ライフサイエンスコーパス: IL-4R

1 IL-4R and PRLR gave only small numbers of thymocytes, wh

2 IL-4R bound to the IL-13/IL-13Ralpha1 complex with slow

3 IL-4R is functional because IL-4 strongly induced activa

4 IL-4R is up-regulated during T cell differentiation by a

5 IL-4R signaling impaired the capacity of Treg cells to s

6 IL-4R-independent proliferation was controlled by a rise

7 tively activated macrophages, but the type 1 IL-4R is also important.

8 Thus, IL-4, acting through the type 1 IL-4R, induces Stat6-dependent IFN-gamma secretion by NK

9 n mice bred to have null mutations of IL-13, IL-4R(alpha), or STAT-6, transgenic IL-10 did not induce

10 n and fibrosis being independent of an IL-13/IL-4R(alpha)/STAT-6 activation pathway.

11 Binding of IL-4 by either the type 1 or 2 IL-4R, or of IL-13 by the type 2 IL-4R, initiates Jak-de

12 IL-13, which signals through the type 2 IL-4R and mimics many IL-4 effects, failed to stimulate

13 thymic microenvironment expresses the type 2 IL-4R complex and is functionally responsive to its know

14 to the IL-13Ralpha1 component of the type 2 IL-4R that is linked to STAT6.

15 e contribution of IL-13 acting at the type 2 IL-4R to immune and functional responses to primary (Hb1

16 of the IL-4R, and IL-13 binds to the type 2 IL-4R, IL-13 has been proposed as an inhibitor that bloc

17 type 1 or 2 IL-4R, or of IL-13 by the type 2 IL-4R, initiates Jak-dependent tyrosine phosphorylation

18 ed phosphorylation of Janus kinases 1 and 3, IL-4R alpha, signal transducer and activator of transcri

19 interferon-gamma (IFNGR) and interleukin 4 (IL-4R) cytokine receptors, in particular, direct the ear

20 We found that receptors for interleukin-4 (IL-4R) are highly expressed in H-RS cells.

21 and type II (IL-4R alpha/IL-13R alpha1/IL-4, IL-4R alpha/IL-13R alpha1/IL-13) ternary signaling compl

22 Th1/2 lineage commitment genes (GATA3, IL-4, IL-4R, STAT4 and TBET) in umbilical cord DNA at birth in

23 These results demonstrate that IL-4/IL-4R interactions on CD8+ T cells play a critical role

24 rocess is critically dependent upon the IL-4/IL-4R signaling pathway.

25 expression activities to a minimally active IL-4R mutant, delta 557.

26 Although IL-4R alpha signals Shc and SH2-containing inositol phos

27 Although IL-4R(-/-) mice displayed a milder course throughout, th

28 tion of V75R576 resulted in expression of an IL-4R alpha with enhanced sensitivity to IL-4.

29 Co-expression of an IL-4R antagonist by the rFPV vaccine further enhanced th

30 hance nuclear GATA-3 accumulation through an IL-4R-dependent action, leading to Th2 differentiation.

31 nt common component shared between IL-13 and IL-4R.

32 e in the binding affinity of both IL-13R and IL-4R complexes.

33 ming a ternary complex with IL-13Ralpha1 and IL-4R.

34 nsic and requires the expression of IL-4 and IL-4R.

35 ugh CD40 signaling can reverse both BCR- and IL-4R-mediated B7h down-regulation.

36 6 impaired the association of IL-2R beta and IL-4R alpha chains with Jak1 but did not have a major im

37 gamma R alpha, IL-10R alpha, IL-2R beta, and IL-4R alpha.

38 L-4R alpha/common gamma-chain (gamma(c)) and IL-4R alpha/IL-13R alpha1, and only the latter is also a

39 o known that the mechanism by which CD40 and IL-4R stimulation on a B cell increases the level of IgG

40 unaffected, but synergism between CD40- and IL-4R-mediated signals is completely ablated.

41 henotype and expressed Kit, FcepsilonRI, and IL-4R on their surface.

42 Thus, functional synergy between Flt3 and IL-4R signaling is critical for Stat-mediated regulation

43 tor, interleukin-2R gamma (IL-2R gamma), and IL-4R alpha.

44 nti-IL-10R-treated IL-4R alpha(-/-) mice and IL-4R alpha x IL-10 double knockouts.

45 ibroblasts showed nearly identical PDGFR and IL-4R activation, gross substrate tyrosine phosphorylati

46 peripheral B cells via the CD40 receptor and IL-4R together lead to IgE synthesis and secretion, but

47 ion, Dectin-1, CD206 (mannose receptor), and IL-4R.

48 s metaplasia and methacholine responses, and IL-4R null mice failed to show RV-induced mucous metapla

49 ing insulin receptor substrate 1/2, Shc, and IL-4R interacting protein, as well as Stat6.

50 lso increases the expression of TGFbetaR and IL-4R, pivotal to Th9 polarization.

51 ducing susceptibility to LV39, wild-type and IL-4R alpha(-/-) mice were treated with anti-IL-10R mAb,

52 responses, through administration of an anti-IL-4R alpha mAb, reversed asthma-like symptoms, when giv

53 tion-dependent and could be reversed by anti-IL-4R Abs.

54 f Vgamma2Vdelta2 T cells was blocked by anti-IL-4R alpha mAb but not anti-IL-4 mAb.

55 unction were attenuated or prevented by anti-IL-4R mAb.

56 cade, three anti-IL-5 biologics and one anti-IL-4R biologic have recently emerged as promising treatm

57 Anti-IL-4 or anti-IL-4R Ab did not diminish IL-4 production by Th2 cells i

58 se using the JAK inhibitor AG490 or the anti-IL-4R(alpha) Ab M1 abrogated the persistence of phosphor

59 n and later reinfected and treated with anti-IL-4R mAb, an antagonist of IL-4 and IL-13 receptor bind

60 sed mRNA for IL-4R beta chain (also known as IL-4R alpha) and IL-13R alpha' chain (also known as IL-1

61 ibody to the IL-4Ralpha chain (also known as IL-4R beta) in surgical/biopsy samples of brain tumor ti

62 arrier populations by selectively augmenting IL-4R alpha-dependent signaling.

63 ing transgenic mice expressing an IL-2R beta/IL-4R alpha chimeric cytokine receptor transgene specifi

64 rotection, CIA was exacerbated in IL-2R beta/IL-4R alpha chimeric receptor transgenic mice, with incr

65 understanding of receptor crosstalk between IL-4R and BCR is summarized along with several possible

66 tor alpha chain (IL-4Ralpha), common to both IL-4R complexes: type 1 (IL-4Ralpha/gammac; IL-4 specifi

67 Membrane-bound IL-4R mRNA expression was significantly elevated 7 days

68 trast to the lack of resistance conferred by IL-4R alpha gene deletion, partial resistance to LV39 wa

69 gulated in susceptible mice and inhibited by IL-4R-signaling in vitro, uncoupling parasite killing fr

70 s in the interleukin-4 receptor alpha chain (IL-4R alpha) have been linked to asthma incidence and se

71 BALB/c mice deficient for IL-4R alpha-chain (IL-4R alpha), while substrain IR173 was highly controlle

72 ed through a high affinity receptor complex (IL-4R).

73 be an important feedback mechanism to dampen IL-4R signaling in airway inflammation.

74 The ability of tyrosine-deficient IL-4Rs to mediate proliferative signaling and STAT phosp

75 pancreatic samples express no or low-density IL-4R.

76 -12 priming does not suppress IL-4-dependent IL-4R up-regulation shows that both IL-4 mRNA and cytoki

77 tein kinase C activation and STAT6-dependent IL-4R signaling.

78 cineurin pathway contribute to desensitizing IL-4R.

79 tive for cell types expressing the different IL-4Rs.

80 ise questions about the importance of direct IL-4R effects on smooth muscle in murine asthma models a

81 ch has previously been shown to downregulate IL-4R subunit alpha cell surface expression and promote

82 rs demonstrating significantly higher DUOX2, IL-4R, and IL-17RA expression in tumors than in adjacent

83 n helminth-infected mice deficient in either IL-4R alpha-chain or Stat6.

84 This action is not dependent on either IL-4R or IL-2R signals and results in OX40 controlling i

85 rastingly, there was no evidence that either IL-4R-dependent or IL-4R-independent/CCR3/IL-5-dependent

86 express high levels of endogenously encoded IL-4Rs.

87 recombinant Fowl Pox Virus (FPV)-gag pol env-IL-4R antagonist prime, intramuscular (i.m.) recombinant

88 ndicate that airway epithelial cells express IL-4R constitutively and that IL-4 directly induces the

89 ivo, mouse airway epithelial cells expressed IL-4R constitutively, and IL-4 (250 ng) increased MUC5 g

90 airway epithelial cells (NCI-H292) expressed IL-4R constitutively, and IL-4 (10 ng/ml) induced MUC2 g

91 The viral vector-expressed IL-4R antagonist transiently inhibited IL-4/IL-13 signal

92 ed by local macrophage populations following IL-4R-dependent in situ proliferation and alternative ac

93 healing lesions in BALB/c mice deficient for IL-4R alpha-chain (IL-4R alpha), while substrain IR173 w

94 nd neck cancer cell lines expressed mRNA for IL-4R beta chain (also known as IL-4R alpha) and IL-13R

95 trovirus containing a mutant of the human (h)IL-4R alpha-chain, Y497F, which is unable to recruit the

96 analyses have identified RAS/NF1, hedgehog, IL-4R, and ALK pathway abnormalities as potential therap

97 4(+) T cells that induced IL-4 receptor(hi) (IL-4R(hi)) CD206(+) alternatively activated macrophages.

98 iched with CD21(low), CD11c(+), FCRL4(high), IL-4R(low) memory B cells.

99 A mutation in the human (hu) IL-4R alpha, Q576R, has been linked with allergy in huma

100 IL-4 signaling through the endogenous human IL-4R(alpha).

101 functional consequences of two of the human IL-4R alpha allelic variants that have been found to ass

102 (IL-4R) type, IL-4Ralpha/IL-2Rgamma (class I IL-4R), whereas endothelial cells express another type,

103 e that gammadelta17 cells express the type I IL-4R and that STAT6 signaling negatively regulates gamm

104 er the common gamma-chain to form the type I IL-4R or with the IL-13R alpha1 chain (IL-13Ralpha1) to

105 ells responded to murine IL-4 via the type I IL-4R, but were unresponsive to IL-13, and did not expre

106 al structures of the complete set of type I (IL-4R alpha/gamma(c)/IL-4) and type II (IL-4R alpha/IL-1

107 other type, IL-4Ralpha/IL-13Ralpha (class II IL-4R).

108 ha1 chain (IL-13Ralpha1) to form the type II IL-4R.

109 entially regulated by the type I and type II IL-4R.

110 d highlight unforeseen roles for the type II IL-4R.

111 e role of IL-13Ralpha1 and the type I and II IL-4Rs in experimental asthma, we examined lung patholog

112 e I (IL-4R alpha/gamma(c)/IL-4) and type II (IL-4R alpha/IL-13R alpha1/IL-4, IL-4R alpha/IL-13R alpha

113 rom Flt3 ligand-deficient mice have impaired IL-4R signaling, with reduced phosphorylation of signal

114 diated suppression of L-CNV was abrogated in IL-4R-deficient mice and in bone marrow chimeras reconst

115 emonstrating that a functional alteration in IL-4R alpha requires the coexistence of two naturally oc

116 ative to wild-type or littermate controls in IL-4R alpha(-/-) mice with complementary defects in IL-1

117 atment further suppressed parasite growth in IL-4R alpha(-/-) mice infected with L. major IR173.

118 17A production, but this was not observed in IL-4R KO and STAT6 KO mice.

119 the size of the VM population is reduced in IL-4R-deficient animals.

120 ephalomyelitis and enhanced remyelination in IL-4R(-/-) mice appeared to be related to a shift toward

121 the importance of juxtatyrosine residues in IL-4R signaling and argue for an essential role of exten

122 To directly assess the role of STAT6 in IL-4R- and CD40-mediated germline transcription and swit

123 ts show that hypoxia significantly increased IL-4R alpha expression in wild-type (WT) control lungs.

124 The cytokine receptor interleukin (IL)-4R, expressed by lymphocytes, is well known for its

125 IL-4 production and requires MPhi-intrinsic IL-4R signaling.

126 d from T15 had enzymatic activity and killed IL-4R+ C1498 cells, but not IL-4R- EL4 cells.

127 In the T cell line CTLL2, ligation of kit/IL-4R alpha induces cellular proliferation.

128 SCF-mediated ligation of kit/IL-4R alpha is sufficient to elicit IL-4-specific gene e

129 f cells expressing the chimeric receptor kit/IL-4R alpha with SCF induces activation of the IL-4R alp

130 t examined the genetics of five of the known IL-4R alpha allelic variants in asthmatic and nonatopic

131 to IL-4 because expression of both membrane IL-4R and the IL-4-neutralizing soluble (s)IL-4R were re

132 single nebulized dose of IL-4R 1,500 microg, IL-4R 500 microg, or placebo after stopping inhaled cort

133 urce of IL-4 receptor (IL-4R) that mobilizes IL-4R signaling pathways and the transcription factor GA

134 This vector-based mucosal IL-4R antagonist/SOSIP booster strategy, which promotes

135 Administration of murine IL-4R antagonist during allergen (OVA) challenge inhibit

136 Each form of the murine IL-4R(alpha) mediated tyrosine phosphorylation of STAT6

137 e human monocytic cell line U937 with murine IL-4R(alpha) cDNA bearing the I or V at position 50 and

138 Nebulized IL-4R has a serum half-life of approximately 1 wk.

139 Thus, through different mechanisms, neither IL-4R nor IL-12R has any clear advantage in polarizing c

140 , although IL-4Ralpha mRNA was expressed, no IL-4R protein was detectable in two adult and one pediat

141 ivity and killed IL-4R+ C1498 cells, but not IL-4R- EL4 cells.

142 levels of IFN-gamma and IL-12Rbeta2 but not IL-4R.

143 Selective augmentation of IL-4R signaling in Treg cells induced their reprogrammin

144 fection experiments with different chains of IL-4R and kinase-deficient JAK1 and JAK2 mutants in CHO

145 h respond to IL-13, gammac is a component of IL-4R but does not appear to be a component of IL-13R.

146 lomyelitis in mice demonstrating deletion of IL-4R and found a correlation with cytokine expression d

147 ls of the primary structural determinants of IL-4R-mediated proliferative signaling.

148 signed to receive a single nebulized dose of IL-4R 1,500 microg, IL-4R 500 microg, or placebo after s

149 Conclusions: A single dose of IL-4R appears safe and effective in moderate asthma.

150 tat6, the transcription factor downstream of IL-4R that is required for Th2 differentiation.

151 ocess is mediated by continued engagement of IL-4R(alpha), suggesting enhanced responses of V50 IL-4R

152 sion of IL-13R alpha1 and mRNA expression of IL-4R alpha compared with Th0, Th1, or Th2 polarized cel

153 We examined the expression of IL-4R by using a monoclonal antibody to the IL-4Ralpha c

154 hese results establish uniform expression of IL-4R on head and neck cancer cell lines and IL-4 toxin

155 In addition, expression of IL-4R on the cell surface of various normal brain tissue

156 Th cells instead show elevated expression of IL-4R subunit alpha on cell surface, sensitized IL-4/STA

157 ny studies have implicated the importance of IL-4R alpha in the development of allergic inflammation

158 CD4 cells can secrete IL-4 independently of IL-4R signals, but how this secretion is regulated is no

159 tiated WT Th1 cells was not due to a lack of IL-4R expression or phosphorylation.

160 B cells had a significantly higher level of IL-4R and CD23 expression than B7.1+ B cells.

161 tested (n = 7) expressed no or low levels of IL-4R.

162 ted regarding IL-4R, the exact mechanisms of IL-4R-mediated signaling pathways in human B cells are n

163 ors; however, prior engagement of CD40 or of IL-4R produces an alternate signaling pathway in which B

164 rine-rich ID-1 region in this new program of IL-4R signal transduction observed in activated T cells.

165 nine substitution at position 576 (Q576R) of IL-4R alpha has been associated with severe asthma, espe

166 play an important role for the regulation of IL-4R-mediated JAK/STAT signaling.

167 ut not IFN-gamma, suggested a direct role of IL-4R-mediated events.

168 ounting for this result were the strength of IL-4R and CD40 signaling and relative rates of cell prol

169 he investigation of the subunit structure of IL-4R demonstrated that head and neck cancer cell lines

170 ining domains within the cytoplasmic tail of IL-4R alpha play in IL-4-mediated protection from apopto

171 pe II alveolar epithelial cell expression of IL-4Rs in mice sensitized and challenged with Af, and in

172 d STAT1, whereas PD-L2 expression depends on IL-4R alpha and STAT6.

173 that gammac is not a component of IL-13R or IL-4R systems in these cells.

174 that block binding to either IL-13Ralpha1 or IL-4R inhibited the TR-FRET signal formed by the ternary

175 hibited by costimulation with either CD40 or IL-4R.

176 s no evidence that either IL-4R-dependent or IL-4R-independent/CCR3/IL-5-dependent immunity influence

177 expression in DCs developed from STAT6-/- or IL-4R alpha-/- mice.

178 ected in mice deficient in IL-4 synthesis or IL-4R triggering.

179 that human brain tumors in situ overexpress IL-4R compared with normal brain tissues, thus confirmin

180 However, during the chronic phase, IL-4R(-/-) mice exhibited extensive remyelination and an

181 bound less effectively to the phosphorylated IL-4R/GST fusion protein than that in IFNGR(-/-) Th1 cel

182 Modified Vaccinia Ankara Virus (MVA)-gag pol-IL-4R antagonist boost followed by an i.m SOSIP-gp140 bo

183 murine IL-4 mutant (C118 deletion) protein (IL-4R antagonist) inhibited IL-4- and IL-13-induced STAT

184 These data suggest that the Q576R IL-4R alpha- chain polymorphism may mitigate disease exp

185 their expression of interleukin-4 receptor (IL-4R) and IL-13R subunits.

186 d IL-13 and the heterodimeric IL-4 receptor (IL-4R) complexes that they interact with play a key role

187 The IL-4 receptor (IL-4R) in B cells is composed of two chains, the IL-4-bi

188 The interleukin 4 receptor (IL-4R) is a central mediator of T helper type 2 (T(H)2)-

189 We found that interleukin 4 receptor (IL-4R) knockout and downstream signal transducer and act

190 n of the alpha-subunit of the IL-4 receptor (IL-4R) might be relatively resistant to the gain-of-func

191 nd based on the expression of IL-4 receptor (IL-4R) on most acute myeloid leukemia cases.

192 ) mice with enhanced interleukin-4 receptor (IL-4R) signaling exhibited STAT6-dependent impaired gene

193 ng damage, whereas subsequent IL-4 receptor (IL-4R) signaling reduced elevations in IL-17 mRNA levels

194 that dimerization of Interleukin-4 receptor (IL-4R) subunits is a pivotal step for JAK/STAT signal tr

195 tion is driven by a source of IL-4 receptor (IL-4R) that mobilizes IL-4R signaling pathways and the t

196 to IL-4, T cells express one IL-4 receptor (IL-4R) type, IL-4Ralpha/IL-2Rgamma (class I IL-4R), wher

197 17 cells expressed the type I IL-4 receptor (IL-4R), and IL-4 increased STAT6 phosphorylation in gamm

198 To target interleukin-4 receptor (IL-4R), we used a recombinant protein fusing circularly

199 ss a high density of interleukin-4 receptor (IL-4R), whereas normal ovarian tissues tested (n = 7) ex

200 rate- to high-density surface IL-4 receptor (IL-4R), whereas normal pancreatic samples express no or

201 and IL-13 activate the type 2 IL-4 receptor (IL-4R), which contains the IL-13Ralpha1 and IL-4Ralpha c

202 xpress high affinity interleukin-4 receptor (IL-4R), which is an attractive target for receptor-direc

203 IL-4 receptor (IL-4R)-deficient CD8+ T cells specific for the circumspo

204 Soluble recombinant human IL-4 receptor (IL-4R; Nuvance; altrakincept) inactivates naturally occu

205 l lines also express surface IL-4 receptors (IL-4R) and IL-4 binds to IL-4R on one cell line studied

206 of plasma membrane interleukin-4 receptors (IL-4R).

207 IL-4 receptors (IL-4Rs) are also expressed by nonhematopoietic cells as

208 Although IL-4 receptors (IL-4Rs) but not IL-12Rs are expressed on naive CD4(+) T

209 Although IL-4 signals through two receptors, IL-4R alpha/common gamma-chain (gamma(c)) and IL-4R alph

210 omain with that of other cytokine receptors: IL-4R, IL-9R, and prolactin receptor (PRLR).

211 lth of information has accumulated regarding IL-4R, the exact mechanisms of IL-4R-mediated signaling

212 uncharacterized role for STUB1 in regulating IL-4R signaling, which might provide a new strategy for

213 by IL-4 treatment, and this effect requires IL-4R.

214 bition of inflammatory cytokines in resident IL-4R-expressing epidermal cells and thereby alters the

215 e IL-4R and the IL-4-neutralizing soluble (s)IL-4R were reduced in Il21r(-/-) mice.

216 A haplotype analysis revealed a single IL-4R alpha haplotype that was associated with allergic

217 ombination therapy between IL-12 and soluble IL-4R (sIL-4R) on the established infection of HSV-1 in

218 ys after conidia challenge; however, soluble IL-4R mRNA expression was increased 30 days after conidi

219 the anti-inflammatory activities of soluble IL-4R (sIL-4R).

220 s are arrested at the double-negative stage, IL-4R, IL-9R, or PRLR all imparted some progression to t

221 10 was not due to down-regulation of surface IL-4R because pretreatment with these cytokines did not

222 To target IL-4R, we have developed IL-4 cytotoxin, in which circul

223 t during chronic filarial infection and that IL-4R-independent/IL-5- and CCR3-dependent pathways are

224 hus confirming our previous conclusions that IL-4R in brain tumors may serve as an attractive target

225 e cell analysis experiments demonstrate that IL-4R/Stat6 signaling, while influencing the final frequ

226 These results indicate that IL-4R-targeted cytotoxin may be a useful agent for the m

227 In this study, we show that IL-4R is expressed by breast and ovarian cancer cell lin

228 y analysis at the plasma membrane shows that IL-4R subunit dimerization is indeed a strictly ligand-i

229 These data suggest that IL-4R exerts a negative regulatory role on oligodendrocy

230 The IL-4R alpha-chain (IL-4Ralpha) contains a putative ITIM

231 The IL-4R induces proliferation and gene expression through

232 ponents of a receptor complex for IL-13, the IL-4R and a low affinity IL-13-binding chain, IL-13R alp

233 In response to IL-4, the IL-4R activates a set of phosphotyrosine binding domain-

234 i-IL-10R mAb, and in a genetic approach, the IL-4R alpha(-/-) mice were crossed with BALB/c IL-10(-/-

235 assay targeting the interaction between the IL-4R and the binary complex.

236 sed levels of IL-4 could be explained by the IL-4R being unavailable to neutralize this cytokine in I

237 lity is that in the absence of gamma(c), the IL-4R alpha chain is able to transduce signals by homodi

238 es, suggesting a direct contribution for the IL-4R pathway to the heightened susceptibility of co-inf

239 overlap of their functions results from the IL-4R alpha-chain forming an important functional signal

240 Patients in the IL-4R 1,500 microg group also required significantly les

241 ithdrawal of corticosteroids, but not in the IL-4R 500 microg group or the placebo group (p < 0.05).

242 at an additional level of specificity in the IL-4R signaling mechanism exists and may partially expla

243 eral commonly occurring polymorphisms in the IL-4R(alpha) have been associated with atopy in humans;

244 complex receptor system, which includes the IL-4R alpha-chain, IL-4Ralpha, and at least two other ce

245 Memory CD8+ T cells lacking the IL-4R are unable to establish a stable population residi

246 Engagement of the IL-4R activates multiple signaling pathways, including t

247 through a receptor complex consisting of the IL-4R alpha chain and the common gamma chain (gamma c),

248 cytoplasmic and transmembrane domains of the IL-4R alpha chain was generated.

249 -4R alpha with SCF induces activation of the IL-4R alpha-associated kinase JAK-1 and the transcriptio

250 chanisms of binding and stabilization of the IL-4R and IL-13R complexes, we compared the effects of s

251 Analyses of the IL-4R in factor-dependent cell lines led to the developm

252 lpha' is a novel functional component of the IL-4R system and that JAK1 and JAK2 mediate IL-4-induced

253 ed gammac) is shown to be a component of the IL-4R system, whereas in nonhematopoietic cells, gammac

254 IL-13Ralpha' forms a novel component of the IL-4R system.

255 c is absent and it is not a component of the IL-4R system.

256 )2 protein and the cytoplasmic domain of the IL-4R(alpha) chain that harbors the Stat6 docking sites.

257 m resides in the extracellular domain of the IL-4R(alpha).

258 ecause STAT6 is a downstream effector of the IL-4R, and IL-13 binds to the type 2 IL-4R, IL-13 has be

259 (gamma(c)) is a functional component of the IL-4R, yet cells lacking gamma(c) are able to respond to

260 Together, these data demonstrate that the IL-4R alpha cytoplasmic domain is sufficient to activate

261 Further, we found that the IL-4R gene regulation domain (amino acids 557-657) conta

262 Signaling through the IL-4R alpha-chain (IL-4Ralpha) is crucial for the develo

263 tive and antiapoptotic signaling through the IL-4R in 32D cells; however their role in regulating nor

264 duced by NKT cells and signaling through the IL-4R-STAT6 pathway, are necessary for down-regulation o

265 rotein produce IL-4 mutants that bind to the IL-4R alpha-chain with high affinity, but do not induce

266 The IL-4 toxin binds specifically to the IL-4R and is highly cytotoxic to glioblastoma cells, as

267 different signalling pathways coupled to the IL-4R complexes and examine the possible mechanisms of D

268 f STAT6 by inhibiting its recruitment to the IL-4R.

269 TAT6 proteins induced by IL-4 binding to the IL-4R.

270 IL-13, the only other cytokine that uses the IL-4R-STAT6 pathway.

271 te gamma'-chain, which can interact with the IL-4R alpha chain to mediate signaling, is expressed on

272 +) and CD8(+) T cells were detected with the IL-4R antagonist adjuvanted strategy compared to the una

273 e specifically coimmunoprecipitated with the IL-4R as well as with phosphatidylinositol 3-kinase (p85

274 (IL-21R) shows significant homology with the IL-4R, and CD4+ Th2 cells are an important source of IL-

275 paired IL-4/IL-13 activation of AAMs through IL-4R types 1 and 2.

276 IL-4 and lose the ability to signal through IL-4R.

277 IL-4 signaling through IL-4R alpha/gamma(c) suppresses Ca2T6 and SPRR gene expr

278 14, CD54, FcgammaR1, FcalphaR, CD120b, TLR5, IL-4R, CCR1, p47(phox), p40(phox), IL-8, CXCL1, Nramp1,

279 ace IL-4 receptors (IL-4R) and IL-4 binds to IL-4R on one cell line studied with low affinity ((k)d =

280 otoxin [IL4(38-37)-PE38KDEL] is cytotoxic to IL-4R-expressing cells, we tested whether primary GBM ex

281 d to be highly and specifically cytotoxic to IL-4R-positive head and neck cancer cells, as determined

282 atically reduced in both anti-IL-10R-treated IL-4R alpha(-/-) mice and IL-4R alpha x IL-10 double kno

283 ion much less efficiently than did wild-type IL-4R, requiring 150-fold more IL-4 to reach maximal CD2

284 Moreover, VIL-4 seemed to use IL-4R alpha for signaling and activation, as the VIL-4-i

285 alpha), suggesting enhanced responses of V50 IL-4R when IL-4 is limiting.

286 of phosphorylated STAT6 observed in the V50-IL-4R(alpha)-expressing cells.

287 IL-4 triggers the apoptosis of Th1 cells via IL-4R alpha/IL-13R alpha 1, thus explaining the Th2 bias

288 in BALB/c strain mice and that signaling via IL-4R can be an important factor in the generation of pr

289 Whereas IL-4R antagonist blocked responses to both cytokines, sh

290 em during the acute phase in WT mice whereas IL-4R(-/-) animals expressed higher levels of IL-6 and I

291 on occurs through Ca2+ mobilization, whereas IL-4R down-regulation occurs through a distinct Stat6-de

292 However, whether IL-4R are expressed in brain tumors in situ has not been

293 of IL-13 or IL-13R110Q and IL-13Ralpha1 with IL-4R using surface plasmon resonance and time-resolved

294 gene-subsets and individual genes (FLG with IL-4R and CCL17; r < -0.4, P < .05).

295 (IL-13R alpha 1), which heterodimerizes with IL-4R alpha.

296 amma-chain, which is known to be shared with IL-4R in immune cells.

297 cores stabilized among patients treated with IL-4R 1, 500 microg, despite abrupt withdrawal of cortic

298 Treatment with IL-4R produced significant improvement in FEV(1) on Day

299 mbilical cord methylation of CpG loci within IL-4R with atopic eczema at 12 months (median ratio 1.02

300 lpha and an IL-4 double mutein (R121D/Y124D, IL-4R antagonist) on IL-4- and IL-13-mediated responses.