ライフサイエンスコーパス: IL-2

1 IL-2 and IFNgamma in response to CMVpp65 were enhanced w

2 IL-2 expression is blocked in naive, but not activated o

3 IL-2 feedback had no effect on Th1- or Th17-signature cy

4 IL-2 is a pleiotropic cytokine that promotes the differe

5 IL-2 priming increased the activity of mTORC1, and inhib

6 IL-2- and alphaKG-sensitive CTCF sites in T cells were a

7 IL-2/JES6-1 injection before or after hapten sensitizati

8 Also, they have low IFN-gamma, IL-17F, IL-2, and IL-12 levels, with increased IL-10 production

9 ed interferon-gamma, interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, tumor necrosis factor-alpha, epi

10 factor (TNF)-alpha, interleukin (IL)-1beta, IL-2, IL-6, and IL-8-were determined using a multiplex b

11 th concentrations of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor

12 as associated with lower levels of IL-1beta, IL-2 and IL-4 (P<0.05).

13 erleukin (IL)-10, IL-12p70, IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8 and tumour necrosis factor-alpha.

14 Interleukin 2 (IL-2) promotes Foxp3(+) regulatory T (Treg) cell respons

15 factor alpha (TNF-alpha), and interleukin 2 (IL-2) secretion by CD8(+) T cells.

16 (+) T cells) that coexpressed interleukin-2 (IL-2) (66.4%) and/or tumor necrosis factor alpha (TNF-al

17 factor alpha (TNF-alpha), and interleukin-2 (IL-2) (P < 0.001) and splenic and lung CD8(+) T cells ex

18 tivated by cytokines from the interleukin-2 (IL-2) family to promote cell proliferation and to inhibi

19 Interleukin-2 (IL-2) has an essential role in the expansion and functio

20 ted T cell receptor (TCR) and interleukin-2 (IL-2) signaling and upregulated PD-1, leading to diminis

21 ine correlates with defective interleukin-2 (IL-2) signaling in memory CD4 T cells from HIV-infected

22 strongly augmented IFN-gamma, interleukin-2 (IL-2), and TNF-alpha production.

23 d LTBI from controls included interleukin-2 (IL-2), monocyte chemotactic protein 2 (MCP-2), interfero

24 We found that aspects of the interleukin-2 (IL-2)-sensitive effector gene program in CD4(+) and CD8(

25 TCR]) and cytokines examined (interleukin 2 [IL-2], IL-4, IL-10, IL-17A, and gamma interferon [IFN-ga

26 ct in the expression of CD25 (interleukin-2 [IL-2] receptor alpha chain) on Ad5-elicited CD4 T cells,

27 factor alpha [TNF-alpha], and interleukin-2 [IL-2]) and type 17 (IL-17A and/or IL-17F) cytokines and

28 vation markers (CD107, CD154, interleukin-2 [IL-2], tumor necrosis factor [TNF], and IFN-gamma) and m

29 naling pathway that stabilizes interleukin-2(IL-2), IL-4, and IL-10 messenger RNA (mRNA) transcripts.

30 rgence of an anergic and regulatory CTLA-4(+)IL-2(low)Foxp3(-) T cell population, where the tolerance

31 and cytokines downstream of mTOR activation (IL-2, IL-6, and IL-13), whereas in late PVR vitreous, cy

32 th decreased expression of the high affinity IL-2 receptor (CD25).

33 tration of an engineered mouse serum albumin/IL-2 fusion with an Fc fusion to an integrin-binding pep

34 atory T cells, and CTLA-4 blockade alongside IL-2 treatment in vivo prevented the decrease in CD80 an

35 es and coexpression of IFN-gamma, TNF-alpha, IL-2, IL-17, and/or IL-22 in CD4 T cells and IFN-gamma-e

36 mutation decreased STAT5 binding and altered IL-2-induced Il2ra gene expression, revealing that indiv

37 Although IL-2 is produced by all polarized Th subsets to some lev

38 Although IL-2 was able to induce robust proliferation of gammadel

39 Although IL-2/mAb complexes can be efficacious in cGVHD, a cautio

40 Il2ra as the top-ranked gene regulated by an IL-2-activated STAT5-bound superenhancer and one of the

41 We identified an IL-2-JAK-independent SRC family Tyr-kinase-controlled si

42 s equipped to suppress Th17 cells through an IL-2/STAT5-dependent mechanism.

43 showed a low content in IL 10-2, IL 6-3 and IL 2-6.

44 BiG efficiently inhibited IL-15- and IL-2-dependent functions of primary cells, including CD8

45 y higher levels of IL-10, IL-1beta, IL-4 and IL-2 in both MCI groups (P<0.001), while there was no si

46 n analysis of IFN-gamma and of TNF-alpha and IL-2 revealed that T cell responses consist of two types

47 uction of IFN-gamma but not of TNF-alpha and IL-2.

48 he coproduction of IFN-gamma, TNF-alpha, and IL-2.

49 nhibiting Bruton's tyrosine kinase (BTK) and IL-2-inducible T cell kinase (ITK).

50 Furthermore, dendritic cell- and IL-2/7-dependent T cell survival was found to be indepen

51 ediated through contact with CD4 T cells and IL-2 production by CD4 T cells and Vgamma9 T cells thems

52 es (IL-10) in the bronchoalveolar fluid, and IL-2 and IFN-gamma cytokines in restimulated splenocyte

53 fluenza-infected mice produced IFN-gamma and IL-2 but not IL-5 on stimulation with the aforementioned

54 IFN-gamma and IL-2 results for subjects >/= 70 years old were signific

55 caused by reduced secretion of IFN-gamma and IL-2.

56 ree key cytokines: TNF-alpha, IFN-gamma, and IL-2.

57 e former Tregs produced copious IFNgamma and IL-2.

58 25, IL-33, thymic stromal lymphopoietin, and IL-2.

59 xhibited reduced Ag-driven proliferation and IL-2 secretion in vitro.

60 crospheres; TGF-beta1, Rapamycin (Rapa), and IL-2).

61 ineered to release TGF-beta1, Rapamycin, and IL-2, to locally sustain a microenvironment that promote

62 cts of cysLTs, PGD2, IL-33, IL-25, TSLP, and IL-2 alone or in combination on ILC2s were defined by us

63 l death was prevented with neutralizing anti-IL-2 Ab or STAT5/JAK3 inhibitors, indicating that STAT5

64 ntigen loads are translated into appropriate IL-2 production to ensure adequate responses against pat

65 We also show that Tregs from AA patients are IL-2-sensitive and expandable in vitro, suggesting novel

66 r maximal release of some cytokines, such as IL-2 and IL-6.

67 racellular calcium concentration, as well as IL-2 gene expression.

68 JAG1-induced NF-kappaB activation as well as IL-2-induced STAT5 activation were essential for the pro

69 paradoxically robust, rapid, cell-autonomous IL-2 and IFNgamma production, equip liver CD8 TRM to sur

70 e observation that the soluble factors BAFF, IL-2, and IL-21 induce memory and DN B cell activation a

71 ermore, at low antigen concentrations binary IL-2 expression safeguards by its spatial distribution s

72 CD83 inhibited T cell proliferation, blocked IL-2 secretion, and rendered T cells unresponsive to fur

73 roduction and STAT5 activation, and blocking IL-2 responses eliminates the difference in IL-9 product

74 egrates mitogenic signals downstream of both IL-2 and the TCR, yet marks an invariant minimal thresho

75 he effect of lipoxin A4 on PP5 activation by IL-2 plus IL-4.

76 globally analyzed enhancer elements bound by IL-2-activated STAT5 and IL-21-activated STAT3 in T cell

77 AT pathway blocked proliferation elicited by IL-2 and IL-15, but only an inhibitor targeting the PI3K

78 dly superenriched at genes highly induced by IL-2 and that IL-2-activated STAT5 binding induces new a

79 tion of effector memory phenotype induced by IL-2.

80 wnstream differentiation signals mediated by IL-2.

81 ty of TCR signaling that is not modulated by IL-2, thereby restricting responses to low-affinity or l

82 ffector differentiation that is regulated by IL-2 and IL-12 signaling and the combined activities of

83 itch to glycolysis, which can be restored by IL-2.

84 hibit proliferation of T cells stimulated by IL-2 and by antigen presentation using a Theileria-trans

85 ry, displaying impaired expression of CD62L, IL-2, Eomesodermin, and CXCR4, which resulted in impaire

86 like its effects on conventional Treg cells, IL-2 inhibits TFR cell responses.

87 These expressed the common IL-2/IL-15 receptors and another subset of APOBEC3G anti

88 s were often associated with loci containing IL-2- and alphaKG-sensitive genome organization patterns

89 ditions of IL-2 deficiency, and, conversely, IL-2 represses Flicr expression.

90 ta revealed that Janus kinases (JAKs) couple IL-2 receptors to the coordinated phosphorylation of tra

91 These findings implicate the IFNbeta/CREM/IL-2 axis in regulating T-lymphocyte function during chr

92 pies, such as administration of the cytokine IL-2, adoptive cell transfer (ACT) and the recent succes

93 the T-cell antigen receptor and the cytokine IL-2, but its role in T-cell immunity in vivo has not be

94 those activated by the endogenous cytokines IL-2, IL-4, and IFN.

95 gs reduced the serum levels of Th1 cytokines IL-2 and IL-12, and Th2 cytokines IL-4 and IL-10, partic

96 with steroid-refractory cGVHD received daily IL-2 (1 x 10(6) IU/m(2)) for 12 weeks.

97 uding the expansion of DN T cells, decreased IL-2, and increased IL-17 production.

98 tion of IFNgamma, in addition to a defective IL-2 receptor signaling machinery and a defective commun

99 Functional analysis revealed defective IL-2 and TNF production yet retained expression of IFN-g

100 These data identify DC-derived IL-2 as a key mediator of alum adjuvanticity in vivo and

101 Using chimeric mice, we show that DC-derived IL-2 is required for maximal Ag-specific proliferation o

102 ced with MAGE-A3 TCR plus systemic high-dose IL-2.

103 tudy, we investigated the effect of low-dose IL-2 administration on Treg function and corneal allogra

104 D25(high) cells are unresponsive to low-dose IL-2 and in patients have marked proliferative ability,

105 Low-dose IL-2 provides durable clinical improvement in active cGV

106 Treatment with low-dose IL-2 significantly increased frequencies of CD4CD25Foxp3

107 ovel therapeutic approaches such as low-dose IL-2 therapy and/or expanded autologous Tregs and meriti

108 promoted IL-17 production and downregulated IL-2 production.

109 was observed on DCs in vivo following early IL-2 treatment.

110 Mechanistically, early IL-2 treatment enhanced CTLA-4 expression on regulatory

111 effector CD8 T cell numbers, but only early IL-2 signals enhance memory numbers.

112 -9 and IRF4 expression are rescued by either IL-2 or constitutively active STAT5, but not NFATc1.

113 f STAT3 correlates with increased endogenous IL-2 production and STAT5 activation, and blocking IL-2

114 r late (days 4-6) administration of enhanced IL-2 signals increase peak effector CD8 T cell numbers,

115 Exogenous IL-2 restores the phenotypic changes and overall gene-ex

116 uld be readily corrected by adding exogenous IL-2 to the co-cultures.

117 Critically, exogenous IL-2 restores Myc expression in RTEs, driving aerobic gl

118 Furthermore, the addition of exogenous IL-2 enhanced PEM Treg phosphorylated STAT5 signaling co

119 CD4 T cells, and administration of exogenous IL-2 following Ad5 immunization partially restored CD4 T

120 OX40 L and JAG1 in the presence of exogenous IL-2.

121 tantly, the uptake of exosomes, derived from IL-2 stimulated CD4+ T cells, effectively promoted react

122 profile of up to four functions (IFN-gamma(+)IL-2(+)Perforin(+)Granzyme B(+)).

123 bset of M. tuberculosis-specific IFN-gamma(+)IL-2(-)TNF-alpha(+) CD4 T cells.

124 uded both protective (CD107a(-)/IFN-gamma(+)/IL-2(+)/TNF-alpha(+) CD4(+) T cells, CD107a(-)/IFN-gamma

125 ha(+) CD4(+) T cells, CD107a(-)/IFN-gamma(+)/IL-2(+)/TNF-alpha(+) CD8(+) T cells) and detrimental (CD

126 lls) and detrimental (CD107a(+)/IFN-gamma(+)/IL-2(-)/TNF-alpha(-) CD8(+) T cells) subsets.

127 cells expressing high amounts of IFN-gamma, IL-2 and TNF.

128 ectors defined by coexpression of IFN-gamma, IL-2, and CD107a after vaccination.

129 69) expression, and production of IFN-gamma, IL-2, and granzyme B.

130 inflammatory cytokines TNF-alpha, IFN-gamma, IL-2, and IL-17.

131 t demonstrated either high (IL-8, IFN-gamma, IL-2, IL-6, and IL-1beta) or low (IL-15, TNF-alpha, IL-1

132 lcNAc levels and in the absence of O-GlcNAc, IL-2 production and proliferation were compromised.

133 nfluenza infection model, we found that high IL-2 concentrations at the peak of the infection prevent

134 ype 2 cytokine-secreting cells and highlight IL-2 as a critical component in optimal cytokine product

135 However, it is not clear how IL-2 affects T follicular regulatory (TFR) cells, a cell

136 Aldesleukin (Proleukin; recombinant human IL-2), which is administered at high doses to activate t

137 ression of IL-2Ralpha, resulting in impaired IL-2 signaling and ultimately leading to increased apopt

138 ulating this cellular circuit culminating in IL-2 production could have clinical benefits in settings

139 HC ligand followed by ligand-free culture in IL-2, we found that ligand density determined the freque

140 roinflammatory microenvironment deficient in IL-2 leads to impaired function and increased susceptibi

141 aT-17 cells to be enriched, not depleted, in IL-2-deficient mice.

142 aired antigen presentation, and a failure in IL-2-dependent Treg homeostasis.

143 depletion re-established the CHS response in IL-2/JES6-1-treated mice.

144 of several interleukin receptors, including IL-2 and IL-7 receptors.

145 vated T cells that corresponded to increased IL-2 mRNA levels.

146 There was increased IL-2 and IL-12 and reduced IL-4 immunostaining in VUE le

147 days resulted in rapid mortality, indicating IL-2/mAb complexes can drive conventional T-cell (Tcon)-

148 -2 silences directly constitutive or induced IL-2 expression through the ARRE-2.

149 nificantly decreased T-cell receptor-induced IL-2, IFN-gamma, and GM-CSF expression.

150 Increases of general inflammatory (IL-2), innate (IL-1beta), and some TH1/interferon (IFN-g

151 tion of kynurenine found in plasma inhibited IL-2 signaling through the production of reactive oxygen

152 Ld-IL-2 induced Treg expansion and activation that elicited

153 anded and activated by low doses of IL-2 (ld-IL-2) inducing immunoregulation without immunosuppressio

154 ro cultures, IL-23 induced IL-17 and limited IL-2 production, whereas T follicular helper and double

155 ammatory Tregs (RORc(High/+), Helios(Low/-), IL-2(+), IFN-gamma(+), and IL-8(+)) compared with typica

156 ION is associated with higher VEGF and lower IL-2 concentrations without a change in other inflammato

157 In contrast, lytic IL-2/Fc or IL-10/Fc had no effect.

158 Recipients were treated with lytic IL-2/Fc, nonlytic IL-2/Fc, TGF-beta/Fc, or IL-10/Fc fusi

159 Mechanistically, IL-2 production was compromised in weakly stimulated T c

160 gene expression and show that STAT5 mediates IL-2-induced chromatin looping at superenhancers to pref

161 ld TCR signaling in the context of mitogenic IL-2 signals, thereby rendering CD8 T cells exquisitely

162 In an acute GVHD (aGVHD) model, IL-2/mAb complexes given for only 4 days resulted in rap

163 TGF-beta/Fc and nonlytic IL-2/Fc exert a synergistic effect in promotion of alloe

164 ts were treated with lytic IL-2/Fc, nonlytic IL-2/Fc, TGF-beta/Fc, or IL-10/Fc fusion proteins to pro

165 The combination of nonlytic IL-2/Fc and TGF-beta/Fc had a synergistic effect to prom

166 beta/Fc (5- or 10-day treatment) or nonlytic IL-2/Fc (10-day treatment) fusion proteins to the condit

167 expression of SAP in SLE T cells normalized IL-2 production, calcium (Ca(2+)) responses, and tyrosin

168 signaling and Treg differentiation, but not IL-2 expression.

169 ker upregulation (CD69, CD25, CD154, NUR77), IL-2 production, or clonal expansion.

170 The absence of IL-2 also resulted in higher IL-17 production and the em

171 d cytokine (IL233) bearing the activities of IL-2 and IL-33 for efficient targeting to Tregs.

172 In a skin transplant model, the addition of IL-2 synergizes with CNIs treatment, promoting intragraf

173 Furthermore, the addition of IL-2 to in vitro cultures of sorted gammadeltaT-17 cells

174 Interestingly, addition of IL-2 to LTE4 and epithelial cytokines significantly ampl

175 -)MRL.lpr mice produced increased amounts of IL-2 and reduced amounts of IL-17 compared with T cells

176 d subsequent expression of IFN-gamma, and of IL-2, depends on calcium-induced de novo transcription a

177 onse of gammadeltaT-17 cells upon arrival of IL-2-producing adaptive immune cells at the site of infl

178 l microenvironment where the availability of IL-2 is limited.

179 unction approaches, we found that capture of IL-2 was dispensable for the control of CD4(+) T cells b

180 regs in mice express ST2, and coinjection of IL-2 and IL-33 increased the number of Tregs in lymphoid

181 Hence, the combination of IL-2 and CNIs constitutes an optimal immunomodulatory re

182 optosis showed that cytokine combinations of IL-2 plus IL-4 as well as TNF-alpha plus IFN-gamma, or I

183 /mL; P = .010) and the mean concentration of IL-2 (5.56 +/- 1.27 pg/mL) was significantly lower in th

184 licr is particularly marked in conditions of IL-2 deficiency, and, conversely, IL-2 represses Flicr e

185 a simple network based on the consumption of IL-2 by Treg cells in their suppressor function.

186 cytokine, which utilizes the cooperation of IL-2 and IL-33 to enhance Treg- and ILC2-mediated protec

187 IL-3 and primary CD8(+) T cells depleted of IL-2 that are differentiating toward memory cells.

188 ively expanded and activated by low doses of IL-2 (ld-IL-2) inducing immunoregulation without immunos

189 D8 T cells become responsive to low doses of IL-2 more quickly than CD4 T cells, and propose that thi

190 e CD8 T cells are responsive to low doses of IL-2.

191 urn accounts for the differential effects of IL-2 on the minimal TCR signaling threshold for prolifer

192 ubset was more susceptible to the effects of IL-2 than Vgamma4(+) gammadeltaT-17 cells.

193 These data highlights the existence of IL-2 trans-presentation between NK cells in the local mi

194 c dendritic cell accumulation, expression of IL-2 and indoleamine 2,3-dioxygenase were evident in TLR

195 ermore, PGE2 downregulated the expression of IL-2 receptor alpha (CD25).

196 on followed by the concomitant expression of IL-2.

197 binding protein (OMCP) and a mutated form of IL-2 with poor affinity for IL-2Ralpha.

198 We demonstrate a direct impact of IL-2 and IL-15, two common gamma-chain-dependent cytokin

199 showed a significant reduction in levels of IL-2 (p < 0.0001) after treatment with abatacept, indica

200 e significantly decreased, and the levels of IL-2 in the serum of AOM rats increased after KJT treatm

201 ct, exhibited significantly higher levels of IL-2 receptor (IL-2R) signaling compared with those in l

202 patients have similar circulating levels of IL-2, whereas SLE patients exhibit elevated BAFF and DN

203 n, the latter by promoting endocytic loss of IL-2 receptor-alpha (CD25).

204 ented IRI more efficiently than a mixture of IL-2 and IL-33.

205 The number of IL-2-dependent FoxP3(+) regulatory T cells is increased

206 function that are stable in the presence of IL-2 and IL-23.

207 D28 monoclonal antibodies in the presence of IL-2, IL-15, and IL-1beta.

208 silencing B7-H4 increased the production of IL-2 and IFNgamma from autologous cells; a process media

209 cells, as indicated by reduced production of IL-2 and reduced T cell proliferation.

210 cells, characterized by robust production of IL-2 as well as key Th1-type cytokines IFN-gamma and TNF

211 mouse splenocytes led to down-regulation of IL-2, a key cytokine involved in T-cell proliferation.

212 limp-1, a known transcriptional repressor of IL-2.

213 leased by DCs, even when T cell secretion of IL-2 is intact.

214 Mechanistically, GTIs blocked secretion of IL-2 that normally feeds back in a paracrine manner to p

215 ed mRNA stability and inhibited secretion of IL-2, IL-4, and IL-10.

216 This study identifies a series of IL-2-induced cellular changes that regulates the NKG2D r

217 taneous aldesleukin in the Adaptive Study of IL-2 Dose on Regulatory T Cells in Type 1 Diabetes (DILT

218 Ab in the absence of an exogenous supply of IL-2.

219 mic Treg cells exhibit reduced dependence on IL-2 but unchanged rates of proliferation and apoptosis.

220 ced in all patients with pDGS, especially on IL-2 stimulation.

221 presence of IL-2Ralpha, BiG had no impact on IL-2-dependent regulatory T cell proliferation.

222 culture experiments in the presence of only IL-2 demonstrated that independent of their CD28 express

223 feration per se, it is essential for optimum IL-2 production by Teff cells.

224 tivated NKp30/MAPK/IL-12 (interleukin-12) or IL-2 (interleukin-2) pathway was susceptible to NK lysis

225 ur analysis shows that Treg depletion and/or IL-2 neutralization can effectively improve the treatmen

226 fusion proteins of IL-10/Fc, TGF-beta/Fc, or IL-2/Fc would enhance allogeneic bone marrow cell (BMC)

227 by the individual production of IFN-gamma or IL-2, and a multifunctional CD8(+) T cell profile of up

228 expression, and the production of IL-12 p70, IL-2, IL-6, and TNF-alpha by beta-glucan-stimulated DCs.

229 n compete for a limiting supply of paracrine IL-2 generated by autoreactive CD4(+) T cells in respons

230 of proinflammatory cytokines, in particular IL-2, distinguish the cyclotide from other marketed drug

231 e CXCR3(+)CCR6(-)CCR4(-)CXCR5(-) and produce IL-2, as well as low levels of TNF-alpha.

232 T cells, gammadeltaT-17 cells do not produce IL-2, but express Blimp-1, a known transcriptional repre

233 s uric acid crystals, induces DCs to produce IL-2 following initiation of actin-mediated phagocytosis

234 increases the capacity of T cells to produce IL-2, which overcomes TGFbeta-mediated suppression.

235 am by the NF-kappaB pathway, and it promoted IL-2 production and proliferation.

236 or response element (ARRE)-2 of the proximal IL-2 promoter.

237 Five cytokines (G-CSF, GM-CSF, IL-1-ra, IL-2 and IL-16) were significantly increased in MPs from

238 anti-CD3 mAb, anti-CD28 mAb, and recombinant IL-2 induced expression of LAP on naive CD4(+) T cells,

239 presented impaired proliferation and reduced IL-2 production on anti-CD3/CD28 stimulation and decreas

240 cells increased serum IFN-gamma but reduced IL-2 concentrations, leading to upregulation of PD-L1 ex

241 of transcription 3 phosphorylation, reduced IL-2 production, and enhanced activation and survival.

242 ter Ad5 immunization could be due to reduced IL-2-mediated signaling.IMPORTANCE During viral infectio

243 , the master transcription factor regulating IL-2 expression.

244 le, we show that alum adjuvanticity requires IL-2 specifically released by DCs, even when T cell secr

245 secondary outcomes, using a highly sensitive IL-2 assay, the observed plasma concentrations of the dr

246 Both serum IL-2, IL-4, and IL-6 and endothelial cell markers were a

247 s of immune dysregulation, including soluble IL-2 receptor alpha chain, CD45RO(+)CD4(+) effector T ce

248 Serum soluble IL-2 receptor alpha chain levels and in vitro immunoglob

249 e was associated with decreased BCG-specific IL-2(+) CD4(+) T-cell frequency and proliferation.

250 Our results suggest that suboptimal IL-2 signaling possibly plays a role in reduced Th1 deve

251 They support IL-2-mediated gene expression and the functions of the T

252 combination with IL-12, or more surprisingly IL-2, it induced striking and rapid TCR-independent IFN-

253 hed at genes highly induced by IL-2 and that IL-2-activated STAT5 binding induces new and augmented c

254 Here, we demonstrate that IL-2/7/9 stimulation activates Erk and Akt pathways down

255 2D responsiveness in NK cells and found that IL-2 upregulates expression of the amino acid transporte

256 We previously found that IL-2, which is critical for Treg homeostasis, upregulate

257 on CD4(+) T cells, thus we hypothesized that IL-2 and IL-33 cooperate to enhance Treg function.

258 Taken together, these data indicate that IL-2 can augment the gammadeltaT-17 response in favor of

259 Our central finding is that IL-2 was made when each TCR interacted with selecting or

260 In this study, we report that IL-2-dependent Tr cells in the spleen compete for a limi

261 We further show that IL-2 signaling in memory CD4 T cells is improved by the

262 in dual-costimulated T cells we showed that IL-2 induced IL-36R gene expression in a JAK/STAT-depend

263 These results suggest that IL-2 bound on CD25 of one NK cells triggered IL-2 signal

264 unction in inflamed tissues and suggest that IL-2 supplementation, particularly if used in conjunctio

265 nce corresponding to its binding site in the IL-2 gene promoter.

266 turally close to IL-2 and shares with it the IL-2 beta and gamma receptor (R) subunits.

267 atter, Ets-2 participates in a change of the IL-2 promoter architecture, possibly to facilitate a qui

268 ion and protein binding to the ARRE-2 of the IL-2 promoter are part of a strictly regulated process t

269 of one of the two signalling subunits of the IL-2 receptor, the beta chain (CD122) (mean decrease = 5

270 ition of mTORC1 abrogated the ability of the IL-2-primed NK cells to produce IFN-gamma in response to

271 Common to both cytokine receptors, the IL-2 receptor beta (IL2Rbeta) chain is selectively maint

272 onfirming and extending these findings, TNF, IL-2, and IL-21 also synergistically triggered the proli

273 Furthermore, we identify TNF, IL-2, and IL-21 as CD4(+) T-cell cytokines that synergis

274 hese effects are caused by reduced access to IL-2, because Tregs remain capable of translocating NFAT

275 priming and potentiates their activation to IL-2.

276 eas STAT5 phosphorylation and DNA binding to IL-2 receptor alpha (IL2RA) are reduced or not affected

277 pic cytokine, which is structurally close to IL-2 and shares with it the IL-2 beta and gamma receptor

278 e overcome by early or prolonged exposure to IL-2, or by addition of IL-12 to cultures, revealing tha

279 ransduction and T cell activation leading to IL-2 production.

280 mmunocytokine (IC), an anti-GD2 Ab linked to IL-2, can activate T and NK cells resulting in antitumor

281 was aberrantly phosphorylated in response to IL-2 stimulation.

282 IL-2 bound on CD25 of one NK cells triggered IL-2 signaling of neighboring NK cells.

283 Unexpectedly, IL-2 reduces this threshold in CD8 but not CD4 T cells,

284 TAT5-regulated genes in patient T cells upon IL-2 stimulation.

285 Determine the impact of cytolytic versus IL-2 receptor antibody (IL-2RA) induction on acute rejec

286 The response is induced via IL-2 receptor common gamma chain cytokines and a Janus k

287 In vivo, IL-2 enhances ILC210 generation and is associated with d

288 In this way, IL-2 may act to curtail the innate-like response of gamm

289 se data reveal a signaling framework wherein IL-2-JAK-controlled pathways coordinate with IL-2-indepe

290 We further identified a mechanism by which IL-2- and alphaKG-sensitive metabolic changes regulated

291 Stimulation of effector cells with IL-2 downregulated mRNA expression of inhibitory NKR-P1A

292 Priming of human NK cells with IL-2 is necessary to render them functionally competent

293 contrast, soluble CD40L in combination with IL-2 and IL-21 induces these activities in both memory a

294 scribe that soluble BAFF in combination with IL-2 and IL-21 is a T cell contact-independent inducer o

295 memory T cell-derived T cells compared with IL-2.

296 IL-2-JAK-controlled pathways coordinate with IL-2-independent networks of kinase activity and provide

297 reduced proliferation after stimulation with IL-2 or IL-15, suggesting that STAT5 signaling is affect

298 ficient CD4(+) T cells upon stimulation with IL-2 or upon activation by allogeneic dendritic cells, b

299 NK cells was potentiated by stimulation with IL-2.

300 sensitized mice into recipients treated with IL-2/JES6-1 showed impaired CHS.