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 shares a common beta subunit receptor with both IL-

10 IL-3 stimulation yielded the most numbers of differentia

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

12 IL-3, a cytokine secreted by activated T lymphocytes, is

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

14 IL-3-deprivation induces apoptosis correlating with upre

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

16 IL-3-upregulated genes may provide a foundation for rese

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

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

19 the parental MSCs, including IL-1beta, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-13,

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

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

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

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

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

25 ese cells depend on exogenous interleukin-3 (IL-3) for growth, but this dependence can be compensated

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

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

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

29 ogene (c-MYC) and exposure to interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor

30 imulating factor (GM-CSF) and interleukin-3 (IL-3), have not received much attention.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 1alpha (Spearman's rho 0.242, P = 0.009) and IL-3 (rho 0.189, P = 0.043) responses after TNF-alpha/IL

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

51 ted human Th cells is modulated by IL-4, and IL-3 regulates the effector functions of Th2 cells.

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

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

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

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

56 report a sustained production of GM-CSF and IL-3 from IgM(+) and IgM(-)/IgG(+) CD138(+) Blimp-1(+) i

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

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

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

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

61 h potential isotype switching of GM-CSF- and IL-3-producing IgM(+) B1 B cells.

62 3 (10-fold) when cocultured with A549 EC and IL-3, without exogenous allergen or IgE cross-linking st

63 Furthermore, IL-3R expressing and IL-3-secreting Th cells were high in house dust mite-all

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

65 n for 24 hours with anti-IgE, C5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosino

66 Cytokines, such as GM-CSF, IFN-gamma, and IL-3, which are typically found in patients with allergi

67 y and stimulated with GM-CSF, IFN-gamma, and IL-3.

68 pates in the resolution of inflammation, and IL-3 and IL-5 may also have such properties.

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

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

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

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

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

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

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 hlight NFATc2-driven production of autocrine IL-3 as a critical and cell type-specific component for

78 tion of IL-9 critically depends on autocrine IL-3 acting via the sustained activation of STAT5 on the

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

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

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

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

83 IgE, C5a, fMLP, and IL-3 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

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

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

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

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

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

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

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

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

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

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

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

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

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

97 required for IL-4 production after combined IL-3 and IL-33 treatment in mice.

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

99 In conclusion, IL-3 produces a distinct eosinophil gene expression prog

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

101 peractivated MAP kinase signaling, conferred IL-3 hypersensitivity and sensitized the cells to variou

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

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

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

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

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

107 GM-CSF, IL-3, and IL-5 commonly upregulated 252 genes and downre

108 The beta common chain cytokines GM-CSF, IL-3, and IL-5 regulate varied inflammatory responses th

109 erize the transcriptomic profiles of GM-CSF, IL-3, and IL-5 stimulation on human circulating eosinoph

110 olunteers and stimulated with either GM-CSF, IL-3, or IL-5 for 48 h.

111 GM-CSF/IL-3(+) B1 B cells originate in the spleen of infected m

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

113 cytokines/chemokines IL-1beta, CXCL1, CXCL5, IL-3, CXCL2, CCL3, and CCL4, but decreased levels of IL-

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

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

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

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

118 1 and PDL2), and immune activation elements (IL-3, IFN-beta, TIM1, and TLR2) was seen in tissues, wit

119 -33 challenge, but the addition of exogenous IL-3 enhances IL-13 production.

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

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

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

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

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

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

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

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

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

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

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

131 , 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,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 ort that IVIG directly induces activation of IL-3-primed human basophils, but IL-33 and other cytokin

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

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

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

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

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

180 lmost completely abrogates the expression of IL-3 in both cell types.

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

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

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

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

185 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

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

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

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

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

190 Moreover, Th2 cells in presence of IL-3 show increased expression of type 2 effector cytoki

191 lthy donors were cultured in the presence of IL-3, IL-33, GM-CSF, thymic stromal lymphopoietin, or IL

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

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

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

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

196 human Th cells and also examined the role of IL-3 in effector functions of these cells.

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

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

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

200 However, the role of IL-3 in regulation of T cell functions is not fully deli

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

219 bition of apoptosis could be due to released IL-3, IL-5, and GM-CSF found in supernatants.

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

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

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

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

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

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

226 Furthermore, we demonstrate that IL-3 acts independently and synergistically with IL-1bet

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

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

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

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

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

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

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

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

235 Previously, we have reported that IL-3 plays an important role in development of regulator

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

237 5 priming, and in this article, we show that IL-3, a member of the IL-5 family, also augments fMLP-st

238 Our results suggest that IL-3 may play an important role in regulating allergic i

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

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

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

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

243 3/ITD N676K mutations, and activation of the IL-3 compensatory pathway were all negated by fluvastati

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

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

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

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

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

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

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

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

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

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

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

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

256 ular mice in which the cells were exposed to IL-3 or GM-CSF delivered using a cotransduction strategy

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

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

259 24p3 expression and apoptosis in response to IL-3 withdrawal.

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

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

262 h is specifically upregulated in response to IL-3.

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

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

265 CL12 and thymic stromal lymphopoietin (TSLP)/IL-3-dependent upregulation of CXCR4.

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

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

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

269 1 (HSV-1), whereas granzyme-B induction upon IL-3/IL-10 stimulation was normal.

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

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

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

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

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

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

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

277 be secreted by multiple cell types, whereas IL-3 is mostly restricted to T cells, yet innate respons

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

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

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

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

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

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

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

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

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

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

288 Short-term incubation with IL-3 dose-dependently upregulated MRGPRX2 expression in

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

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

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

292 In mast cells stimulated with IL-3 and IL-33, the Il9 CNS-25 enhancer is a potent regu

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

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

295 ontrast, when basophils were stimulated with IL-3, loss of STIM2, but not STIM1, reduced basophil IL-

296 3c including in response to stimulation with IL-3 alone.

297 ces of prolonged eosinophil stimulation with IL-3.

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

299 y-mass spectrometry following treatment with IL-3, IL-5 or granulocyte-macrophage colony-stimulating

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