ライフサイエンスコーパス: IL-15

1 IL-15 activates signaling by the beta and common gamma (

2 IL-15 activates STAT5 proteins, which can form dimers or

3 IL-15 administered to patients with malignancy yielded d

4 IL-15 and IL-21 production appears to feed back on CD4(+

5 IL-15 disorders play pathogenetic roles in organ-specifi

6 IL-15 enhanced TGF-beta-mediated conversion through Ras:

7 IL-15 equally sustains wild-type and Il7ra(-/-) ILC surv

8 IL-15 induced the phosphorylation of AKT, which led to t

9 IL-15 is a potential target for such a treatment because

10 IL-15 is an essential cytokine known to promote T cell s

11 IL-15 KO mice showed improved survival, attenuated hypot

12 IL-15 may be an effective therapeutic target for the att

13 IL-15 mediates membrane recruitment of Otub1, which inhi

14 IL-15 promotes the cytotoxic phenotype, elevates CX3CR1

15 IL-15 regulates central and effector memory CD8 T cell (

16 IL-15 SA treatment also exacerbated septic shock caused

17 IL-15 SA treatment amplified endotoxin shock, which was

18 IL-15 superagonist N-803, currently involved in a clinic

19 IL-15 treatment also rescued the in vitro cytotoxicity d

20 IL-15, a pleiotropic cytokine, stimulates generation of

21 IL-15, a stromal cell-associated cytokine found within s

22 IL-15-activated CD40L(+) ILC3s helped B-cell survival, p

23 IL-15/IL-15Ra superagonist complex-activated CD8(+)CD122

24 3.1] vs 59.1 pg/ml [39.2, 119.4]; p = .003), IL-15 (12.0 pg/ml [12.0, 12.0] vs 12.0 pg/ml [12.0, 126.

25 s for interleukin (IL)-4, IL-6, IL-8, IL-10, IL-15, granulocyte colony-stimulating factor (GCSF), MCP

26 fter activation with interleukin-12 (IL-12), IL-15, and IL-18, exhibit potent antitumor responses, an

27 We report that upon activation with IL-12, IL-15, and IL-18 human NK cells express NKG2D ligands of

28 ically, glucocorticoids together with IL-12, IL-15, and IL-18 not only upregulate PDCD1 transcription

29 Interleukin 15 (IL-15) is an essential cytokine for the survival and pro

30 Interleukin 15 (IL-15) is implicated in the pathophysiology of coeliac d

31 Interleukin 15 (IL-15) is one of the most important cytokines that regul

32 e with high mortality rates; interleukin 15 (IL-15) is strongly implicated in its pathophysiology.

33 limiting the availability of interleukin 15 (IL-15), and administration of IL-15/IL-15Ralpha or immun

34 oduces the overexpression of interleukin-15 (IL-15) in the gut epithelium and lamina propria that is

35 Interleukin-15 (IL-15) is essential for the development and maintenance

36 CH1 and RBPJ, as well as the interleukin-15 (IL-15) receptor complex, the latter enhancing IL-15 auto

37 a key negative regulator of interleukin-15 (IL-15) signaling in natural killer (NK) cells.

38 Interleukin-15 (IL-15) signaling induced miR-142 expression, whereas glo

39 pletion and treated with the interleukin-15 (IL-15) superagonist N-803 (J.

40 Low doses of interleukin-15 (IL-15) that mimic exercise responses in the circulation

41 phocytes and increased serum interleukin-15 (IL-15).

42 nd was mimicked by exogenous interleukin-15 (IL-15).

43 homeostatic pathway defined by IL-15/IL-15R (IL-15 receptor) interaction and the inflammasome pathway

44 on with soluble or surface-bound IL-15Ralpha-IL-15 complex resulted in Stat5 phosphorylation and NK c

45 ow here that membrane-associated IL-15Ralpha-IL-15 complexes are transferred from presenting cells to

46 docytosis of membrane-associated IL-15Ralpha-IL-15 provides a mode of regulating NK cells that is not

47 ition of metalloprotease-induced IL-15Ralpha-IL-15 shedding from trans-presenting cells, whereas S6 p

48 noclonal antibodies in the presence of IL-2, IL-15, and IL-1beta.

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

50 in hampered secretion of interleukin (IL)-7, IL-15, and IL-6, cytokines being involved in thymic T ce

51 -9, IL-10, fibroblast growth factor 2, IL-7, IL-15, and transforming growth factor alpha) but lower l

52 for interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21.

53 of Shp-2 as a molecular nexus bridging acute IL-15 signaling with downstream metabolic burst and NK c

54 hanistically, Shp-2 deficiency hampers acute IL-15 stimulation-induced raise in glycolytic and respir

55 Neutralisation of the high-affinity IL-15 receptor binding subunit, IL-15ralpha in elderly m

56 Although IL-15 has been implicated in the pathogenic hyperimmune

57 Although IL-15 is essential for NK cell homeostasis in vivo, it i

58 mbinant cytokines (rIL-15, rTNFalpha) and an IL-15 receptor neutralising antibody.

59 es, as memory CD8 T cells proliferated in an IL-15-dependent manner.

60 cluding the possibility that retention of an IL-15 transpresenting support system is key to extending

61 Following stimulation with an IL-15/IL-15Ra superagonist complex, Ly-49(+) CD8 Tregs e

62 XCL9) or T cell modulatory (IL-4, IL-12, and IL-15) cytokines.

63 Interleukin 2 and IL-15 are two closely related cytokines, displaying impo

64 ation and molecular association of IL-2 (and IL-15) receptor chains in the ER/Golgi, which became mor

65 y blocked proliferation elicited by IL-2 and IL-15, but only an inhibitor targeting the PI3K/Akt/mTOR

66 Interleukin-2 (IL-2) and IL-15 play pivotal roles in T cell activation, apoptosis

67 n radio-resistant host cells in an IL-2- and IL-15-dependent manner.

68 investigated the interplay between IL-32 and IL-15 and their role in NK cell activity.

69 D3/28-activated T cells expanded in IL-7 and IL-15 produced greater expansion of memory stem T cells

70 toxicity of TECs and restored their IL-7 and IL-15 secretion.

71 in (gammac) receptor but that, like IL-7 and IL-15, induced expression of the lineage-specifying tran

72 proliferation in response to IL-2, IL-7, and IL-15 but not following TCR engagement.

73 ion was heritably preserved during IL-7- and IL-15-mediated in vitro cell proliferation.

74 tion is a physiologic feature of asthma, and IL-15 might have an important role in asthma pathogenesi

75 ntify a synergistic activity of TGF-beta and IL-15 in this cellular conversion.

76 ded in vitro in the presence of TGF-beta and IL-15, IL-9 was the most abundant among 16 analyzed cyto

77 lex interaction between gluten, genetics and IL-15-driven tissue inflammation, this mouse model provi

78 ere assessed in Il15 gene-deficient mice and IL-15-overexpressing mice in an allergen-induced murine

79 e and accumulate in the spleen where TCR and IL-15/STAT5 signaling promotes their conversion to CD8al

80 C57BL/6 wild-type (WT) and IL-15(-/-) mice were sensitized and challenged with oval

81 investigate the effects of AMG 714, an anti-IL-15 monoclonal antibody, on the activity and symptoms

82 e onset of AIDS were comparable between anti-IL-15- and control-treated groups in both cohorts.

83 In both cohorts, anti-IL-15 was highly efficient at blocking IL-15 signaling i

84 AMG 714 is the first anti-IL-15 monoclonal antibody to be investigated for the tre

85 Furthermore, anti-IL-15-treated mice showed significantly reduced conjunct

86 aluated memory Th17 cell depletion with anti-IL-15 antibody as a strategy to abrogate the severe exac

87 Treatment with anti-IL-15 antibody decreased the enlarged memory Th17 pool i

88 However, RM treated with anti-IL-15 during primary infection manifested accelerated re

89 K cell depletion through treatment with anti-IL-15 monoclonal antibody during chronic SIVagm infectio

90 As IL-15 is required for Ly-49(+) CD8 Treg development, we

91 f malignant Lin(-)IEL lines as powerfully as IL-15.

92 ly isolated NK cells with cytokines, such as IL-15, IL-12, or IL-18, does not activate LFA-1 but incr

93 bited IFN-gamma and oncostatin M, as well as IL-15 and IL-21, activity and resulted in clinical and h

94 Because IL-15 promotes NK cell activation, we investigated the i

95 anscriptional analysis revealed that besides IL-15, IL-32 was the only other cytokine expressed by hu

96 Su et al demonstrate associations between IL 15 serum levels and the outcome of patients with Stev

97 Finally, synergy between IL-15 and IL-21 was observed only upon CD137 engagement

98 ng compounds, 36 of which were found to bind IL-15, to inhibit the binding of IL-15 to the IL-2Rbeta

99 Diverse approaches are developed to block IL-15 action.

100 Blocking IL-15 signals also significantly impacts tissue-specific

101 anti-IL-15 was highly efficient at blocking IL-15 signaling in vivo, causing 1) profound depletion o

102 Both IL-15 and CpG DNA are elevated in microbe-draining lymph

103 o enforce NK cell responses to activation by IL-15 and IL-2.

104 uated the restoration of mortality caused by IL-15 SA.

105 nation of the homeostatic pathway defined by IL-15/IL-15R (IL-15 receptor) interaction and the inflam

106 IFN-gamma production, which was enhanced by IL-15.

107 TOR pathway blocked proliferation induced by IL-15 as well as the CD4(+) T-cell cytokines.

108 DNA damage response molecules are reduced by IL-15, as indicated by Western blotting and immunofluore

109 Aspergillus species extract-challenged CC10-IL-15 bitransgenic mice exhibited significantly reduced

110 d compared with non-doxycycline-exposed CC10-IL-15 bitransgenic mice.

111 ther validated in doxycycline-inducible CC10-IL-15 bitransgenic mice.

112 proliferation of NK, NK-T, and CD8+ T cells, IL-15 plays important roles in innate and adaptative imm

113 given immediately prior to septic challenge, IL-15-neutralizing IgG M96 failed to protect against sep

114 healing of aged skin depend upon circulating IL-15.

115 -1-related alarmins, as well as the cytokine IL-15, which is important for T cell and NK cell homeost

116 d synergy between two stimulating cytokines, IL-15 and IFN-alpha, which, given together, constitute a

117 cell development, associated with defective IL-15-dependent cell survival.

118 s of sepsis was assessed in IL-15-deficient (IL-15 knockout, KO) mice.

119 (-)IELs is driven by epithelial cell-derived IL-15.

120 Death of NK cells resulted from diminished IL-15 receptor signaling within miR-142-deficient mice,

121 ion and survival when treated with high dose IL-15 or IL-2.

122 er in vitro PBMC restimulation with low-dose IL-15, alone or in combination with inactivated H3N2 vir

123 -32alpha also acted on DCs by downregulating IL-15-induced IL-18 production, an important cytokine in

124 CL-2/BIM ratio, which rapidly dropped during IL-15 withdrawal.

125 o achieve major cancer therapeutic efficacy, IL-15 will be used in combination therapy, and combinati

126 ata demonstrate that mice with an endogenous IL-15 deficiency are susceptible to the development of s

127 In conclusion, endogenous IL-15 does not directly augment the pathogenesis of seps

128 Help signals enhance IL-15-dependent maintenance of central memory T (T(CM))

129 L-15) receptor complex, the latter enhancing IL-15 autocrine signaling.

130 Exogenous IL-15 exacerbates the severity of sepsis by activating N

131 However, exogenous IL-15 may have a limited impact on patients with cancer

132 2-deficient mice by treatment with exogenous IL-15/IL-15Ralpha complexes.

133 mice, most myeloid cells in the TME express IL-15 with CD11b(+)Ly6C(hi) cells being the most abundan

134 rough trans-presentation by cells expressing IL-15 bound to the alpha chain of the IL-15 receptor (IL

135 hat cooperates with an ILC3 survival factor, IL-15, to induce proliferation of human ILC3s, as well a

136 describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL and suggest targeting o

137 Finally, IL-15 robustly stimulated the PI3K/Akt/mTOR and MEK/ERK

138 phatic tissues, and unraveling the basis for IL-15-driven B-CLL growth could illuminate new therapeut

139 VHD, donor T cells compete with NK cells for IL-15 thereby inducing profound defects in NK-cell recon

140 are activated and functionally important for IL-15->CD122/yc signaling in ODN-primed cells expressing

141 These follicles were strongly positive for IL-15, which was primarily presented in its membrane-bou

142 dies revealed that T cells were required for IL-15-induced LGC formation, involving a direct contact

143 nst leukemia cells and was also required for IL-15-mediated NK cell survival through an anti-apoptoti

144 pe 1 (TH1)-related markers interferon-gamma, IL-15, and granulocyte-macrophage colony-stimulating fac

145 study provides mechanistic insight into how IL-15 controls the generation of memory CD8 T cells and

146 Additionally, we found that a human IL-15 agonist (ALT-803) improved airway resistance and c

147 T-PCR confirmed positive synergistic hypoxia/IL-15 interactions for genes of key regulatory and metab

148 Thus, the newly identified IL-15-AKT-XBP1s signaling pathway contributes to enhance

149 ditional analytes (IP-10, IL-12/23p40, IFNy, IL-15) were found to be elevated in HIV/HCV coinfection

150 scovering small-molecule inhibitors impeding IL-15/IL-15R interaction.

151 are dispensable for the induction of AAD in IL-15-deficient mice.

152 , the pathogenesis of sepsis was assessed in IL-15-deficient (IL-15 knockout, KO) mice.

153 highly proapoptotic splice variant of BIM in IL-15-activated NK cells.

154 uppressed the enhancement of eosinophilia in IL-15(-/-) animals to levels observed in WT mice, but ha

155 Trx1 and thiol levels were higher in IL-15- than in IL-2-primed NK cells.

156 ence of microenvironmental signals including IL-15, and were capable of polarizing both blood and col

157 ISH(-/-) iPSC-NK cells demonstrate increased IL-15-mediated JAK-STAT signaling activity.

158 led between ILC3s and B cells: ILC3s induced IL-15 production in B cells through B cell-activating fa

159 that IL-32alpha acts on NK cells to inhibit IL-15-mediated STAT5 phosphorylation and to suppress the

160 BiG efficiently inhibited IL-15- and IL-2-dependent functions of primary cells, in

161 Engagement of GITR inhibited IL-15-mediated activating signaling events in NK cells,

162 e tested whether tofacitinib, which inhibits IL-15 signaling by blocking Jak3, might decrease CD8-dep

163 Intravenous IL-15 treatment rescued chronological aging-induced heal

164 Mice lacking IL-15 have selective defects in populations of several p

165 After stimulation with the gammac-ligand IL-15, gammac-deficient keratinocytes show significantly

166 Like IL-15, these cytokines were found to increase the phosph

167 t of T(VM) at least in part through limiting IL-15 trans-presentation by CD11b+ dendritic cells.

168 ty of the IL-15 superagonist receptor-linker-IL-15 (RLI), designed to bypass the need of endogenous I

169 IFN-gamma, IL-2, IL-6, and IL-1beta) or low (IL-15, TNF-alpha, IL-12 p70, IL-17A, GM-CSF, IL-12 p40,

170 ve macrophages with the potential to mediate IL-15 signals critical for optimal outcomes of pregnancy

171 Moreover, exercise or exercise-mimicking IL-15 treatment rescued the age-associated decrease in e

172 pproach, leading to the first small-molecule IL-15 inhibitor with sub-micromolar activity.

173 Moreover, IL-15 as well as type I IFN, which regulates IL-15, was

174 trogen signaling pathway, signaling by MST1, IL-15 production, MSP-RON signaling pathway, and IL-12 s

175 to the maternal-fetal interface direct novel IL-15-responsive macrophages with the potential to media

176 In the absence of IL-15, OVA-challenged mice exhibited enhanced bronchial

177 Despite the abundance of IL-15-expressing cells, the relative levels of sIL-15 co

178 nterleukin 15 (IL-15), and administration of IL-15/IL-15Ralpha or immune suppression with rapamycin c

179 In analyses of IL-15 reporter mice, most myeloid cells in the TME expre

180 und to bind IL-15, to inhibit the binding of IL-15 to the IL-2Rbeta chain or the proliferation of IL-

181 104(+)CCL21(+) mTEC(low) that are capable of IL-15-transpresentation for regulating NKT1 and NKT17.

182 d NK cells by functioning as a checkpoint of IL-15-mediated priming.

183 s confirmed that autocrine concentrations of IL-15 also support myogenesis.

184 so indirectly augmented by very low doses of IL-15, which increased induction of myeloid cell-derived

185 ationale for its key functions downstream of IL-15.

186 e phenotype was independent of the effect of IL-15 or TGF-beta on mTOR, as the culture of NK cells in

187 The effects of IL-15 on human skeletal muscle growth and development re

188 Finally, expression of IL-15 correlated with cytolytic immune functions in pati

189 housed in EE, in mediating the expression of IL-15 in CD11b(+) cells.

190 Disruption in homeostasis of IL-15 is linked to poor maternal and fetal outcomes duri

191 ll functions and argue for implementation of IL-15 in adoptive NK-cell cancer therapy.

192 Infusion of IL-15-activated CD8 Tregs may serve as an innovative cel

193 ur findings suggest a feedback inhibition of IL-15-mediated NK cell activity by IL-32alpha.

194 Moreover, the association of high levels of IL-15 expression with inflammatory and autoimmune diseas

195 The novel mechanism of IL-15 transfer to the surface of antigen-processing DCs

196 8(+) T cells and re-established mortality of IL-15 KO mice during septic shock.

197 Overexpression of IL-15 in both the epithelium and the lamina propria is r

198 sing DCs may explain the enhanced potency of IL-15:IL-15Ralpha-coated nanoparticles for antigen deliv

199 ctivation of the CD137 axis, and presence of IL-15 (or its membranous form) and IL-21.

200 the IL-2Rbeta chain or the proliferation of IL-15-dependent cells or both.

201 Finally, up-regulation of IL-15 expression in muscle, with increased secretion of

202 our study reveals the dynamic regulation of IL-15 in the TME and its importance in antitumor immunit

203 We tested the hypothesis that regulation of IL-15 is critical for preservation of allergen-induced a

204 itumor responses; however, the regulation of IL-15 within the tumor microenvironment (TME) is unclear

205 To understand the role of IL-15 in SIV infection and pathogenesis, we treated two

206 rates the location-dependent central role of IL-15 in the pathogenesis of coeliac disease.

207 ndant, indicating there is a large source of IL-15 protein in tumors that lies sequestered within the

208 We then show that antagomiR-214 treatment of IL-15 transgenic mice with spontaneous, miR-214-overexpr

209 feration and are not critically dependent on IL-15 for their maintenance.

210 ced H4K12ac, enhancing the effect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokines while

211 in soluble factors release, such as MCP-1 or IL-15.

212 omparison to CAR T cells expressing IL-18 or IL-15.

213 proliferation after stimulation with IL-2 or IL-15, suggesting that STAT5 signaling is affected.

214 the in vivo relevance of this pathway in our IL-15 transgenic mouse model of CTCL by showing that int

215 response to IL-15 alone (CD25) and H3N2 plus IL-15 (CD25 and IFN-gamma) was enhanced postvaccination.

216 t NOD macrophages inadequately trans-present IL-15.

217 of canonical target genes, SD-Foxo1 promoted IL-15-mediated CD8 T cell survival in vitro and survival

218 Despite reduced IL-15 trans-presentation, NOD Ly-49(+) CD8 Tregs can eff

219 IL-15 as well as type I IFN, which regulates IL-15, was required for establishing normal numbers of C

220 ression of distant secondary tumors required IL-15 expression.

221 iNKT cell development requires IL-15, and we found that sgammac interfered with IL-15 s

222 r with primary infection, with a rhesusized, IL-15-neutralizing mAb (versus an IgG isotype control) f

223 Treatment with IL-15 superagonist (IL-15 SA, IL-15/IL-15Ralpha complex) regenerated NK and mCD8(+) T

224 d with our observation that myotubes secrete IL-15 in response to TNFalpha stimulation supports the n

225 Sequential IL-15 or antigen exposure followed by TGFbeta induces li

226 High serum IL-15 levels were associated with high peak blood CAR(+)

227 n of advanced-stage lymphoma, and high serum IL-15 levels were associated with the effectiveness of t

228 onses occurs despite deficiencies in several IL-15-dependent cell types including NK, NKT, and gammad

229 2 and is distinct from activation by soluble IL-15.

230 anted with various tumor cell lines, soluble IL-15/IL-15Ralpha complexes (sIL-15 complexes) are abund

231 These results may explain the strict IL-15 dependence of NK cells and illustrate how the cell

232 As a result, adoptive transfer of such IL-15-addicted NK cells is associated with cellular stre

233 Treatment with IL-15 superagonist (IL-15 SA, IL-15/IL-15Ralpha complex) regenerated NK and

234 We report that cell surface IL-15 expression is upregulated during lymphopenia induc

235 terestingly, the cellular profile of surface IL-15 expression is distinct in each model.

236 caffold for creating multispecific, targeted IL-15-based immunotherapeutic agents and may serve as a

237 of various antagonistic approaches targeting IL-15.

238 In this study, we demonstrate that IL-15 influences the generation of memory CD8 T cells by

239 Previous studies have provided evidence that IL-15 expression within human tumors is crucial for opti

240 Lastly, we provide evidence that IL-15 induced by inflammatory signals in response to lym

241 We report our novel finding that IL-15 has a potent inhibitory effect on the airway obstr

242 In this study, we found that IL-15 is a potent inducer of IL-32alpha in DCs.

243 Here, we found that IL-15, a cytokine that induces M1 macrophage differentia

244 These findings led us to hypothesize that IL-15 stimulation could reveal a similar effect for acti

245 We hypothesized that IL-15 promotes the pathogenesis of sepsis by maintaining

246 We therefore hypothesized that IL-15(-/-) mice will have reduced inflammatory responses

247 These data indicate that IL-15 induces LGC formation through the direct interacti

248 Overall, these results indicate that IL-15 or its analogs represent promising therapies for t

249 NFalpha stimulation supports the notion that IL-15 serves to mitigate inflammatory skeletal muscle lo

250 We made a novel observation that IL-15 deficiency promotes baseline airway resistance in

251 Mechanistically, we observed that IL-15-mediated protection of airway obstruction is assoc

252 Here, we report that IL-15(-/-) mice developed enhanced allergic responses in

253 Here we show that IL-15 also mediates homeostatic priming of CD8(+) T cell

254 Last, we show that IL-15 complexes delivered locally to mucosal tissues wit

255 We show that IL-15 induces signal transducer and activator of transcr

256 cell lines and in mouse models suggest that IL-15 promotes myogenesis and may protect against the in

257 dria in uninjured aged skin, suggesting that IL-15 is an essential mitochondrial signal for healing t

258 We discuss how the IL-15-induced changes in gene expression lead to rapid c

259 essing IL-15 bound to the alpha chain of the IL-15 receptor (IL-15Ralpha).

260 rk, we studied the antitumor activity of the IL-15 superagonist receptor-linker-IL-15 (RLI), designed

261 Analysis of the IL-15-treated adherent cell transcriptome identified gen

262 Interestingly, Bim does not restrict the IL-15-driven maturation of CD8alphaalpha cells that is c

263 ht NK cells from MM patients primed with the IL-15 receptor agonist ALT-803 in vivo displayed enhance

264 STAT5 phosphorylation and to suppress their IL-15-induced effector molecule expression and cytolytic

265 hodepletion, the mechanisms regulating these IL-15 responses are unclear.

266 dependent, but can persist partially through IL-15 signalling.

267 Thus, IL-15 support of NK cell and T(EM) homeostasis does not

268 e, we describe a dose-dependent addiction to IL-15 during in vitro expansion of human NK cells, leadi

269 NK cell addiction to IL-15 was tightly linked to the BCL-2/BIM ratio, which r

270 uses aberrant responses of CD8(+) T cells to IL-15, rendering naive CD8(+) T cells hypersensitive to

271 PI3K and STAT5 show that both contribute to IL-15-driven upregulation of mRNA for cyclin D2 and supp

272 Effector mechanisms contributing to IL-15-based priming included improved cytotoxic protein

273 rs and subsequently undergo apoptosis due to IL-15 starvation.

274 t5 DKI NK cells have normal proliferation to IL-15 but are susceptible to death upon cytokine withdra

275 The only cells described to respond to IL-15 at the early maternal-fetal interface have been NK

276 the IL-15R complex (CD122) and responding to IL-15.

277 NK cell activation in response to IL-15 alone (CD25) and H3N2 plus IL-15 (CD25 and IFN-gam

278 lower production of IFN-gamma in response to IL-15 and reduced proliferation after stimulation with I

279 eightened cytokine production in response to IL-15 compared with PBMC collected at baseline; these re

280 genes(2,3)-that was activated in response to IL-15 in human NK cells.

281 In response to IL-15, CD122+Macs activate the ERK signaling cascade and

282 de repeats 1 (IFIT1) promoter in response to IL-15, whereas STAT5 phosphorylation and DNA binding to

283 Ly-49(+) CD8 Tregs can effectively transduce IL-15-mediated survival signals when they are provided.

284 nts, compared with scrambled control-treated IL-15 transgenic CTCL mice.

285 se-3 activation and profound cell death upon IL-15 withdrawal.

286 CD8alphaalpha T(unc) are dependent upon IL-15/IL-2Rbeta signaling and PLZF for their development

287 lung cancer may benefit from therapies using IL-15-primed NK cells.

288 ; these responses were further enhanced when IL-15 was combined with H3N2.

289 Whereas IL-15 has well-established roles in stimulating lymphocy

290 h B cell-activating factor receptor, whereas IL-15, a potent growth factor for ILC3s, induced CD40 li

291 To determine whether IL-15(-/-) mice have attenuated allergic responses in a

292 e studies demonstrate that the form in which IL-15 is expressed, its kinetics and cellular sources, a

293 d for myeloid cells were anticorrelated with IL-15 treatment and LGC formation.

294 und agonistic antibodies in combination with IL-15 drove robust proliferation and activation of CD3-C

295 and IFN-inducible genes that correlated with IL-15 treatment and LGC-type multinucleated giant cell f

296 5, and we found that sgammac interfered with IL-15 signaling to suppress iNKT cell generation in the

297 synergistic activity with RLI, but not with IL-15.

298 igm by demonstrating that brief priming with IL-15 markedly enhanced the antitumor response of CD56br

299 increase in CD4(+) T cells was recorded with IL-15 receptors, APOBEC3G and CC chemokines, the latter

300 Treatment with IL-15 superagonist (IL-15 SA, IL-15/IL-15Ralpha complex)