ライフサイエンスコーパス: IL-2R

1 IL-2R signaling influences two discrete aspects of immun

2 IL-2R signaling is essential for regulatory T cell (Treg

3 IL-2R signaling was also important for CD8(+) T cell imm

4 IL-2R signaling was indispensable for T(reg) cell homeos

5 IL-2R stimulation results in a G(1) cell cycle arrest, c

6 IL-2R-derived signals are also required for their matura

7 = 90), increased levels of IL-8 (P < .001), IL-2R (P < .001), IL-12 (P < .001), IL-15 (P = .001), an

8 ss high levels of CD44, B220, and the IL-15R/IL-2R, and undergo fas-dependent apoptosis.

9 reased interleukin-1beta (IL-1beta), IL-1RA, IL-2R, IL-6, IL-8, IL-10, IL-12, IL-13, IL-15, tumor nec

10 IL-1RA, and marked splenomegaly; and IL-1RA, IL-2R, IP-10, MIP-1beta, and JAK2V617F.

11 Expression of IL-2, IL-2R-alpha, and the major G(1) cell cycle regulatory pr

12 IL-2-IL-2R interactions, rather than antibody-antigen targeti

13 onsistent with a stepwise assembly from IL-2/IL-2R alpha to IL-2/IL-2R alpha/IL-2R beta to IL-2/IL-2R

14 pwise assembly from IL-2/IL-2R alpha to IL-2/IL-2R alpha/IL-2R beta to IL-2/IL-2R alpha/IL-2R beta/ga

15 alpha to IL-2/IL-2R alpha/IL-2R beta to IL-2/IL-2R alpha/IL-2R beta/gamma(c).

16 not appear to be a direct role for the IL-2/IL-2R autocrine pathway within the microenvironment of t

17 the lethal autoimmunity associated with IL-2/IL-2R deficiency.

18 activates Tregs to broadly induce their IL-2/IL-2R gene program and provide a molecular underpinning

19 D4+CD25+ T(reg) cells, we show that the IL-2/IL-2R interaction is active in the thymus at the earlies

20 The IL-2/IL-2R interaction is important for development and perip

21 l, we investigated the possibility that IL-2/IL-2R interactions contribute to the deletion of self-re

22 Furthermore, disruption or blockade of IL-2/IL-2R interactions in vivo during Ag-mediated selection

23 subunit forms the largest of the three IL-2/IL-2R interfaces, which, together with the high abundanc

24 Because the IL-2/IL-2R signaling pathway has been implicated in thymocyte

25 We found that IL-2/IL-2R signaling was associated with a PI3K-dependent/AKT

26 al, and memory in part through enhanced IL-2/IL-2R signaling.

27 ia, suggesting a mechanism by which the IL-2/IL-2R system may impact this widespread vascular patholo

28 cate that the essential function of the IL-2/IL-2R system primarily lies at the level of the producti

29 This augments the activation of the IL-2/IL-2R/STAT5 pathway and enhances cell proliferation in r

30 thymocytes up-regulate expression of IL-2RS: IL-2R(+) double-positive and CD4 single-positive thymocy

31 tic value of these five cytokines, and IL-8, IL-2R, IL-12, and IL-15 remained significant when risk s

32 A two-cytokine (IL-8/IL-2R) -based risk categorization delineated prognostica

33 Aberrant IL-2R signaling in CD4(+) T-cells of type 1 diabetic sub

34 hich is essential for formation of an active IL-2R.

35 T cells failed to express the high affinity IL-2R (CD25) while proliferating in vivo, irrespective o

36 IL-2 and the expression of the high affinity IL-2R (CD25).

37 ion of IL-2 production and its high affinity IL-2R alpha-chain (CD25).

38 racterized by up-regulation of high affinity IL-2R, but a failure to produce IL-2, and uncoupling of

39 egulatory T cells up-regulated high affinity IL-2R, but failed to produce IL-2, express cyclins or c-

40 process using mAbs against the high affinity IL-2R, CD25, and IL-2 in prolonging skin allograft survi

41 T cells (Tregs) displaying the high-affinity IL-2R (alpha-beta-gamma trimers).

42 2-mediated upregulation of the high-affinity IL-2R (CD25) and a subsequent increase in the sensitivit

43 rkers, CD27 and CD11b, and the high-affinity IL-2R (CD25) following infection.

44 helper NK cells expressed the high-affinity IL-2R and were hyperresponsive to IL-2.

45 ibition of IL-2 production and high-affinity IL-2R expression.

46 The lack of high-affinity IL-2R in IL-2Ralpha KO mice increases circulating IL-2 t

47 Expression of the high-affinity IL-2R on gammadeltaT-17 cells prompted us to investigate

48 ction of IL-2 and induction of high-affinity IL-2R upon TCR engagement has precluded a clear distinct

49 Despite expression of the high-affinity IL-2R, CD4(+)CD25(+) regulatory T cells (Tregs) are hypo

50 ion of the other chains of the high-affinity IL-2R, indicating an autonomous and previously unappreci

51 chain (CD25), required for the high-affinity IL-2R, remain poorly understood.

52 on of CD25, a component of the high-affinity IL-2R, was also reduced in response to IL-2 or after in

53 -intoxicating cells expressing high-affinity IL-2R.

54 able to a pre-existing intermediate affinity IL-2R complex and/or hyperactive Jak activity.

55 titutively express the intermediate-affinity IL-2R (beta-gamma dimers) and play a critical role in an

56 T(M) cells through its abundant low-affinity IL-2R, resulting in systemic CD8(+) T(M) cell dominance.

57 neutralization of IL-2 in mice abrogated all IL-2R signaling in Treg cells, but was well tolerated an

58 to bind to the interleukin 2 receptor alpha (IL-2R alpha; CD25)-expressing tumor cells.

59 a R beta L, IFN-gamma R alpha, IL-10R alpha, IL-2R beta, and IL-4R alpha.

60 zation of the receptor subunits IL-2R alpha, IL-2R beta, and gamma(c).

61 ly from IL-2/IL-2R alpha to IL-2/IL-2R alpha/IL-2R beta to IL-2/IL-2R alpha/IL-2R beta/gamma(c).

62 2/IL-2R alpha/IL-2R beta to IL-2/IL-2R alpha/IL-2R beta/gamma(c).

63 he IL-2R pathway and suggest that an altered IL-2R signaling signature may be a biomarker for type 1

64 An IL-2R-signaling mutant that lowers STAT5 activation read

65 rived factor/TRX, originally described as an IL-2R alpha-inducing factor.

66 re we show that up-regulation of Bcl-2 by an IL-2R lacking IL-2Rbeta tyrosine residues leads to incre

67 Further, CD25, an IL-2R alpha chain, and lytic granules of NK cells in soc

68 ther vascular smooth muscle cells express an IL-2R.

69 s on CIA using transgenic mice expressing an IL-2R beta/IL-4R alpha chimeric cytokine receptor transg

70 the GM-CSF binding results in delivery of an IL-2R signal.

71 G patients were combined in a meta-analysis, IL-2R, IL-1RA, and CXCL9 (P = .013, .042, and .0012) wer

72 e colony-stimulating factor, IL-1Ralpha, and IL-2R were serially analyzed in 31 BOS+ and matched 31 B

73 IL-2- and IL-2R-deficient mice are not completely devoid of Foxp3+

74 cellular IL-2, as well as increased CD28 and IL-2R alpha-chain (CD25) expression.

75 During this phase, signals from CD28 and IL-2R cooperate with the TCR to "tune" this threshold by

76 stinct signals transduced via TCR, CD28, and IL-2R for their development and maintenance.

77 y reduced the day-14 percentages of CD3+ and IL-2R+ cells in allogeneic BMT mice, producing results s

78 ns cells at 6 days after infection, CD4+ and IL-2R+ T cells at 5 days after infection, enhanced DTH,

79 mab, IL-2 serum concentrations increased and IL-2R bg signaling induced STAT5 phosphorylation and sus

80 Effects of MV on signaling via the TCR and IL-2R and proliferation or apoptosis of activated primar

81 ive outcome of signaling through the TCR and IL-2R.

82 Interestingly, the addition of an anti-IL-2R-alpha monoclonal antibody profoundly inhibited IL-

83 mmunosuppression regimen (rapamycin and anti-IL-2R monoclonal antibody [mAb]) or the base immunosuppr

84 Cyclosporine, tacrolimus, and anti-IL-2R monoclonal antibody therapy abrogated the effect o

85 Animals receiving the LEA29Y/rapamycin/anti-IL-2R regimen (n = 5) had significantly prolonged islet

86 reas 35 nonsensitized patients received anti-IL-2R.

87 nts as nonsensitized patients receiving anti-IL-2R induction.

88 es direct induction of apoptosis by the anti-IL-2R antibodies in vivo.

89 Furthermore, induction treatment with anti-IL-2R mAb did not prevent the development of these regul

90 dependent, the GMIL2R delivers an augmented IL-2R signal exclusively to CD8(+) T cells responding to

91 examined the effect of delivering augmented IL-2R signals selectively to CD8(+) T cells responding t

92 Thus, to deliver enhanced autocrine IL-2R signals to CD8(+) T cells, we established a transg

93 s capable of augmented, regulated, autocrine IL-2R signaling after target recognition by means of exp

94 CD8+ memory T cells lacking the high-avidity IL-2R results in a failure to repopulate the effector po

95 n CLPs are delivered via IL-2 receptor beta (IL-2R beta) intracellular domains.

96 e previously reported an association between IL-2R mutations and susceptibility to visceral leishmani

97 , we explored a molecular connection between IL-2R signaling and Ets1.

98 , our findings provide a direct link between IL-2R subunit signaling and Ets1 expression and helps to

99 Helix A of IL-2 wedges tightly between IL-2R beta and gamma(c) to form a three-way junction tha

100 this effect depends on the presence of both IL-2R beta and gamma(c) chains and Jak3.

101 e post-transcriptional regulation of Ets1 by IL-2R signaling in human NK cells.

102 the activation of the NF-kappa B pathway by IL-2R signals in NK cells involves activation of the IKK

103 e some of the parallel pathways triggered by IL-2R signaling are sensitive to the effects of rapamyci

104 function and was treated de novo with CsA/c-IL-2R mAb/Pred (n=21; group 2).

105 This pilot study suggests that a SRL/c-IL-2R mAb/Pred induction regimen provides excellent acut

106 CD4(+) T cells and CD25(+) (IL-2R) T cells were stimulated the most by 85A and 85B,

107 Combined signals from the TCR, CD28, IL-2R, and TGF-beta R promote Foxp3 expression in activa

108 okines within the IL-2 receptor gamma chain (IL-2R gamma) superfamily that possess similar and unique

109 do the dominant negative forms of the common IL-2R beta and gamma chains.

110 Conversely, IL-2R signaling was not required for Th cell function.

111 way sequentially linking CD28 costimulation, IL-2R signaling, and mTOR activation as important requir

112 acrophage colony-stimulating factor (GM-CSF)/IL-2R.

113 ic mouse strain expressing a chimeric GM-CSF/IL-2R (GMIL2R).

114 A divergent IL-2R transcriptional signature is noted for thymic Treg

115 unization protocol with transiently enhanced IL-2R signaling in normal mice led to persistent polyclo

116 s issue, we examined the effect of enhancing IL-2R signals in CD8(+) T cells after antigen stimulatio

117 dritic cells (hDCs) produce IL-2 and express IL-2R alpha-chain (CD25), but the role of IL-2 in DC fun

118 These cells express IL-2R alpha only after culture with specific peptide.

119 mphoma is that very few normal cells express IL-2R alpha, whereas the abnormal T cells in patients wi

120 All the melanoma cell lines expressed IL-2R and -15R.

121 nt of Klrg1(+) Tregs also requires extensive IL-2R signaling.

122 eased, indicating that iron is necessary for IL-2R-mediated signaling.

123 s cellular system revealed a requirement for IL-2R expression for CD40 ligand-initiated, IL-12-driven

124 thermore, we show that, through a functional IL-2R, IL-2 initiates signaling pathways and impacts vas

125 tumor necrosis factor, interleukin-2R gamma (IL-2R gamma), and IL-4R alpha.

126 However, IL-2R signals can potentially promote CD8(+) T cell deat

127 y flow cytometry for the expression of human IL-2R and -15Ralpha.

128 In vivo blockade of the human IL-2R by mAb has been used for immunosuppression in tran

129 we report that administration of a humanized IL-2R blocking Ab induced a 4- to 20-fold expansion of C

130 trated dynamic effects, by which hyperactive IL-2R signaling promoted compensatory transcriptional ev

131 cell lysates but failed to immunoprecipitate IL-2R and HLA Ags.

132 the defect is not a consequence of impaired IL-2R expression or IL-2R signaling capability.

133 Tregs with impaired IL-2R signaling were more prevalent in the thymus than s

134 These data demonstrate that defects in IL-2R/1L-15Rbeta expression can lead to a unique NK-defi

135 However, congenital deficiency in IL-2R results in reduced expression of the Treg cell lin

136 -2 signaling at multiple levels that include IL-2R complex formation and Jak3/Stat5 activation.

137 In contrast, CD28 engagement also increases IL-2R surface expression, but the up-regulation does not

138 Instead, IL-2R signaling was reduced in Tregs and total CD4(+) T-

139 tinib (CP-690,550) and the anti-interleukin (IL)-2R antibody basiliximab, as part of a phase 2 study.

140 fector); the cytokine receptors interleukin (IL)-2R beta , common gamma (C gamma ) chain, IL-7R alpha

141 ation as well as cytolytic activity involves IL-2R beta signals that also up-regulate expression of t

142 , our data support a model in which limiting IL-2R signaling is amplified by thymic Tregs to readily

143 f IL-2-dependent targets is indexed to a low IL-2R signaling threshold and that a substantial proport

144 istinct amounts of IL-2R signaling, with low IL-2R signaling sufficient for many key aspects of Treg

145 pressed a mutant IL-2Rbeta-chain that lowers IL-2R signaling.

146 The general effectiveness of mutant IL-2Rs to support thymic Treg development is partially a

147 n mixed chimeras where the Tregs with mutant IL-2Rs were forced to compete with wild-type Tregs durin

148 ymptoms; IL-2R, IL-12, and transfusion need; IL-2R, IL-8, and leukocytosis; IP-10 and thrombocytopeni

149 2 did not overcome the block, despite normal IL-2R expression.

150 Thus, depending on the amount of IL-2R stimulation, a wide range of TCR signals supports

151 and Treg cells requires distinct amounts of IL-2R signaling, with low IL-2R signaling sufficient for

152 d the role of IL-2Rgammac in the assembly of IL-2R complexes and in ligand binding.

153 eletion of JH7-6 impaired the association of IL-2R beta and IL-4R alpha chains with Jak1 but did not

154 more, an Ab reactive with the alpha-chain of IL-2R complex reduced the viability mediated by IL-2 sec

155 mTOR appears to be the critical component of IL-2R signaling regulating GRAIL expression.

156 7R alpha-chain and the cytoplasmic domain of IL-2R beta-chain in IL-2Rbeta(-/-) mice did not prevent

157 reatment block mTOR activation downstream of IL-2R signaling.

158 Therefore, we examined the effect of IL-2R blockade on Th1 and Th2 cytokine production from h

159 may help explain the paradoxical effects of IL-2R blockade in the 2 species.

160 on provides explanations for the efficacy of IL-2R antibody therapy in uveitis, and suggests that ant

161 iation rate and high-affinity interaction of IL-2R alpha with IL-2 at the cell surface.

162 uction in human Tregs increased the level of IL-2R subunits and promoted tyrosine phosphorylation of

163 ) transgenic mice expressed normal levels of IL-2R subunits.

164 Modulation of IL-2R expression was observed at or above a bexarotene d

165 lines stably expressing deletion mutants of IL-2R that fail to activate PI 3-K have questioned the r

166 We find a distinct pattern of IL-2R signaling in which the Janus kinase/STAT pathway r

167 In the presence of IL-2R(+) MHC class II(+) T cells, IL2NAg fusion proteins

168 l costimulation by LFA-1 is up-regulation of IL-2R expression.

169 sine phosphatase N2, a negative regulator of IL-2R signaling.

170 We questioned whether the restriction of IL-2R gamma-chain (Il-2rgamma)-dependent cytokine signal

171 These findings support the principal role of IL-2R alpha to deliver IL-2 to the signaling complex and

172 perimental efforts to understand the role of IL-2R expression and signaling in the suppressor functio

173 However, the role of IL-2R signaling during thymic Treg development remains o

174 To more precisely define the direct role of IL-2R signaling on CD8(+) T cells during the response to

175 se data suggest that the predominant role of IL-2R signals delivered to responding CD8(+) T cells is

176 regulation, illustrating the specificity of IL-2R beta and gamma subunit signaling on the regulation

177 naling molecules to determine specificity of IL-2R gamma superfamily cytokines.

178 d characterization of a new genetic stock of IL-2R common gamma-chain deficient NOD/LtSz-scid (NOD-sc

179 de, in its affinity for the alpha subunit of IL-2R (CD25).

180 s at the interface with the alpha subunit of IL-2R.

181 immune phenotype in mice lacking subunits of IL-2R.

182 nduced a three- to eightfold upregulation of IL-2R expression in all the melanoma cell lines.

183 s in a manner that is partially dependent on IL-2R and STAT5 signaling.

184 ression during thymic development depends on IL-2R signaling.

185 the basis for this phenomenon by focusing on IL-2R signaling, which is known to promote Th1 and suppr

186 s from mice genetically deficient in IL-2 or IL-2R(alpha) (CD25) expression.

187 oimmunity related with deficiency in IL-2 or IL-2R.

188 ng an adoptive transfer system with IL-2- or IL-2R-deficient TCR transgenic CD8 T cells and MHC class

189 s action is not dependent on either IL-4R or IL-2R signals and results in OX40 controlling initial na

190 CR ligation in the absence of either CD28 or IL-2R signals.

191 consequence of impaired IL-2R expression or IL-2R signaling capability.

192 y, NK cells do not inhibit IL-2 secretion or IL-2R up-regulation and do not induce T cell death.

193 e, directly demonstrating that CD25 promotes IL-2R signaling.

194 ion of pSTAT5, indicating that PP2A promotes IL-2R signaling through multiple mechanisms.

195 d protein phosphatase 2A (PP2A) in promoting IL-2R signaling in Tregs.

196 esponsiveness of the interleukin 2 receptor (IL-2R) and transcription factor STAT5.

197 kers, as measured by interleukin-2 receptor (IL-2R) and transcription factor T bet.

198 -205, B7-1, CD4, and interleukin-2 receptor (IL-2R) antibodies and histopathologic, RT-PCR, and delay

199 re we identify human interleukin-2 receptor (IL-2R) beta chain (IL2RB) gene defects as a cause of lif

200 lasmic domain of the interleukin-2 receptor (IL-2R) beta chain that is involved in the recruitment of

201 expressing the high-affinity IL-2 receptor (IL-2R) consisting of the alpha/p55/CD25, beta/p75/CD122,

202 , none of the 3 chains of the IL-2 receptor (IL-2R) expresses a binding site for PI 3-kinase.

203 lating high-affinity interleukin-2 receptor (IL-2R) expression.

204 as fused to the interleukin (IL)-2 receptor (IL-2R) extracellular domain.

205 The IL-2 receptor (IL-2R) is composed of IL-2Ralpha, IL-2Rbeta, and IL-2Rga

206 The interleukin-2 receptor (IL-2R) is composed of one affinity-modulating subunit (I

207 h chimeric (c-) anti-interleukin-2 receptor (IL-2R) monoclonal antibodies (mAb).

208 hat from circulating interleukin-2 receptor (IL-2R) or IL-8 levels.

209 nes in the interleukin (IL)-2/IL-2 receptor (IL-2R) pathway are associated with type 1 diabetes.

210 ignificantly higher levels of IL-2 receptor (IL-2R) signaling compared with those in lonesome microwe

211 Interleukin-2 receptor (IL-2R) signaling is essential for T regulatory (Treg) ce

212 Interleukin-2 receptor (IL-2R) signaling regulates tolerance and immunity.

213 ation, making unclear whether IL-2 receptor (IL-2R) signals ultimately have a predominantly positive

214 nt expression of the interleukin 2 receptor (IL-2R), are reliant on IL-2 produced by activated T cell

215 mma(c) chains of the interleukin-2 receptor (IL-2R), the heavy chain of the major histocompatibility

216 leukin-2 (IL-2) secretion and IL-2 receptor (IL-2R)-signal transducer and activator of transcription

217 donor T cells, their interleukin-2-receptor (IL-2R) alpha-chain expression and their capacity to indu

218 d more activated ([interleukin-2 receptor+], IL-2R+) CD8+ T cells.

219 ted that Thr-450 is important for regulating IL-2R complex formation, recruitment of JAK3, and activa

220 ed T cell expansion by positively regulating IL-2R signaling and mitochondrial function.

221 In this study, we assess IL-2 release, IL-2R expression, IL-2 signaling, and cell proliferation

222 effects on plasma levels of CXCL10, soluble IL-2R, and IL-1alpha.

223 ique as monitored by serum levels of soluble IL-2R alpha and/or human beta-2-microglobulin (P <.05, t

224 owth as monitored by serum levels of soluble IL-2R-alpha (sIL-2R-alpha) and soluble beta2-microglobul

225 Overall, our data show that strong IL-2R and inflammatory signals act through Dicer and miR

226 they are larger, more granular, and strongly IL-2R positive.

227 mAb that binds the IL-2 receptor a subunit (IL-2R a or CD25) and prevents IL-2 binding.

228 etero-trimerization of the receptor subunits IL-2R alpha, IL-2R beta, and gamma(c).

229 Surprisingly, IL-2R alpha makes no contacts with IL-2R beta or gamma(c

230 Rather, high-affinity T cells sustained IL-2R expression longer and expressed two novel Th cell

231 increased IL-8 and constitutional symptoms; IL-2R, IL-12, and transfusion need; IL-2R, IL-8, and leu

232 domain and the VE-cadherin cytoplasmic tail (IL-2R-VE-cadcyto) was expressed in microvascular endothe

233 under rechallenge conditions that targeting IL-2R by partial mammalian target of rapamycin inhibitio

234 g the activation of CD8(+) T cells, and that IL-2R-dependent activation of the transcription factor S

235 CD25 in peripheral Tregs, we also find that IL-2R signaling is indispensable for Treg homeostasis, w

236 These data indicate that IL-2R signaling in the thymus and the periphery leads to

237 Here we show that IL-2R signaling is required by thymic Tregs at an early

238 er, these observations strongly suggest that IL-2R signals can activate a pathway leading to NF-kappa

239 ion compared with wild type, suggesting that IL-2R signaling is required for efficient OX40-mediated

240 The IL-2R alpha subunit forms the largest of the three IL-2/

241 The IL-2R common gamma-chain (IL-2Rgamma) is shared by recep

242 The IL-2R promotes rapid expansion of activated T cells thro

243 Daclizumab (Dac), an Ab against the IL-2R alpha-chain, inhibits brain inflammation in patien

244 s study was to define genes regulated by the IL-2R-mediated PI3K pathway in T cells.

245 tion of the cell cycle gene cyclin D2 by the IL-2R.

246 greatly diminished expression of CD122, the IL-2R/IL-15R beta-chain, and impaired expression of the

247 y T cells (Tregs) constitutively express the IL-2R alpha-chain (CD25) on their surface.

248 ation of VE-cadherin in cells expressing the IL-2R-VE-cadcyto mutant.

249 ages 2 through 5 months were stained for the IL-2R.

250 ceptor tyrosine kinase that signals from the IL-2R, where activating mutations have been found in div

251 L-12 is shown to stimulate expression of the IL-2R alpha-chain (CD25) to much higher levels than are

252 gulated both the p55 and p75 subunits of the IL-2R and enhanced 5- to 10-fold the susceptibility of T

253 ed against the alpha-chain (Tac/CD25) of the IL-2R are an emerging therapy in both transplantation an

254 , which nearly span the entire length of the IL-2R beta and gamma(c) subunits.

255 Fusion of the A region of the IL-2R beta cytoplasmic tail to IL-7R alpha enables IL-7

256 en linked to a compromised expression of the IL-2R beta subunit (CD122) by old CD8+ T cells.

257 sisted of the extracytoplasmic domain of the IL-2R beta-chain and the cytoplasmic domain of IL-7R alp

258 2, IL-4, and IL-7, through engagement of the IL-2R common gamma-chain.

259 was not linked to altered expression of the IL-2R complex.

260 il dramatically increased endocytosis of the IL-2R in a clathrin-dependent manner.

261 sion of both the p55 and p75 subunits of the IL-2R in T-cell leukemias and p75 in B-cell leukemias.

262 controlling the nonredundant activity of the IL-2R is selective compartmentalization of IL-2-producin

263 te the expression of the three chains of the IL-2R on hDCs and that IL-2 induces STAT5 phosphorylatio

264 ut it was not determined which region of the IL-2R or which pathway was activated to direct this sign

265 helps to explain the interdependence of the IL-2R subunits and Ets1 for NK cell development and func

266 pression of the common gamma(c)-chain of the IL-2R that mediates CD8(+) T cell survival.

267 nding to the extracytoplasmic portion of the IL-2R via this chimeric receptor.

268 scle cells express all three subunits of the IL-2R, and that expression of IL-2Ralpha varies with vas

269 he structure, signaling, and function of the IL-2R, emphasizing the contribution of IL-2 for T cell-d

270 ls in the absence of the other chains of the IL-2R, which are indispensable for IL-2 signaling.

271 Expression of the IL-2R-VE-cadcyto mutant resulted in the internalization

272 TAT5A/5B was triggered via activation of the IL-2R.

273 based on their expression of subunits of the IL-2R.

274 least two, if not all three, subunits of the IL-2R; although, compared with lymphocytes, relatively l

275 G but not anti-CD52 mAb (alemtuzumab) or the IL-2R antagonists causes rapid and sustained expansion o

276 of IL-2Rbeta tyrosines, indicating that the IL-2R engages at least two distinct signaling pathways t

277 It has been shown that the IL-2R is a critical element in the peripheral self-toler

278 owth and differentiation signals through the IL-2R initially favors Ag-specific CD8(+) T cells to dev

279 Signaling through the IL-2R or chimeric IL-2Rbeta/IL-7Ralpha in vivo or the cu

280 emain largely unknown, signaling through the IL-2R represents one feature for the production of T(reg

281 t mice and mice unable to signal through the IL-2R, we hypothesized that the tolerizing role of STAT5

282 is inhibited in mice treated with Ab to the IL-2R beta-chain that blocks signaling by either IL-2 or

283 g through TCR/costimulatory molecules vs the IL-2R.

284 for treatment of type 1 diabetes within the IL-2R pathway and suggest that an altered IL-2R signalin

285 Therefore, IL-2R is required for the progression, functional progra

286 functional maturation and activation through IL-2R binding.

287 nges result from increased signaling through IL-2R.

288 Our observation may have implications to IL-2R blockade therapy and for the potential role of CD5

289 ation, exhibits a reciprocal relationship to IL-2R expression over the time course of activation of P

290 y T cells (Tregs) are hypoproliferative upon IL-2R stimulation in vitro.

291 Using IL-2R mutants and specific pharmacologic inhibitors, we

292 Relying on genetic mouse models where IL-2R signaling was either completely blocked or selecti

293 We asked whether IL-2R subunits could already preassemble and signal effi

294 as proliferation, making it unclear whether IL-2R signals provide a predominantly positive or negati

295 might be due to specificity associated with IL-2R signal transduction or because IL-2 was uniquely p

296 risingly, IL-2R alpha makes no contacts with IL-2R beta or gamma(c), and only minor changes are obser

297 at the immunocytokine associated mainly with IL-2R-expressing innate immune cells, with more bound im

298 The instability primarily occurred with IL-2R(lo) Tregs and was shown, in part, to be the conseq

299 pproach in a clinical trial in patients with IL-2R alpha-expressing leukemias.

300 est a rationale for combining rexinoids with IL-2R-targeted therapies in lymphoid malignancies as wel