ライフサイエンスコーパス: GM-CSF

1 GM-CSF activates IRF5 in vitro and in vivo and can be ad

2 GM-CSF and IL-3 belong to the beta common (betac/CD131)

3 GM-CSF and IL-5 stimulation demonstrated redundancy in e

4 GM-CSF can be secreted by multiple cell types, whereas I

5 GM-CSF causes accumulation of eosinophils, neutrophils a

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

7 GM-CSF intrinsically promotes eosinophil accumulation in

8 GM-CSF is produced by gammadelta T cells via macrophage

9 GM-CSF is required for alveolar macrophage (AM) developm

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

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

12 GM-CSF triggered TGFbeta1 expression by M2 TAMs by activ

13 GM-CSF, but not M-CSF, increased the expression of both

14 GM-CSF, but not M-CSF, reinforced the cellular identity,

15 GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes an

16 GM-CSF-induced MCP-1/CCR2 signaling plays an important r

17 GM-CSF-receptor is increased on HSCs and multipotent pro

18 GM-CSF/IL-3(+) B1 B cells originate in the spleen of inf

19 PD reduced IL-6, MCP-1, GM-CSF, and IFN-gamma in brains of WT mice and reduced I

20 populations of both low-frequency (IL-10(+); GM-CSF(+)) and high-frequency (TNF(+)) cytokine-defined

21 duction of TNF-alpha, IL-6, IL-12p70, IL-10, GM-CSF, VEGF, MIP-1beta, TNF-beta, IFN-alpha2 and IL-7 i

22 6, IL-10, MCP-1, sVCAM-1, MIP-1alpha, IP-10, GM-CSF, M-CSF, TNF-alpha, IFN-gamma, VCAM-1, ICAM-1, PD-

23 oduction of IL-17A, IFN-gamma, IL-10, IP-10, GM-CSF, sFasL, Granzyme A, Granzyme B, Granulysin, and P

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

25 ssays revealed that IL-11 induces IL-17A(+), GM-CSF(+), and IL-21(+)CD4(+) myelin Ag-reactive cells.

26 Blocking IL-1beta, GM-CSF or caspase activation eliminated the type-2 skew

27 ure was also inversely correlated with IL-2, GM-CSF, and eotaxin production to Toll-like receptor lig

28 AML cells, but only in mice producing IL-3, GM-CSF, and SCF transgenically or in regular mice in whi

29 ere cultured in the presence of IL-3, IL-33, GM-CSF, thymic stromal lymphopoietin, or IL-25.

30 mulated NFkappaB activation and boosted IL-4/GM-CSF induced expression of surface markers CD14 and CD

31 The peptides also boosted IL-4/GM-CSF induction of CD14, while only MVWGP and TGSYTEGWS

32 Virus infection prevented IL-6/GM-CSF-mediated differentiation of myeloid suppressors,

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

34 tudies have demonstrated the importance of a GM-CSF->IFN regulatory factor 4 (IRF4)->CCL17 pathway, f

35 It has been reported that a GM-CSF->CCL17 pathway, originally identified in vitro in

36 Previously, our group has shown that a GM-CSF-secreting allogenic pancreatic tumor cell vaccine

37 fering from rheumatoid arthritis underwent a GM-CSF-independent necroptosis following CD44 ligation;

38 for inflammatory pain development in which a GM-CSF->CCL17 pathway appears critical, nerve growth fac

39 In addition, GM-CSF IRF4 signaling upregulated MHC class II expressio

40 In addition, GM-CSF promoted indirect alloantigen presentation, resul

41 d better in patient-derived xenografts after GM-CSF neutralization with lenzilumab.

42 Although GM-CSF has been widely used in dendritic cell (DC) resea

43 sessment, serum CXCL10/IP-10 (P = 0.047) and GM-CSF (P = 0.050) were higher and nasopharyngeal RT-PCR

44 le cytokines including IL6, IL17, MCP-1, and GM-CSF in the tumor-bearing host, and persisted as memor

45 sed serum concentrations of CXCL10/IP-10 and GM-CSF, together with higher nasopharyngeal SARS-CoV-2 v

46 he production of IL-5, IL-6, IL-9, IL-13 and GM-CSF by ILC2 in response to IL-33, with inhibition of

47 matory cytokines: interleukin-17 (IL-17) and GM-CSF.

48 nd IL-23R and secreted IFN-gamma, IL-17, and GM-CSF in response to canonically restricted peptide ant

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

50 int inflammation via production of IL-18 and GM-CSF.

51 mon beta subunit receptor with both IL-5 and GM-CSF but, through alpha-subunit-specific properties, u

52 DIN was administered IV (days 2-5), and GM-CSF was administered subcutaneously (days 6-12).

53 sis could be due to released IL-3, IL-5, and GM-CSF found in supernatants.

54 Neutrophil dysfunction and GM-CSF auto-antibodies are observed in pediatric and adu

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

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

57 produce IL-17A, interferon (IFN)-gamma, and GM-CSF, increasing the susceptibility of the recipients

58 ulocyte colony-stimulating factors (GCSF and GM-CSF) enhance swarming and neutrophil ability to restr

59 virus that coexpresses a PD-L1 inhibitor and GM-CSF.

60 IL-8, MMP9, and GM-CSF were measured by ELISA in HBEC and neutrophils.

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

62 eutrophil accumulation in target organs, and GM-CSF prophylactic or therapeutic blockade substantiall

63 herapeutic target in asthmatic patients, and GM-CSF has been suggested to control various aspects of

64 ted the IL-1beta-induced release of TSLP and GM-CSF, suggesting that the ability of PKM2 to phosphory

65 s in thymic stromal lymphopoietin (TSLP) and GM-CSF in primary tracheal epithelial cells isolated fro

66 Wild-type and GM-CSF receptor alpha (Csf2ra)-deficient mice reconstitu

67 Blockade of CXCL-11 abrogated anti-GM-CSF treatment and induced inflammatory monocytes.

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

69 Our findings show that anti-GM-CSF treatment induces modulatory monocytes that act i

70 Cytokines, such as GM-CSF, IFN-gamma, and IL-3, which are typically found i

71 Thus, Bhlhe40+ GM-CSF+ CD4+ T cells constitute a colitogenic T-cell pop

72 We demonstrate that blocking GM-CSF makes macrophages more permissive of Mtb growth w

73 ciency in GM-CSF or IL-5 alone, loss of both GM-CSF and IL-5 signaling impaired protection against H.

74 networks including genes responding to both GM-CSF and IL-4, which had a higher centrality value in

75 develop via a specific pathway activated by GM-CSF, independent of cDC-restricted (CDP) and monocyte

76 IL-10 counterregulates IRF5 activation by GM-CSF.

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

78 nts of the antimicrobial response induced by GM-CSF.

79 this study, we compared their modulation by GM-CSF and M-CSF in murine primary AMs and IMs.

80 ce accompanied by high levels of circulating GM-CSF and TGFbeta1.

81 TNBC cells lowered the levels of circulating GM-CSF, suppressed TAM recruitment, and decreased the le

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

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

84 IL-17, CCL2, CCL3, CCL4, CCL5, CCL11, G-CSF, GM-CSF and TNF-alpha.

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

86 n the CeA, and a profile of increased G-CSF, GM-CSF, IL-13, IL-6, IL-17a, leptin, and IL-4 that discr

87 4, CCL11, CXCL1, CXCL2, CXCL5, CXCL9, G-CSF, GM-CSF, VEGF, and M-CSF) and chemokine receptors on MDSC

88 We identified Csf2/GM-CSF as a primary complement-dependent inflammatory me

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

90 ut rather via the production of the cytokine GM-CSF, another factor with an established regulatory ro

91 strongly express receptors for the cytokine GM-CSF.

92 The beta common chain cytokines GM-CSF, IL-3, and IL-5 regulate varied inflammatory resp

93 common beta (CSF2RB) chain family cytokines GM-CSF and IL-5.

94 vated their expression of the Th17 cytokines GM-CSF and IL-17F.

95 ented toxicity, whereas perforin deficiency, GM-CSF deficiency, or modulation of the myeloid populati

96 Taken together, we uncover T cell-derived GM-CSF as a key inducer of the chemokine CCL22 and thus,

97 secretion, and we identified T cell-derived GM-CSF as the major inducer of DC-derived CCL22 expressi

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

99 atients were nonrandomly assigned to I/T/DIN/GM-CSF (August 2016 to May 2017).

100 e patients were randomly assigned to I/T/DIN/GM-CSF (February 2013 to March 2015); 36 additional pati

101 I/T/DIN/GM-CSF has significant antitumor activity in patients wi

102 survival for all patients receiving I/T/DIN/GM-CSF were 67.9% +/- 6.4% (95% CI, 55.4% to 80.5%) and

103 acrophage colony-stimulating factor (I/T/DIN/GM-CSF) demonstrated activity in patients with relapsed/

104 d cohort was nonrandomly assigned to I/T/DIN/GM-CSF.

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

106 Transplantation of either GM-CSF or Bhlhe40 knockout donor T cells resulted in sig

107 in ZIP macrophages in the absence of either GM-CSF or IRF4, thus supporting the presence of the new

108 ealthy volunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h.

109 e to mutations in CSF2RA or CSF2RB, encoding GM-CSF receptor subunits); secondary PAP results from va

110 We additionally measured endogenous GM-CSF and IL6 in human serum from n = 14 human subjects

111 Conversely, blockage of endogenous GM-CSF with antibody treatment not only inhibited the in

112 ng proteins (IL-4, 5, 10, 13, 17 A, Eotaxin, GM-CSF, IFNy, MCP-1, TARC, TNFalpha, Total IgE, and Endo

113 Furthermore, we found that exogenous GM-CSF administration improves sepsis survival through e

114 locyte-macrophage colony-stimulating factor (GM-CSF) (6.6-fold), RANTES (14.8-fold), and interferon g

115 locyte-macrophage colony-stimulating factor (GM-CSF) (encoded by Csf2) is a key communicator between

116 locyte-macrophage colony-stimulating factor (GM-CSF) adjuvant or 200 mug GM-CSF alone six times at 14

117 locyte-macrophage colony-stimulating factor (GM-CSF) and C-C motif chemokine ligand 2 (CCL2), both of

118 locyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-3 (IL-3), have not received much

119 locyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4).

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

121 nulocyte-monocyte colony-stimulating factor (GM-CSF) and occurred in a Stat5-dependent manner.

122 locyte-macrophage colony-stimulating factor (GM-CSF) as a potential strategy to manage CART19 cell-as

123 locyte-macrophage colony-stimulating factor (GM-CSF) as well as transcription factor T-bet.

124 locyte-macrophage colony-stimulating factor (GM-CSF) for concentrating dendritic cells (DCs), CpG oli

125 locyte-macrophage colony stimulating factor (GM-CSF) has been identified as a cytokine that mediates

126 locyte-macrophage colony-stimulating factor (GM-CSF) has many more functions than its original in vit

127 locyte-macrophage colony stimulating factor (GM-CSF) in nociceptor activation in male and female mice

128 locyte-macrophage colony-stimulating factor (GM-CSF) in vitro.

129 locyte-macrophage colony-stimulating factor (GM-CSF) is a multipotent cytokine that prompts the proli

130 locyte-macrophage colony-stimulating factor (GM-CSF) production by CD4(+) T cells.

131 locyte-macrophage colony-stimulating factor (GM-CSF) promote graft-versus-host disease (GVHD) by recr

132 locyte-macrophage colony-stimulating factor (GM-CSF) signalling and can be autoimmune (caused by elev

133 locyte-macrophage colony-stimulating factor (GM-CSF) signalling in astrocytes drives the expression o

134 locyte-macrophage colony-stimulating factor (GM-CSF), a myelopoietic growth factor and pro-inflammato

135 locyte-macrophage colony-stimulating factor (GM-CSF), and stem cell factor (SCF) on the experimental

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), signaling.

138 locyte-macrophage colony-stimulating factor (GM-CSF), the Toll-like-receptor-9 agonist cytosine-guano

139 locyte-macrophage colony stimulating factor (GM-CSF), through deregulation of the expression of cell-

140 locyte-macrophage colony-stimulating factor (GM-CSF)-CC-chemokine ligand 17 (CCL17) chemokine axis, o

141 locyte-macrophage colony-stimulating factor (GM-CSF)-induced CD103(+) DC differentiation by suppressi

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

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

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

145 locyte-macrophage colony-stimulating factor [GM-CSF], CCL3, CCL5, and CXCL9) or T cell modulatory (IL

146 ntrations of EGF (epithelial growth factor), GM-CSF, IL-10, CCL2/MCP-1, CCL3/MIP-1a, CXCL10/IP-10, CC

147 addition to its effects as a growth factor, GM-CSF plays an important role in chronic inflammatory a

148 gnificant preclinical data have emerged from GM-CSF deletion/depletion approaches indicating that GM-

149 In contrast, conditioned medium from GM-CSF-treated murine macrophages was able to drive noci

150 e we established the absence of a functional GM-CSF receptor in murine nociceptors, and suggest an in

151 -8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamma, GM-CSF, MIP-1alpha, and Eotaxin-1 in patients with MDD b

152 Finally, we generated GM-CSF-deficient CART19 cells through CRISPR/Cas9 disrup

153 but the transcriptional program that governs GM-CSF production and the mechanism by which GM-CSF link

154 a key transcriptional regulator that governs GM-CSF production by CD4+ T cells and mediates pathologi

155 evel of FGL2 expression with concurrent high GM-CSF expression is associated with higher CD8B express

156 n autoimmune disease, it remains unclear how GM-CSF is regulated at sites of tissue inflammation.

157 lammatory roles of these cytokines; however, GM-CSF also participates in the resolution of inflammati

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

159 The authors identified GM-CSF secretion in a rare population of CD11c(+) CD4(+)

160 filing of GEM-treated tumor cells identifies GM-CSF as one of the most differentially expressed cytok

161 duce two or more of the cytokines, IFNgamma, GM-CSF, and IL-17.

162 In GM-CSF-deficient (Csf2(-/-)) mice, inflammation resoluti

163 tor ZBTB46 and prolonged STAT5 activation in GM-CSF cultures.

164 In contrast to deficiency in GM-CSF or IL-5 alone, loss of both GM-CSF and IL-5 signa

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

166 eal that the expression of genes involved in GM-CSF signaling discriminates between the two subpopula

167 expression), with IRF4 levels being lower in GM-CSF(-/-) ZIP macrophages than in the WT cells.

168 with apoptotic cells significantly increased GM-CSF production and T(H)2 cell differentiation.

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

170 by an agonistic anti-DR3 antibody increases GM-CSF production from ILC3s through the p38 MAPK pathwa

171 Siglec-7 cross-linking inhibited GM-CSF-induced release of eosinophil peroxidase, TNF-alp

172 n Kit inhibition, which reduces intratumoral GM-CSF, leading to the accumulation of Batf3-lineage DC

173 Intriguingly, GM-CSF signaling amplifies inflammatory cytokine product

174 tly in macrophage lineage populations and is GM-CSF dependent, 2) for its action in arthritic pain an

175 odels, the cellular CCL17 expression and its GM-CSF dependence as well as the function of CCL17 in in

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

177 taining protein (CIS) is crucial in limiting GM-CSF signaling not only during inflammatory arthritis

178 associated damaging coding variants with low GM-CSF induced STAT5 stimulation index (GMSI) in pediatr

179 To systematically study and manipulate GM-CSF(+) cells and their progeny in vivo, we generated

180 nnexinV-FITC/7-AAD staining and by measuring GM-CSF-induced mediator release in culture supernatants.

181 Mechanistically, GM-CSF had no adverse effect on regulatory T-cell recons

182 In comparison with WT mice, GM-CSF(-/-) and Irf4(-/-) mice had a reduced ZIP respons

183 its expression of proinflammatory molecules, GM-CSF, and ERK-2, promoting immune homeostasis.

184 rmore, DCs from IL-9R(-/-) mice induced more GM-CSF production by T cells and exacerbated EAE upon ad

185 mulating factor (GM-CSF) adjuvant or 200 mug GM-CSF alone six times at 14-day intervals and then quar

186 strongly enhances differentiation of murine GM-CSF-derived DCs.

187 ibution of non-coding variants in neutrophil GM-CSF signaling and the potential importance of RCL1 an

188 ients and implicated variation of neutrophil GM-CSF signaling in cell function and disease complicati

189 aft model of CRS and neuroinflammation (NI), GM-CSF neutralization resulted in a reduction of myeloid

190 stream of RIG-I, IFN-beta, and IL-4, but not GM-CSF, signaling.

191 eletion of NK cells, or specific ablation of GM-CSF production in NK cells, abrogated disease.

192 L-23 induces loss of ILC3s in the absence of GM-CSF.

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

194 However, the comparative actions of GM-CSF and M-CSF on AMs are incompletely understood.

195 s demonstrate that the activating actions of GM-CSF and M-CSF on primary AMs are not conserved in pri

196 e permissive of Mtb growth while addition of GM-CSF increases bacterial control.

197 er of wild-type T cells or administration of GM-CSF.

198 pective discusses the pleiotropic biology of GM-CSF and the scientific merits behind these contrastin

199 Blockade of GM-CSF or IL-23 reverses anti-DR3 antibody-driven ILC3 l

200 teases in CD44-mediated necroptotic death of GM-CSF-primed human neutrophils.

201 RT19 cells through CRISPR/Cas9 disruption of GM-CSF during CAR-T cell manufacturing.

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

203 irway inflammation to evaluate the effect of GM-CSF signaling deficiency on asthmatic inflammation in

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

205 Key features of GM-CSF biology need to be defined better, such as the re

206 can abrogate GEM-induced hyperexpression of GM-CSF in E0771 cells.

207 increasing recognition of the importance of GM-CSF in autoimmune disease, it remains unclear how GM-

208 the peritoneal cavity occurs independent of GM-CSF, indicating organ specificity.

209 Both administration and inhibition of GM-CSF are currently being therapeutically tested in COV

210 Blockade or knockdown of GM-CSF can partially reduce immunosuppression of Ly6C(hi

211 Knockdown of GM-CSF in tumor cells also delays tumor progression with

212 the ZIP macrophages was altered by a lack of GM-CSF or IRF4 (increased IL-10 secretion and Arg1 mRNA

213 microenvironment by decreasing the level of GM-CSF in tumors while modulating protumoral IL-1alpha,

214 be autoimmune (caused by elevated levels of GM-CSF autoantibodies) or hereditary (due to mutations i

215 g (IRISOE) TNBC cells secrete high levels of GM-CSF in a hypoxia-inducible factor-1alpha (HIF1alpha)-

216 The specific loss of GM-CSF signaling or IRF5 expression in the eosinophil co

217 Loss of GM-CSF signalling or genetic susceptibility to TB (C3HeB

218 eady-state differentiation and maturation of GM-CSF-dependent DCs are insufficiently known.

219 Furthermore, the neutralization of GM-CSF reduced cDC2s activation.

220 -) mice correlates with increased numbers of GM-CSF(+) CD4(+) T cells and inflammatory dendritic cell

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

222 emonstrate that monocytes in the presence of GM-CSF, TGF-beta1, and the Notch ligand DLL4 differentia

223 malaria, we report a sustained production of GM-CSF and IL-3 from IgM(+) and IgM(-)/IgG(+) CD138(+) B

224 Synovial NK cell production of GM-CSF is IL-18-dependent.

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

226 characterize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating

227 However, the molecular properties of GM-CSF-producing cells and the mode of Csf2 regulation i

228 nsing flagellin, AECs trigger the release of GM-CSF in a TLR5-dependent fashion and the doubling of t

229 part of the antistreptococcal repertoire of GM-CSF differentiated MPhi in vitro and in vivo and deli

230 ivo, we generated a fate-map and reporter of GM-CSF expression mouse strain (FROG).

231 We sought to elucidate the role of GM-CSF signaling in asthmatic inflammation.

232 However, to date, the role of GM-CSF signaling in eosinophils in vivo is largely uncle

233 e lymphoid cells, mast cells are a source of GM-CSF in this model, and its pathogenic production is p

234 relating with potential isotype switching of GM-CSF- and IL-3-producing IgM(+) B1 B cells.

235 dentified monocytes as the primary target of GM-CSF; however, its effect on monocyte activation has b

236 Specifically, GH treatment of GM-CSF-primed monocyte-derived macrophages promotes a si

237 immunosuppression in TME via upregulation of GM-CSF and efferocytosis as well as deregulation of lipi

238 ge numbers and their phenotype can depend on GM-CSF- and IRF4-dependent signaling independently of CC

239 These findings shed new light on GM-CSF biology in sterile tissue inflammation and identi

240 Finally, Siglec-7 cross-linking on GM-CSF-activated eosinophils induced phosphorylation of

241 e in which the cells were exposed to IL-3 or GM-CSF delivered using a cotransduction strategy.

242 implicated in asthma) but not IL-5, IL-9 or GM-CSF in response to IL-33.

243 on of monocytes to macrophages with M-CSF or GM-CSF strongly up-regulated full-length Dicer.

244 ctly stimulate myelopoiesis such as G-CSF or GM-CSF.

245 ical damage within the GI tract, positioning GM-CSF as a key regulator of GVHD in the colon and a pot

246 in activating dendritic cells and positions GM-CSF-producing T cells as a critical link between inna

247 mice, we show that synovial NK cells produce GM-CSF in autoantibody-mediated inflammatory arthritis.

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

249 increased the generation of those producing GM-CSF.

250 -CSF, TGF-beta-treated) and proinflammatory (GM-CSF-treated) human monocyte-derived macrophages and m

251 patients, pathogenesis is driven by reduced GM-CSF-dependent cholesterol clearance in alveolar macro

252 infected macrophages correlates with reduced GM-CSF secretion.

253 of encephalitogenic Th17 cells by regulating GM-CSF via Bhlhe40 and inhibiting PD-1 expression.

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

255 Th17 cells that secrete GM-CSF are pathogenic and drive inflammation of the CNS.

256 Previous studies have suggested GM-CSF might directly activate neurons.

257 autoimmune neuroinflammation by suppressing GM-CSF production by CD4(+) T cells through the modulati

258 ics and current issues/questions surrounding GM-CSF biology.

259 ased therapies are in development, targeting GM-CSF signalling, immune modulation and cholesterol hom

260 Clinical trials targeting GM-CSF or its receptor have shown encouraging efficacy a

261 ment and reactivation into a pathogenic Th17/GM-CSF phenotype.

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

263 We demonstrate that GM-CSF signaling, although being largely dispensable for

264 sets (e.g., Th1 and Th17), highlighting that GM-CSF expression not only marks pathogenic Th cells, bu

265 D-induced colonic pathology, indicating that GM-CSF constitutes a nonredundant inflammatory pathway i

266 eletion/depletion approaches indicating that GM-CSF is a potential target in many inflammatory/autoim

267 In addition, we observed that GM-CSF was not regulated by either interleukin 6 (IL-6)

268 We report that GM-CSF applied directly to magnetically purified nocicep

269 These data reveal that GM-CSF and IL-3 are produced during malaria infections,

270 ytometry and ELISA experiments revealed that GM-CSF blockage in monocytes stimulated production of th

271 using flow cytometry and ELISA we show that GM-CSF induces an inflammatory profile in human monocyte

272 We show that GM-CSF induces chemokinesis and promotes eosinophil surv

273 In this study, we show that GM-CSF neutralization with lenzilumab does not inhibit C

274 Furthermore, we show that GM-CSF promotes extramedullary myelopoiesis, tissue-toxi

275 cate that during pulmonary immunization, the GM-CSF released by AECs orchestrates the cross-talk betw

276 ls in tumor control in CRC and introduce the GM-CSF-IRF5 axis as a critical driver of the antitumor a

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

278 Previously, we reported that the GM-CSF/JAK2/STAT3 axis drives liver-associated MDSC (L-M

279 rovides a key brake on signaling through the GM-CSF receptor.

280 These GM-CSF(k/o) CAR-T cells maintained normal functions and

281 ovel approach to abrogate NI and CRS through GM-CSF neutralization, which may potentially enhance CAR

282 studies exploring the macrophage response to GM-CSF or IL4, activated LXR repressed IRF4 expression,

283 fficacy of miltefosine combined with topical GM-CSF (M+GM) versus miltefosine and placebo (M+P) versu

284 ng Mycobacterium tuberculosis infection upon GM-CSF blockade.

285 Using GM-CSF fate reporter mice, we show that synovial NK cell

286 ll infiltrate, and persistent arthritis, via GM-CSF production, as deletion of NK cells, or specific

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

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

289 GM-CSF production and the mechanism by which GM-CSF links adaptive to innate immunity within this tis

290 Treatment of coinfected cells with GM-CSF restores bacterial control.

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

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

293 ynamics in mixed mouse MPhi/DC cultures with GM-CSF, which requires snapshot definition of cellular i

294 The association of Miltefosine with GM-CSF do not improve therapeutic outcome.

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

296 ith birch pollen allergy and stimulated with GM-CSF, IFN-gamma, and IL-3.

297 eosinophils after in vitro stimulation with GM-CSF or IL-5.

298 to 6 increased 50% in patients treated with GM-CSF alone and decreased 23% in patients treated with

299 A combined treatment with GM-CSF and miltefosine was tested to increase the cure r

300 ay 0) was induced in C57BL/6 wild-type (WT), GM-CSF(-/-) , Irf4(-/-) , and Ccl17(E/E) mice.