ライフサイエンスコーパス: IL-3

1 IL-3 also enhances osteoblast differentiation and bone f

2 IL-3 also influences IFN-gamma, CXCL9, and G-CSF product

3 IL-3 amplified the number of PC in vitro, and acted syne

4 IL-3 and GM-CSF were similar to each other with half of

5 IL-3 deficiency protects mice against sepsis.

6 IL-3 efficiently inhibited apoptosis of 32Dp210K/R+Abl c

7 IL-3 increases the expression of mouse chondrocyte-speci

8 IL-3 receptor expression was dramatically up-regulated i

9 IL-3 was largely produced by CD4(+)CD49b(+)NK1.1(-) effe

10 IL-3-dependent, conditional Hoxb8-immortalized progenito

11 IL-3-deprivation induces apoptosis correlating with upre

12 IL-3-driven basophil expansion depended on STAT5 signali

13 IL-3/IFN-gamma marginally up-regulated HLA-DR.

14 gnificantly elevated levels of GM-CSF, IL-2, IL-3, and IFN-gamma.

15 aluated the expression of the interleukin 3 (IL-3) receptor alpha subunit (CD123), an established mar

16 rrow were increased by either interleukin 3 (IL-3) treatment or by adoptive basophil transfer before

17 FGFR1, and NPM/ALK as well as interleukin 3 (IL-3), granulocyte-macrophage colony-stimulating factor

18 e-macrophage (GM)-CSF, G-CSF, interleukin-3 (IL-3) and erythropoietin and decreased their activity.

19 sing Hoxb8 in the presence of interleukin-3 (IL-3) and outgrowing cell lines selected for their poten

20 calin family, is induced upon interleukin-3 (IL-3) deprivation and plays a pivotal role in induction

21 imulating factor (GM-CSF) and interleukin-3 (IL-3) manifest insulitis, destruction of insulin-produci

22 e we report that the cytokine interleukin-3 (IL-3) potentiates inflammation in sepsis.

23 Interleukin-3 (IL-3) regulates cell growth by affecting various process

24 The contribution of interleukin-3 (IL-3), a hematopoietic growth factor and immunoregulator

25 signaling is investigated in interleukin-3 (IL-3)-dependent 32D murine myeloid cells.

26 y of extracellular glutamine, interleukin-3 (IL-3)-dependent cells were unable to maintain TCA cycle

27 protein by screening a murine interleukin-3 (IL-3)-dependent NFS/N1.H7 myeloid cell cDNA library.

28 SF1R fusion protein conferred interleukin-3 (IL-3)-independent growth in BaF3 cells, and induces a my

29 ient mice are unresponsive to interleukin-3 (IL-3)-induced maturation signals, and this correlates wi

30 by stem cell factor (SCF) and interleukin-3 (IL-3).

31 otherapy and to withdrawal of interleukin-3 (IL-3).

32 nhibit the differentiation of interleukin-3 (IL-3)/stem cell factor (colony-forming unit [CFU]-IL3)-d

33 stimulating factor [GM-CSF], interleukin-3 [IL-3], and granulocyte-CSF [G-CSF]) within 7 immunopheno

34 We establish that, unlike GM-CSF or IL-5, IL-3 triggers prolonged signaling through activation of

35 The cytokines IL-5, IL-3, and GM-CSF are crucial for eosinophil development,

36 sinophil-activating cytokines, such as IL-5, IL-3, and GM-CSF, are typically present in atopic diseas

37 portance of targeting ICAM-1 and GM-CSF/IL-5/IL-3 receptor systems as a therapeutic strategy to count

38 Src family member Lyn before cytokine (IL-5/IL-3) priming of blood eosinophils inhibited the synergi

39 on, and production of some cytokines (TNF-a, IL-3) but not others (MCP-1, IL-4).

40 Signaling studies indicate that the BCR-ABL/IL-3 receptor+ NIH 3T3 cells utilize the Gab2/PI-3 kinas

41 Accordingly, IL-3- or IL-33-activated basophils amplified IL-17 relea

42 In addition, IL-3-induced STAT5 activation upregulated the expression

43 Additionally, IL-3 directly activates basophils for IL-13 secretion an

44 that failed to initiate cell division after IL-3 add back.

45 rivation and JAK2-STAT5 overactivation after IL-3 treatment.

46 ional stimuli in vitro, producing IFN-alpha, IL-3, IL-6, IL-12, TNF-alpha, CCL2, CCL3, CCL5, and CXCL

47 Although IL-3 is commonly recognized for its growth factor-like a

48 B activation and reduced the viability of an IL-3-dependent hematopoietic cell line.

49 ctly through TSLPR and indirectly through an IL-3-mediated basophil autocrine loop.

50 1alpha (Spearman's rho 0.242, P = 0.009) and IL-3 (rho 0.189, P = 0.043) responses after TNF-alpha/IL

51 SOCS2 can enhance interleukin-2 (IL-2)- and IL-3-induced STAT phosphorylation following and potentia

52 are required for IL-13 production: IL-33 and IL-3.

53 was shown, on the basis of GM-CSF, IL-5, and IL-3 detection assays, Ab neutralization, and sensitivit

54 astic stromal cells (c-Kit ligand, IL-6, and IL-3) shifted the cultures toward myelopoiesis.

55 formation as well as natural killer cell and IL-3 signaling.

56 ed because mice deficient in both GM-CSF and IL-3 also responded to IL-7 with increased myelopoiesis.

57 e mice faithfully expressed human GM-CSF and IL-3 and developed pulmonary alveolar proteinosis becaus

58 paired hematopoietic responses to GM-CSF and IL-3 in patients with T1D and in NOD mice, indicate that

59 at IL-7 treatment in vivo induced GM-CSF and IL-3 production by T cells with memory phenotype.

60 t produce myelopoietic cytokines (GM-CSF and IL-3), and these effector CD4(+) T cells are induced fro

61 etic growth factors, particularly GM-CSF and IL-3.

62 mma and the beta-common cytokines GM-CSF and IL-3.

63 phage-colony stimulating factor (GM-CSF) and IL-3 genes in hematopoietic cells.

64 ends the half-life of TNF-alpha, GM-CSF, and IL-3 mRNA, as well as a chimeric beta-globin mRNA report

65 uced by cytokines such as M-CSF, GM-CSF, and IL-3.

66 3 (10-fold) when cocultured with A549 EC and IL-3, without exogenous allergen or IgE cross-linking st

67 tion in the presence of stem cell factor and IL-3.

68 luding in response to type I interferons and IL-3.

69 discovered a decrease in IL-3 production and IL-3-dependent mast cell development in Batf(-/-) mice.

70 ells represses KIT-induced proliferation and IL-3-mediated maturation by inhibiting the expression of

71 vation inhibited phosphorylation of RPS6 and IL-3-enhanced semaphorin-7A translation.

72 nerate mast cells when stimulated by SCF and IL-3, and, of these, the most active were those in the C

73 ells after a further incubation with SCF and IL-3.

74 Coexpression of MN1-TEL and IL-3, but not SCF, rapidly caused a fatal myeloprolifera

75 hibited in the presence of neutralizing anti-IL-3 receptor (CD123) Abs.

76 found that the IL-3 complex (IL-3 plus anti-IL-3 Ab) greatly facilitated the differentiation of GMPs

77 We predict that autocrine IL-3 activity resulting from low-level IgE/FcepsilonRI c

78 We show that in human basophils, IL-3 but no other stimulus induces de novo expression of

79 TSLP could elicit basophil responses in both IL-3-IL-3R-sufficient and -deficient environments, and g

80 IL-3 receptor expression was not affected by IL-3 or STAT5.

81 ng differential activation of eosinophils by IL-3, GM-CSF, and IL-5.

82 The increased RANKL expression by IL-3 induces mononuclear osteoclasts; however, it does n

83 role of c-Abl in Jak2 activation induced by IL-3 cytokine growth factor in 32D hematopoietic cells.

84 c-Abl kinase activity induced by IL-3 is required for IL-3-stimulated Jak2 and Jak1 activ

85 S159 phosphorylation of MCL-1 was induced by IL-3 withdrawal or PI3K inhibition and prevented by AKT

86 by HRF/TCTP is distinct from that induced by IL-3.

87 ts noted that CD32b could be up-regulated by IL-3 (3- to 12-fold).

88 and activators of transcription 5 (STAT5) by IL-3 inhibits RANKL-induced osteoclastogenesis through t

89 es of both c-Abl and Jak2 were stimulated by IL-3 in 32D cells.

90 ssion; and serum markers (CCL2, CCL5, CCL11, IL-3, and thymic stromal lymphopoietin) at 3 time points

91 basophil mobilization despite intact T-cell IL-3 production, and supplementation of mice with immune

92 ogenous population of early apoptotic cells (IL-3 deprived BaF3 cells), we show that iC3b opsonized a

93 e induction of Ccn3/Nov in control KL cells, IL-3 alone could induce Ccn3/Nov mRNA in control KL and

94 ional heterogeneity exists between classical IL-3-elicited basophils and thymic stromal lymphopoietin

95 We found that the IL-3 complex (IL-3 plus anti-IL-3 Ab) greatly facilitated the differen

96 Each mutant conferred IL-3 factor-independent proliferation to Ba/F3 cells, an

97 Stimulation with a mixture containing IL-3, IL-6, stem cell factor, thrombopoietin, and Flt3 l

98 fy regions of the locus required for correct IL-3 gene expression.

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

100 uced by NK cells or cytokines (e.g., GM-CSF, IL-3).

101 equired a combination of Abs against GM-CSF, IL-3, and anti-Flt3 ligand to achieve maximum neutraliza

102 GM-CSF, IL-3, and IL-5 are proinflammatory cytokines that contro

103 hroid cells in either normal, Rag1 or GM-CSF-IL-3-deficient mice, suggesting that IL-7 might directly

104 Whereas cultured IL-3-dependent murine MCs from wild-type mice were resis

105 al cells with the basophil-specific cytokine IL-3 (0.01-10 ng/ml) promoted basophil and eosinophil, b

106 this study, we demonstrate that the cytokine IL-3 induces the activation of the Ca(2+)-dependent phos

107 ival are largely controlled by the cytokines IL-3 and stem cell factor (SCF).

108 s in the presence of KITLG and the cytokines IL-3, IL-9, and IL-6 promoted the development of a singl

109 ence of kit ligand (KITLG) and the cytokines IL-3, IL-9, and IL-6 under serum-free conditions, or by

110 that IL-5 and perhaps other betac cytokines (IL-3 and granulocyte/macrophage colony-stimulating facto

111 1 and PDL2), and immune activation elements (IL-3, IFN-beta, TIM1, and TLR2) was seen in tissues, wit

112 -33 challenge, but the addition of exogenous IL-3 enhances IL-13 production.

113 whereas IL-5, GM-CSF, and to a lesser extent IL-3 promote survival of mature eosinophils.

114 MYSM1 interacts with nuclear factor IL-3 (NFIL3, also known as E4BP4), a critical factor for

115 owever, the precise roles of nuclear factor, IL-3-regulated (NFIL3) in IL-4 signaling are unknown.

116 Both male and female IL-3 KO mice had increased splenomegaly and were more an

117 th stem cell factor (SCF), Flt3-ligand (FL), IL-3, and GM-CSF and measurement by multiparametric flow

118 ase activity induced by IL-3 is required for IL-3-stimulated Jak2 and Jak1 activation.

119 This finding is different from IL-3, which also primes basophils for histamine release,

120 Immature BM-derived MCs from IL-3 +SCF cultures, when administered i.v., accumulated

121 versed osteoclast development recovered from IL-3-mediated inhibition.

122 Furthermore, IL-3 enhances RANKL expression in mesenchymal stem cells

123 Furthermore, IL-3 increases the serum OPG level in adult mice.

124 Furthermore, IL-3 inhibited RANKL-induced osteoclast differentiation

125 , or IL-12p40 nor mAb blockade of IFN-gamma, IL-3, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17A, IL-12p40,

126 w levels of growth-regulated oncogene (GRO), IL-3, and IL-10.

127 However, how IL-3 protects cartilage degeneration is not yet known.

128 These data provide novel insights into how IL-3, acting directly on endothelium, can cause basophil

129 However, IL-3 did not inhibit osteoblast differentiation of osteo

130 To overcome this, we generated human IL-3/GM-CSF knock-in (hIL-3/GM-CSF KI) mice.

131 The closely linked human IL-3 and GM-CSF genes are tightly regulated and are expr

132 NIH 3T3 cells transduced with the human IL-3 receptor alpha and beta chains were highly suscepti

133 on of CD32B/C on eosinophils, and identified IL-3 as a potent inducer of CD32- and alphaMss2-mediated

134 derstanding of immune activation, identifies IL-3 as an orchestrator of emergency myelopoiesis, and r

135 This study identifies IL-3 as a potent inducer of RANKL expression in human ba

136 These observations identify IL-3 and its downstream intracellular signals as novel t

137 solated basophils following either anti-IgE, IL-3 or fMLP stimulation.

138 TNF-alpha (but not IL5, IL-3, eotaxin-1 or GM-CSF) was detected in supernatants

139 activation of Jak2 in 32D cells and impaired IL-3 independent growth, which was rescued by overexpres

140 mice by culturing their bone marrow cells in IL-3-enriched conditioned medium.

141 m cell factor (SCF) but not when cultured in IL-3 alone.

142 cells to survive for >3 wk when cultured in IL-3 and SCF, a defect that was reversed by the addition

143 igrated in response to CCL2 when cultured in IL-3+stem cell factor (SCF) but not when cultured in IL-

144 Moreover, we discovered a decrease in IL-3 production and IL-3-dependent mast cell development

145 in bone marrow and splenic erythropoiesis in IL-3 KO mice, as evidenced by higher levels of erythroid

146 ion-site mutant (MCL-1(S159A)), expressed in IL-3-dependent cells, showed enhanced stability upon IL-

147 14083 and by documenting CD274 expression in IL-3-depleted BaF3 cells transfected with the wild-type

148 d with granulocytic colonies was observed in IL-3/IL-6/SCF or GM-CSF, but not G-CSF, even in 0.01 mic

149 CD34- cells that can be propagated in IL-3 but grow slowly, if at all, in SCF, although they e

150 ]) were found to be significantly reduced in IL-3 KO mice during early stages of infection.

151 togenesis, suggesting a key role of STAT5 in IL-3-mediated inhibition of osteoclast differentiation.

152 Furthermore, increased IL-3 production by CD8(+) T cells was also observed, str

153 -sensitive enhancer at -37 kb that increased IL-3 promoter activity 40-fold.

154 ion of NIH/3T3 cells expressing ALK, induces IL-3 independent growth of Ba/F3 cells expressing ALK, a

155 The abnormal responses seen in infected IL-3 KO mice may be due to the lack of IL-3 during devel

156 ipheral blood neutrophils lower, in infected IL-3 KO mice than in WT counterparts.

157 -stage malaria was investigated by infecting IL-3-deficient (knockout [KO]) mice with Plasmodium berg

158 n IL-3Ralpha-neutralizing antibody inhibited IL-3-mediated proliferation and STAT5 activation.

159 cells with 1 muM imatinib mysylate inhibited IL-3 stimulated kinase activities of both c-Abl and Jak2

160 Interestingly, IL-3 decreases soluble RANKL by reducing ectodomain shed

161 Interestingly, IL-3 reduces the degeneration of articular cartilage and

162 Interestingly, IL-3 restores RANKL expression in adult mice by enhancin

163 wild type (WT) and rendered BaF3 cells into IL-3-independent growth, while NPM-ALK L182R, L256R, L25

164 agar, whereas BCR-ABL+ NIH 3T3 cells lacking IL-3 receptor expression did not.

165 Although stimulation with a mixture lacking IL-3 prevented the induction of Ccn3/Nov in control KL c

166 may be acting similar to the natural ligand, IL-3.

167 Male IL-3 KO mice, but not female mice, were more resistant t

168 hosphoinositide 3-kinase (PI3K)/Akt mediates IL-3-repressed 24p3 through regulation of Foxo3a.

169 ne and that PI3K/Akt (but not MAPK) mediates IL-3-regulated 24p3 expression in hematopoietic cells.

170 s were first cultured for 3 days in 10 ng/mL IL-3, the concentration-dependence of histamine release

171 Moreover, IL-3 downregulated IL-1beta- and TNF-alpha-induced expre

172 Moreover, IL-3 increases membrane RANKL by activating the JAK2/STA

173 Moreover, IL-3 showed the preventive and therapeutic effects on ca

174 In addition, CSL362 also neutralized IL-3-mediated rescue of TKI-induced cell death.

175 Notably, the increased ability of IL-3 to induce the production of proteins, such as semap

176 Unexpectedly, the absence of IL-3 or of basophil LN recruitment played little role in

177 R-blocking Ab (CD123) before the addition of IL-3 inhibited basophil rolling and adhesion, implicatin

178 Even addition of IL-3 to T cell-basophil co-cultures failed to induce all

179 expression profiling and RT-qPCR analyses of IL-3-stimulated Ba/F3-beta cells led to the identificati

180 howed that c-Abl bound to the betac chain of IL-3/IL-5/GM-CSF receptors.

181 rved in both FL5.12 Bcl-xL cells depleted of IL-3 and primary CD8(+) T cells depleted of IL-2 that ar

182 pletely abolished the synergistic effects of IL-3 priming on fMLP-induced ERK1/2 phosphorylation.

183 in circulating eosinophils and expression of IL-3 receptors, whereas airway eosinophilia and eosinoph

184 The importance of IL-3-induced TNF secretion was demonstrated by the failu

185 lus IRS-1 renders these cells independent of IL-3 owing to the activation of ALK by endogenous MK.

186 en shown to respond to TSLP independently of IL-3 by increasing functional thymic stromal lymphopoiet

187 g mRNA levels suggests a unique influence of IL-3 on translation.

188 trongyloides venezuelensis and injections of IL-3, each of which induces marked basophilia in wild-ty

189 ected IL-3 KO mice may be due to the lack of IL-3 during development, to the lack of IL-3 in the infe

190 k of IL-3 during development, to the lack of IL-3 in the infected mature mice, or to both.

191 myeloid progenitors expressed low levels of IL-3 receptor.

192 Apoptosis appeared to be due to loss of IL-3 signaling, because TNF-deficient cells were less re

193 ese cells require the continuous presence of IL-3 (a STAT5 activator) for survival.

194 ory molecules in the absence and presence of IL-3 and IFN-gamma by flow cytometry.

195 of autocrine and/or paracrine production of IL-3 and GM-CSF in the increased proliferation and myelo

196 s that is characterized by the production of IL-3.

197 Readdition of IL-3 after deprivation demonstrated that Bax activation

198 region enabled correct in vivo regulation of IL-3 gene expression in T cells, mast cells, and myeloid

199 s due at least in part to down-regulation of IL-3 receptor alpha (IL-3Ralpha) surface expression in t

200 results reveal a previously unknown role of IL-3 in recruiting basophils to the LN and demonstrate t

201 ably, our studies indicate the novel role of IL-3 in regulating bone homeostasis in important skeleta

202 However, the role of IL-3 in regulation of osteoblast-osteoclast interactions

203 In this study, we investigated the role of IL-3 on cartilage degeneration under both in vitro and i

204 In this study, we investigated the role of IL-3 on the regulation of osteoblast-specific molecules,

205 e of domains it shares with binding sites of IL-3 and granulocyte-macrophage colony-stimulating facto

206 Now, we report that the stress of IL-3 growth factor withdrawal up-regulates JAZ expressio

207 Treatment of IL-3 and serum-starved 32D cells with 1 muM imatinib mys

208 did show an increased proportion of IL-5- or IL-3-producing CD4(+) T cells.

209 suppresses apoptosis due to 24p3 addition or IL-3 deprivation.

210 resence or absence of cytokine (TNF-alpha or IL-3), and examined for indices of maturation and for th

211 thropoietin, tumor necrosis factor-alpha, or IL-3, also promoted IL-4 signaling.

212 IL-4 as well as TNF-alpha plus IFN-gamma, or IL-3, GM-CSF, and IL-5 alone significantly diminished th

213 Stimulation with anti-IgE or IL-3 resulted in strong upregulation of basophil CD203c

214 In humans with sepsis, high plasma IL-3 levels are associated with high mortality even afte

215 uce IL-13 in response to IL-18 or IL-33 plus IL-3.

216 STAT5 deficiency prevented IL-3-mediated inhibition of osteoclastogenesis, suggesti

217 at innate response activator B cells produce IL-3, which induces myelopoiesis of Ly-6C(high) monocyte

218 me that basophils themselves rapidly produce IL-3 (within 4 h) in response to IgE-dependent activatio

219 aneously either with IL-3 or after prolonged IL-3 culturing.

220 rial metabolism and cell growth by promoting IL-3-dependent glutamine uptake and metabolism.

221 The up-regulated IL-3 receptor expression was not affected by IL-3 or STA

222 role in mast cell development by regulating IL-3-induced differentiation of mast cell progenitor cel

223 ate that STAT5 contributes to the remarkable IL-3-mediated inhibition of RANKL-induced osteoclastogen

224 ChIP assays using 32D cells revealed IL-3-induced binding of STAT5A/B to a gamma-interferon-a

225 e presence of optimal concentrations of SCF, IL-3, IL-6, and Epo.

226 e well-described basophil-activating stimuli IL-3 and anti-IgE.

227 alveolar lavage eosinophils had more surface IL-3 and granulocyte-monocyte colony-stimulating factor

228 airway eosinophils, it is important to take IL-3 and GM-CSF into account to efficiently reduce tissu

229 om virtually all normal donors; and (6) that IL-3 upregulates the expression of both activating and i

230 Our findings demonstrate that IL-3 induced specific expansion of basophils by directin

231 wever, initial pilot studies discovered that IL-3 could markedly up-regulate CD32 expression and firs

232 In this study, we established that IL-3 played an important role in the rapid and specific

233 nowledge, we provide the first evidence that IL-3 has therapeutic potential in amelioration of degene

234 We found that IL-3 increases RANKL expression at both the transcriptio

235 We have found that IL-3 stimulation of bone marrow cells induces the produc

236 Overall, our results indicate that IL-3 plays a critical role in suppressing protective imm

237 We previously reported that IL-3 inhibits osteoclast differentiation and pathologica

238 We recently reported that IL-3 is more potent than IL-5 or GM-CSF in maintaining t

239 Previously, we have reported that IL-3, a cytokine secreted by activated T cells, protects

240 5 priming, and in this article, we show that IL-3, a member of the IL-5 family, also augments fMLP-st

241 These data also suggest that IL-3 modifies only the sensitivity of signalling element

242 l, to our knowledge for the first time, that IL-3 differentially regulates two functional forms of RA

243 oding mouse eosinophil peroxidase, CCR3, the IL-3/IL-5/GM-CSF receptor common beta-chain, and the tra

244 , whereas BCR-ABL+ NIH 3T3 cells lacking the IL-3 receptor do not utilize the Jak2 pathway, but still

245 nt and IgER-independent stimuli modulate the IL-3-mediated RANKL expression in a time- and stimulus-d

246 3/ITD N676K mutations, and activation of the IL-3 compensatory pathway were all negated by fluvastati

247 d thymocytes and cytokine deprivation of the IL-3 dependent cell line BaF3.

248 y of these DHSs mirrored the activity of the IL-3 gene, and included a highly inducible cyclosporin A

249 t to account for the in vivo activity of the IL-3 gene.

250 determined whether forced expression of the IL-3 receptor would allow oncogenic transformation of NI

251 are commonly thought to be the source of the IL-3 that primes for these basophil responses.

252 dicate that Bcr-Abl oncoprotein requires the IL-3 receptor/Jak2/Stat5 pathways for oncogenic transfor

253 e found that in primary patient samples, the IL-3 receptor alpha chain CD123 was highly expressed on

254 We found that the IL-3 complex (IL-3 plus anti-IL-3 Ab) greatly facilitate

255 We also found that the IL-3 complex treatment resulted in approximately 4-fold

256 We found that the IL-3 receptor-alpha (IL-3Ralpha) is a promising candidat

257 (-/-) mice, we report in this study that the IL-3/IL-3R system is absolutely required to recruit circ

258 that basophils rapidly bind and utilize the IL-3 they produce, as evidenced by functional and phenot

259 The response of these cells to IL-3 is stimulated synergistically by SCF, and we presen

260 ponsive than their wild-type counterparts to IL-3-mediated survival.

261 hen compared to IL-5, continuing exposure to IL-3 further induced degranulation of eosinophils on agg

262 leukemic mice exhibited hypersensitivity to IL-3 deprivation and JAK2-STAT5 overactivation after IL-

263 more vigorously than EL cells in response to IL-3 and stem cell factor.

264 24p3 expression and apoptosis in response to IL-3 withdrawal.

265 regulated kinase (ERK) and S6 in response to IL-3, which supports defects in activating the phosphati

266 he failure of Jak2 activation in response to IL-3.

267 On transfer to IL-3, IL-6, and SCF to induce myelopoiesis, levels of gr

268 Survival of Ba/F3 cells transformed to IL-3 independence by the ERBB2 extracellular domain muta

269 acellular cytokines, and receptors for TSLP, IL-3, and eotaxin in blood, bone marrow, and sputum baso

270 However, the mechanism underlying IL-3-mediated inhibition of osteoclast differentiation i

271 Upon IL-3 withdrawal, protein levels of MCL-1 decreased but w

272 direct interaction between Cn and Gab2 upon IL-3 stimulation, and Akt can regulate this interaction.

273 1 (HSV-1), whereas granzyme-B induction upon IL-3/IL-10 stimulation was normal.

274 endent cells, showed enhanced stability upon IL-3 withdrawal and conferred increased protection from

275 ve sites (DHSs) spanning the entire upstream IL-3 intergenic region revealed the existence of a compl

276 the previously identified proximal upstream IL-3 enhancers were insufficient to account for the in v

277 Using IL-3(-/-) and IL-3Rbeta(-/-) mice, we report in this stu

278 d heterogeneity between TSLP-elicited versus IL-3-elicited basophils.

279 Importantly, these in vitro IL-3-induced modifications were recapitulated in vivo on

280 , and to a lesser extent the spleen, and was IL-3 dependent.

281 Trichinella-induced basophil responses were IL-3-IL-3R independent but critically dependent on TSLP-

282 tudy was to identify the mechanisms by which IL-3 distinctively affects eosinophil function compared

283 However, the molecular mechanism by which IL-3 regulates 24p3 expression remains largely unknown.

284 protein translation in cells activated with IL-3, GM-CSF, or IL-5.

285 d to establish the impact of activation with IL-3 on IgG-driven eosinophil degranulation.

286 eptors for IL-5 share a common ss-chain with IL-3 and GM-CSF receptors.

287 When compared with IL-3 and G-CSF, GM-CSF hypersensitivity was cytokine spe

288 L-13 secretion from basophils cotreated with IL-3, with minimal effects on histamine and IL-4.

289 other stimuli, basophils were cultured with IL-3 alone.

290 agents were added simultaneously either with IL-3 or after prolonged IL-3 culturing.

291 IL-13), which are all markedly enhanced with IL-3 pretreatment.

292 s may be mediated by direct interaction with IL-3 receptor.

293 Basophils in medium alone or with IL-3 +/- anti-IgE were coincubated with TSLP, IL-33, or

294 primary blood eosinophils after priming with IL-3/GM-CSF, and small interfering RNA-mediated knockdow

295 purified basophils even when stimulated with IL-3 plus IFN-gamma.

296 rison to normal counterparts stimulated with IL-3, GM-CSF, and SCF.

297 3c including in response to stimulation with IL-3 alone.

298 ces of prolonged eosinophil stimulation with IL-3.

299 Mice treated with IL-3, which increased basophil pool sizes, and mice rece

300 under at least one condition, treatment with IL-3, it is possible to markedly blunt the loss of syk,