK cells led to secretion of GM-CSF and other chemokines, known to promote placental

221 3.1 deficiency led to decreased secretion of GM-CSF from in vitro polarized Th1 and Th17 cells.

222 TNF-alpha (but not IL5, IL-3, eotaxin-1 or GM-CSF) was detected in supernatants of ex vivo eosinoph

223 ported that IL-3 is more potent than IL-5 or GM-CSF in maintaining the ERK/p90S6K/RPS6 ribosome-direc

224 In addition, unlike IL-5 or GM-CSF, IL-3 induced expression of CD32B/C (FCGRIIB/C) s

225 rotic aortas after stimulation with M-CSF or GM-CSF by using quantitative autoradiography.

226 ophages stimulated with M-CSF (MPhiM-CSF) or GM-CSF (MPhiGM-CSF).

227 alone, as well as in combination with LPS or GM-CSF in CS-exposed mice.

228 interaction of HuR and miR-466i orchestrates GM-CSF expression in Th17 cells.

229 nce-labeled specific antibodies against OSM, GM-CSF, and hematopoietic cell-specific markers.

230 both, or placebo; HLA-A2-negative patients, GM-CSF or placebo.

231 the tumor-draining lymph nodes of IL-12 plus GM-CSF-treated tumor-bearing mice revealed that whereas

232 nnate lymphoid cells producing predominantly GM-CSF are expanded in synovial tissues from patients wi

233 ltures of central nervous system ECs produce GM-CSF, G-CSF, IL-6, Cxcl1, and Cxcl2.

234 tion relatively well, whereas mice producing GM-CSF can succumb from left ventricular rupture, a comp

235 wild-type C57BL/6 mice capable of producing GM-CSF and GM-CSF-deficient mice infected with a moderat

236 rate that MAIT cells promote early pulmonary GM-CSF production, which drives the differentiation of i

237 Increased pulmonary GM-CSF production in response to infection is primed by

238 e patients were randomly assigned to receive GM-CSF, PV, both, or placebo; HLA-A2-negative patients,

239 Conversely, administration of recombinant GM-CSF enhanced neutrophil NADPH oxidase function, conid

240 T cell-dependent Ab production, have reduced GM-CSF-specific autoantibody and do not develop PAP.

241 lencing GPR65 in primary CD4 T cells reduces GM-CSF production.

242 To determine whether EGFR regulates GM-CSF as well as key asthma characteristics in vivo, mi

243 y in AEC and demonstrate that EGFR regulates GM-CSF production and the severity of established diseas

244 However, whether HuR regulates GM-CSF expression in Th17 cells has not been fully inves

245 determine whether EGFR signalling regulates GM-CSF production by cultured human AEC in response to H

246 ore, underlying immune mechanisms regulating GM-CSF-specific IgG in aPAP are not well understood.

247 showed that FTY720 triggers MDSCs to release GM-CSF via S1P receptor 3 (S1pr3) through Rho kinase and

248 from monocytes in response to tumor-released GM-CSF.

249 of CD8(+) T lymphocytes and did not require GM-CSF, as mpJX-594 variants that expressed human, mouse

250 fied vaccinia Ankara (MVA) expressing rhesus GM-CSF (MVA/GM-CSF) on the immunogenicity and protection

251 odel is based on the NOD-scid IL2rg(null)SCF/GM-CSF/IL3 (NSG-SGM3) strain of mice engrafted with huma

252 Despite inducing distinct activation states, GM-CSF and M-CSF stimulated progressive but similar leve

253 ted kinase (ERK) in monocytes and subsequent GM-CSF responses.

254 stinal Csf2 expression and elevated systemic GM-CSF cytokine concentrations.

255 idia and demonstrates a benefit for systemic GM-CSF administration.

256 However, therapies that directly target GM-CSF function could lead to undesirable side effects,

257 % CI, -30.2 to +17.6]; P = .61) or more than GM-CSF alone (mean difference, +28.7 m [95% CI, +5.1 to

258 These findings demonstrate that GM-CSF can be used to enhance detection of inflammation.

259 Our data demonstrate that GM-CSF deficiency led to a reduction in: 1) total lung l

260 Results demonstrate that GM-CSF is required for cholesterol clearance in macropha

261 In this study, we demonstrated that GM-CSF signaling plays an essential role in antifungal d

262 In this work, we provide evidence that GM-CSF drives CCL17 production by acting through an IFN

263 These findings support the hypothesis that GM-CSF and MMP9 promote the protumorigenic effect of WAT

264 therapeutic target, bolstering the idea that GM-CSF is a major orchestrator of the leukocyte supply c

265 These findings indicate that GM-CSF can mediate inflammation and pain by regulating I

266 Our data indicate that GM-CSF drives chronic tissue damage and disability in EA

267 In this study, we show that GM-CSF augments the accumulation of MOG35-55-specific T

268 Collectively, these results show that GM-CSF promotes the local differentiation, accumulation,

269 We previously showed that GM-CSF protects against progressive fungal disease using

270 Mice that lack the GM-CSF receptor beta chain (GM-CSFRbeta) developed invas

271 Ablation of the GM-CSF receptor alleviated the monocyte response and inh

272 immunized with the parent virus LBNSE or the GM-CSF-expressing RABV (LBNSE-GM-CSF).

273 mediated immune diseases and it suggests the GM-CSF-eosinophil axis as an attractive therapeutic targ

274 a distinct subpopulation of cells within the GM-CSF bone marrow-derived DC culture based on their abi

275 nes and chemokines, whereas therapeutically, GM-CSF blockade markedly reduces cardiac disease.

276 These GM-CSF-educated cancer cells exhibit enhanced ability of

277 F promotes M. tuberculosis clearance through GM-CSF-dependent mechanisms and enhances host defense ag

278 at chronic exposure of colon cancer cells to GM-CSF, which harbor its receptor, leads to occurrence o

279 signaling as an intrinsic pathway central to GM-CSF priming-induced eosinophil tissue migration.

280 We also showed that Sema4D was comparable to GM-CSF in its induction of MDSC.

281 ) Th17 cells, and that HuR binds directly to GM-CSF mRNA 3'UTR.

282 ophils undergo necroptosis after exposure to GM-CSF followed by the ligation of adhesion receptors su

283 expression is up-regulated after exposure to GM-CSF or the Dectin-1 agonist zymosan.

284 enefits of exercise but do not support using GM-CSF to treat walking impairment in patients with PAD.

285 ot correctly localized to the alveoli, where GM-CSF is produced.

286 rive dendritic cell differentiation, whereas GM-CSF alone leads to macrophage differentiation.

287 ed with attention control + placebo, whereas GM-CSF did not significantly improve walking performance

288 ared with GM-CSF alone; to determine whether GM-CSF alone improves 6-minute walk more than placebo an

289 To determine whether GM-CSF combined with supervised treadmill exercise impro

290 lular and molecular mechanisms through which GM-CSF enhances antifungal host defenses, we investigate

291 mpared with exercise alone and compared with GM-CSF alone; to determine whether GM-CSF alone improves

292 anti-inflammatory Mvarphis upon culture with GM-CSF or M-CSF, respectively (subsequently referred to

293 f), when CD4(+) T-cells are co-cultured with GM-CSF derived bone marrow dendritic cells (G-BMDCs).

294 rom human monocytes cultured for 7 days with GM-CSF and IL-6.

295 ined from monocytes cultured for 5 days with GM-CSF+IL-4 or isolated from peripheral blood (CD1c+ DC)

296 bone marrow-derived DCs differentiated with GM-CSF or treating them with soluble OX40 L and JAG1 in

297 Incubation of human macrophages with GM-CSF resulted in increased glycolysis and increased 2-

298 Treatment of mice with GM-CSF increased MDSC accumulation, and adoptive transfe

299 treatment mimicked the effects observed with GM-CSF neutralization and MMP9 inhibition, suggesting th

300 Without GM-CSF signaling, surfactant-exposed macrophages massive