ライフサイエンスコーパス: IL-7R

1 IL-7R alpha +CD8+ T cell percentages were directly corre

2 IL-7R blockade following anti-CD4- and anti-CD8-mediated

3 IL-7R blockade reduced human T cell homing to the gut an

4 IL-7R is first expressed on common lymphoid progenitor c

5 IL-7R receptor signaling appears to function in specific

6 IL-7R-dependent signals have been clearly shown to regul

7 IL-7R-expressing B-ALL cells grew in culture in response

8 IL-7R-mediated activation of the transcription factor ST

9 ined through a concerted regulation of Gfi-1-IL-7R-controlled cytokine responsiveness and ERK-mediate

10 Importantly, antigen-specific IL-6Ralpha(+)IL-7R(+) CD4(+) T cells emerge from the effector populat

11 xpression of the receptor for interleukin 7 (IL-7R).

12 A significant increase in IL-7, IL-7R, and IFN-gamma protein expression was found in dev

13 IL-7, IL-7R, and IFN-gamma protein expression was significantl

14 disease activity have higher levels of IL-7, IL-7R, and TNF-alpha in RA monocytes, suggesting a feedb

15 otein secretion and gene expression of IL-7, IL-7R, IFN-gamma, MC1R, NF-kappaB, phosphorylated NF-kap

16 positive or negative modulation of the IL-7-IL-7R signaling axis.

17 us DCs and to examine the importance of IL-7/IL-7R alpha for DC development in vivo, we used IL-7R al

18 uggesting a feedback regulation between IL-7/IL-7R and TNF-alpha cascades in myeloid cells that is li

19 w for the first time that expression of IL-7/IL-7R in myeloid cells is strongly correlated with RA di

20 e studies have focused on the effect of IL-7/IL-7R in T cell development and function.

21 occi while high IL-7 levels may reflect IL-7/IL-7R pathway dysfunction in T cells, both of which coul

22 erplay between IFN-gamma/IFN-gammaR and IL-7/IL-7R pathways.

23 The IL-7/IL-7R signaling axis participates in cell survival, and

24 een IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previously been proposed, but has no

25 ss the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics during CNS

26 In pro-B cells, IL-7/IL-7R signaling induces histone hyperacetylation and nuc

27 The present study highlights perturbed IL-7/IL-7R T cell signaling through STAT5 as a potential mech

28 Additionally, IL-7R deletion resulted in delayed growth and proliferat

29 We show that the functional high-affinity IL-7R is expressed on both naive and memory Tregs, and e

30 After IL-7R deletion in a generally normal lymphoid environmen

31 enetic variation in the IL-7 receptor-alpha (IL-7R) gene is associated with susceptibility to human t

32 Although IL-7R remained significant for poor overall survival, al

33 ation with antigenic LCMV peptides, although IL-7R expression was reduced in the NIK KO CD8 T cells.

34 are shown to express LT alpha 1 beta 2 in an IL-7R alpha-dependent manner.

35 Kit activated Jak3 in an IL-7R-dependent manner.

36 and CD127, molecules that make up IL-15R and IL-7R, respectively, than other memory T cells.

37 sion protein transactivated all but IL-6 and IL-7R in the absence of TNF stimulation.

38 ion of the cytokine receptors IL-6Ralpha and IL-7R.

39 , for the first time, regulators of IL-7 and IL-7R expression in RA fibroblasts, RA peripheral blood

40 Although the role of IL-7 and IL-7R has been implicated in the pathogenesis of rheumat

41 Expression of IL-7 and IL-7R in RA and normal synovial tissue was demonstrated

42 Expression and regulation of IL-7 and IL-7R in RA peripheral blood in vitro-differentiated mac

43 Here we discuss the central role of IL-7 and IL-7R in the lymphoid system and highlight the impact of

44 stimulation modulated expression of IL-7 and IL-7R on RA macrophages and HMVECs.

45 IL-7 and IL-7R were coexpressed on RA synovial tissue lining and

46 at adult B cell development in IL-7(-/-) and IL-7R alpha(2/-) mice is arrested at the pre-pro-B cell

47 tain the expression of L-selectin, CCR7, and IL-7R molecules.

48 These T cells, expressing CD62L, CCR7, and IL-7R, failed to produce IFN-gamma, but had the capacity

49 Mice deficient for both CXCL13 and IL-7R alpha displayed a striking absence of LNs, includi

50 expression of CXCL9, its receptor CXCR3, and IL-7R on peritoneal cells from mertk-/- mice.

51 ound to be due to competition between DN and IL-7R-expressing DP cells for endogenous IL-7, which res

52 ents include the cytokine receptors Flk2 and IL-7R as well as the transcription factors PU.1, Ikaros,

53 , as well as the cytokine receptors Flk2 and IL-7R.

54 f lymphoid progenitors that express Flk2 and IL-7R.

55 luding increased expression of IFN-gamma and IL-7R, reduced expression of programmed death-1, and dec

56 High expression of both IL7R and IL-7R signaling signature in the colon before treatment

57 cts of three of the genes--IL-2RG, Jak3, and IL-7R alpha--are components of cytokine receptors, and t

58 in nonhematopoietic cells shows that Kit and IL-7R signaling pathways directly interact.

59 s among size, differentiation phenotype, and IL-7R alpha status in blood did not hold in tonsillar ti

60 ly Ag-driven memory T cell proliferation and IL-7R expression, with subsequent changes in memory T ce

61 (lo)) short-lived effector cells (SLECs) and IL-7R(hi) memory precursor effector cells (MPECs) capabl

62 Pre-TCR and IL-7R signals regulate beta-selection of thymocytes and

63 pancreatic islet allograft survival if anti-IL-7R treatment was started 3 weeks before graft.

64 t to DETCs, these Vgamma5-negative cells are IL-7R(hi)CCR6(hi) retinoic acid-related orphan receptor

65 om control animals, developmentally-arrested IL-7R(+)B220(+)CD19(-)NK1.1(-)Ly-6C(-) cells failed to e

66 ation of gammac-containing receptors such as IL-7R, similar to the interaction between Kit and Epo-R.

67 vel and potent chemoattractant that attracts IL-7R(+) monocytes through activation of the PI3K/AKT1 a

68 nsequently, beta-catenin expression augments IL-7R signaling in thymocytes during positive selection

69 Immunodeficient B6 (IL-7R(-/-) Kit(w41/w41)) mice lacking adaptive cells (B6

70 Because IL-7R was a plausible candidate for driving the homeosta

71 f transgenic IL-7R on their surface, because IL-7R signal transduction is actively suppressed in pres

72 Thus, the cooperation between IL-7R and alpha2beta1 integrin can represent an importan

73 The functional cooperation between IL-7R and alpha2beta1 integrin involves activation of th

74 To examine the role of IL-7, we blocked IL-7R signaling with neutralizing Abs.

75 correlated with the down-regulation of both IL-7R and CD27, suggesting that KLRG1 marks dominant, en

76 signals for survival and proliferation, but IL-7R signals are normally extinguished by the immature

77 sm and suggest that control of glycolysis by IL-7R may contribute to the well-described roles of IL-7

78 ytes, were less efficiently reconstituted by IL-7R alpha KO donor cells, whereas myeloid lineage cell

79 CD4(+)CCR6(+)IL-7R(+)T cells from human tonsils produced IL-10 follow

80 In SLE patients, CD4(+)CCR6(+)IL-7R(+)T cells were associated with the presence of pat

81 ells, of which the majority expressed CD127 (IL-7R) and CCR7.

82 f established memory precursor marker CD127 (IL-7R).

83 ntifying a developmentally restricted CD19(-)IL-7R(+) progenitor compartment, which transitions from

84 nous ETV6 locus show expansion of the CD19(-)IL-7R(+) compartment, show a partial block in B lineage

85 CD19+/IL-7R- cells were smaller and did not proliferate on MS-

86 IL-7 induced STAT5 phosphorylation in CD19+/IL-7R+ pro-B cells and human B-lineage acute lymphoblast

87 FACS-purified CD19+/IL-7R+ cells were larger and, when replated on MS-5, und

88 Both circulating and LN CD4+ CD3- IL-7R alpha hi cells are shown to express LT alpha 1 bet

89 ociated with local accumulation of CD4+ CD3- IL-7R alpha hi hematopoietic cells that deliver lymphoto

90 cling, hyperresponsive memory-like CD8+CD44+ IL-7R- T cells which do not require costimulation for ef

91 + T cell expansion and acquisition of CD45RO+IL-7R+IL-15R+ phenotype.

92 IL)-2R beta , common gamma (C gamma ) chain, IL-7R alpha , IL-15R alpha; and proliferative responses

93 We found that human Th17 cells coexpress IL-7R and the collagen-binding integrin alpha2beta1 (CD4

94 emonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15

95 Here, using a conditional IL-7R transgenic model, we were able to test directly wh

96 Retroviral expression of a chimeric GM-CSF/IL-7R, in which binding of GM-CSF by T cells leads to IL

97 ytokine receptor required in PP development, IL-7R alpha.

98 fection and were committed to downregulating IL-7R.

99 that blockade of PD-1 on tumor DCs enhanced IL-7R expression on CD8 T cells.

100 lopment on IL-7, all B-2 progenitors express IL-7R.

101 Bone marrow cells expressing IL-7R and B220 generated erythroid colonies in vitro in

102 B mice showed that leukemia cells expressing IL-7R were found in enlarged thymuses.

103 g resulted in rapid proliferation, extensive IL-7R down-regulation, and the lowest yield of HA-specif

104 umably why DP thymocytes normally extinguish IL-7R gene expression.

105 PU.1 results in a severe reduction in Flk2+, IL-7R+ lymphoid progenitors as well as impaired expressi

106 stinal ILCs and attenuated colitis following IL-7R blockade.

107 -) ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice

108 hat human blood eosinophils express mRNA for IL-7R alpha (CD127) and its common gamma chain (CD132).

109 The role for IL-7R expression in the differentiation of effector T ce

110 lpha in vivo suggested an important role for IL-7R in immediate and long-term T-cell survival.

111 e IL-7 and HGF (c-Met) receptors, which form IL-7R/c-Met complexes on the surface of CLPs and pre-pro

112 ation in bone marrow, signals emanating from IL-7R and pre-BCR are thought to synergistically induce

113 to undergo differentiation after escape from IL-7R signaling.

114 pts for killer cell lectin-like receptor G1, IL-7R, and CD57 implied that lung CD8(+) T cells in COPD

115 ed, including the putative PU.1 target genes IL-7R and EBF but not B220, and can produce immunoglobul

116 Unlike IL-7R(hi) MPECs, KLRG1(hi) IL-7R(lo) SLECs relied on IL-15, but IL-15 could not sus

117 In contrast, KLRG1(hi)IL-7R(lo) cells, which appear terminally differentiated

118 ell lectin-like receptor G1 high (KLRG1(hi))/IL-7R(lo) short-lived effector cells that expressed gran

119 ratory has previously shown that CD62L(high) IL-7R(high) central memory T (T(CM)) cells mediate prote

120 nvert from an activated phenotype (CD25(high)IL-7R(low)CD44(high)) to a resting memory phenotype (IL-

121 anisms regulating T-cell homeostasis and how IL-7R and TCR signaling are coordinated are largely unkn

122 Our data demonstrate how IL-7R signaling represses Igk germline transcription and

123 with LIC potential and report that impaired IL-7R signaling hampers engraftment and progression of p

124 sion partially rescues B cell development in IL-7R alpha(-/-) mice.

125 in combination with activating mutations in IL-7R, JAK1, or LCK, and down-regulation of CD45 express

126 pre-pro-B cells upon IL-7 stimulation or in IL-7R alpha(-/-) pre-pro-B cells by activation of STAT5,

127 A expression restores V(D)J recombination in IL-7R(-/-) B cells, demonstrating that IL-7 regulates H

128 Increased IL-7R alpha was revealed by surface staining, and increa

129 revealed by surface staining, and increased IL-7R alpha mRNA was documented by using reverse transcr

130 -specific effector CD8(+) T cells, increased IL-7R expression was not a reliable marker of CD4(+) mem

131 beta and-gamma, IkappaBepsilon, interleukin (IL)-7R, and Naf-1) were used to determine whether they w

132 fferentiate into interleukin-7 receptor(lo) (IL-7R(lo)) short-lived effector cells (SLECs) and IL-7R(

133 KLRG1(lo)IL-7R(hi) T cells homed to the T cell zone using pertuss

134 ller cell lectin-like receptor G1 (KLRG1)(lo)IL-7R(hi) effector and memory cells, which are long-live

135 gamma yielded conditioned memory despite low IL-7R expression.

136 , leading to a higher frequency of KLRG1(low)IL-7R(high)CD62L(high) memory T cells.

137 omogeneous memory cells that are CD62L(low), IL-7R(high), and imbued with an enhanced capacity to pro

138 s that divided three times that had marginal IL-7R expression and no IFN-gamma raised base level home

139 expressed high levels of stem cell markers, IL-7R and RORgammat, consistent with the newly described

140 lighting the relevance that targeting normal IL-7R signaling may have in future therapeutic intervent

141 In the absence of IL-7R expression, effector cells transferred into "full"

142 In the absence of IL-7R signaling, IL-15/IL-15R interaction is dispensable

143 fication occurred normally in the absence of IL-7R signaling, in contrast to a recently proposed mode

144 gested that pre-BCR-dependent attenuation of IL-7R signaling returns the H chain loci to an inaccessi

145 Thus, attenuation of IL-7R/STAT5 signaling is not required for allelic exclus

146 Blockade of IL-7R by anti-IL-7Ralpha antibody resulted in eliminatio

147 ress this issue, we examined the capacity of IL-7R-dependent signaling to support Treg cell productio

148 y, similar in many respects to deficiency of IL-7R, gammac, and Jak3.

149 ors were used to reconstitute development of IL-7R(-/-) hemopoietic progenitors by transducing the re

150 -2R beta-chain and the cytoplasmic domain of IL-7R alpha-chain in IL-2Rbeta(-/-) mice led to Treg cel

151 lts suggest that transient downregulation of IL-7R signaling is a necessary event for induction of EB

152 Importantly, in vivo excision of IL-7R led to T cell atrophy that was characterized by de

153 control subjects, with reduced expression of IL-7R alpha in the central memory and effector memory su

154 We identified reduced surface expression of IL-7R and concomitant limited responsiveness to IL-7 sig

155 in the airways gradually lost expression of IL-7R and IL-15R, did not respond to IL-7 and/or IL-15,

156 e performed an analysis of the expression of IL-7R components (CD127 and CD132) on CD4(+) and CD8(+)

157 Thus, selective expression of IL-7R identifies memory cell precursors, and this marker

158 erated a model for conditional expression of IL-7R in mature T cells.

159 phabeta T cells, and increased expression of IL-7R in the thymus of mice expressing Cre under the pro

160 s study, we show that enforced expression of IL-7R on multipotential stem cells does not influence ly

161 TNFalpha activation increased expression of IL-7R only.

162 nt could either reflect unique expression of IL-7R or IL-7, or it could indicate that the IL-7R deliv

163 lly, T-bet also suppressed the expression of IL-7R, a key molecule involved in controlling intestinal

164 was associated with increased expression of IL-7R-alpha, decreased expression of killer cell lectin-

165 ng IL-7 availability via their expression of IL-7R.

166 at it can duplicate many of the functions of IL-7R.

167 of beta-catenin results in the generation of IL-7R-, Egr-, and TGFbeta-expressing pre-DP thymocytes t

168 several important downstream target genes of IL-7R signaling in T cells and thymocytes that provide a

169 Sequestration of IL-7 or impairment of IL-7R signaling after allograft transplantation abolishe

170 The importance of IL-7R signaling in TRUC disease was highlighted by the d

171 tional resting memory cells independently of IL-7R expression.

172 ar mechanism for the inhibitory influence of IL-7R signaling on DP thymocyte development.

173 etectable reactivities showed high levels of IL-7R alpha expression.

174 omeostasis in lymphoid organs, the levels of IL-7R and IL-15R expression likely set a threshold for t

175 Importantly, we showed that the levels of IL-7R expression and the capacity of HIV-specific CD8 T

176 MAIT cells also expressed high levels of IL-7R, and we showed that IL-7, a cytokine produced by h

177 ive proliferation, expressed lower levels of IL-7R, responded less to IL-7, IL-12, or IL-23 cytokines

178 that in HIV-infected individuals the loss of IL-7R (CD127) expression defines the expansion of a subs

179 ed low in vivo proliferation, maintenance of IL-7R expression, and the highest memory T cell yield.

180 s partially reconstituted in the presence of IL-7R and Jak3.

181 an immune response and that reexpression of IL-7R is a key checkpoint in the regulation of this proc

182 Therefore, the down-regulation of IL-7R on DP cells is an "altruistic" act required for ma

183 venting pre-BCR-dependent down-regulation of IL-7R signaling should interfere with allelic exclusion.

184 CH1, which is a transcriptional regulator of IL-7R expression.

185 o known as PTPN2, as a negative regulator of IL-7R-STAT signaling in T cell progenitors, contributing

186 and maintenance, despite the resemblance of IL-7R to other cytokine receptors and the apparent shari

187 ia progression; however, the significance of IL-7R/IL-7 signaling in T-ALL pathogenesis and its contr

188 mitochondrial prosurvival gene and target of IL-7R signaling, partly rescued the differentiation bloc

189 modifications were lost after termination of IL-7R-STAT5 signaling, and the transcription factor E2A

190 Furthermore, the upregulation of IL-7R in CD4(+)CD44(+) lymphocytes suggests that the act

191 ity of cells to recycle IL-7 is dependent on IL-7R alpha-chain (CD127) and endocytosis, consistent wi

192 -distal V(H) genes are uniquely dependent on IL-7R signaling, which is thought to establish local chr

193 bs exhibited the same differential effect on IL-7R expression in human as in mouse cells, suggesting

194 o evidence of a deficiency in plasma IL-7 or IL-7R expression, and IL-7 concentration correlated posi

195 ting effector T cells (CD28(-)CD95(+) and/or IL-7R/CD127(-)) and a high percentage of CD4(+)CD25(+) T

196 of the MHC class I molecules (Kb or Db), or IL-7R, or devoid of T cell renewal via adult thymectomy,

197 to determine the developmental lymphoid (or IL-7R alpha) dependency of various DCs and to examine th

198 is strongly associated with an overexpressed IL-7R signaling pathway and point to IL-7R as a relevant

199 ower IL-7 responsiveness; indeed, percentage IL-7R alpha -positive values showed a tight inverse corr

200 ressing an effector memory T cell phenotype (IL-7R+ CD62low) was dramatically diminished in mice immu

201 w)CD44(high)) to a resting memory phenotype (IL-7R(high)CD25(low)CD44(high)) 1 day after antigenic wi

202 etween different virus-specific populations, IL-7R alpha therefore appears to be more susceptible to

203 ct1, the key adaptor for the IL-17 receptor (IL-7R), formed a complex with the inducible kinase IKKi

204 er expression of the interleukin-7 receptor (IL-7R alpha) and by lower IL-7 responsiveness; indeed, p

205 IL-7 receptor (IL-7R) and T-cell receptor (TCR) signaling are pivotal f

206 ling function of the interleukin 7 receptor (IL-7R) and the pre-T-cell antigen receptor.

207 rosstalk between the interleukin 7 receptor (IL-7R) and the precursor to the B cell antigen receptor

208 ceptor (pre-BCR) and interleukin 7 receptor (IL-7R) coordinate pre-B cell population expansion with s

209 by promoting upregulation of IL-7 receptor (IL-7R) expression.

210 The interleukin-7 receptor (IL-7R) is a crucial T-cell developmental pathway that is

211 Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of a

212 Signaling through the IL-7 receptor (IL-7R) is required for development and maintenance of th

213 Interleukin-7 receptor (IL-7R) levels are tightly controlled during ontogeny: hi

214 enes involved in the interleukin-7 receptor (IL-7R) pathway and T cell receptor (TCR) signaling and t

215 t that key transcripts of the IL-7 receptor (IL-7R) pathway are accumulated in inflamed colon tissues

216 mocytes require interleukin (IL)-7 receptor (IL-7R) signals for survival and proliferation, but IL-7R

217 The IL-7 receptor (IL-7R) stimulated glucose uptake and cell-surface locali

218 required the function of the IL-7 receptor (IL-7R), and contributed to maintenance of humoral tolera

219 The interleukin-7 receptor (IL-7R), via its activation of the JAK-STAT pathway, prom

220 om signaling via the interleukin 7 receptor (IL-7R).

221 Interleukin 7 (IL-7) and its receptor (IL-7R alpha) are known to mediate lymphopoiesis, and IL-

222 The cytokine IL-7 and its receptor, IL-7R, are critical for T cell and, in the mouse, B cell

223 mouse MAITs expressed the cytokine receptors IL-7R, IL-18Ralpha, and IL-12Rbeta and the transcription

224 by the signaling of two opposing receptors, IL-7R and the pre-BCR.

225 date to this model in which three receptors, IL-7R, pre-BCR, and CXCR4, work in concert to coordinate

226 iver versus bone marrow environment, reduced IL-7R/STAT5 levels promote immunoglobulin kappa gene rec

227 lenic memory CD8 T cells also down-regulated IL-7R and IL-15R expression and failed to undergo homeos

228 irectly whether CD8 effector T cells require IL-7R expression for their differentiation into resting

229 alization of Glut1 in a manner that required IL-7R Y449, which promoted rapid signal transducer and a

230 d to be dependent on IL-15, because the same IL-7R-deficient effector cells were rapidly lost from IL

231 dergone four divisions expressed significant IL-7R, produced IFN-gamma, and yielded rapid and robust

232 fic selection, we created T-lineage-specific IL-7R alpha chain (IL-7Ralpha) transgenic (Tg) mice in w

233 y activating the transcription factor STAT5, IL-7R signaling maintains proliferation and represses Ig

234 Mi-2beta also supported IL-7R signaling, survival, and proliferation by repressi

235 hat the direct effects of IFN-gamma suppress IL-7R expression on Ag-specific effector CD8 T cells, bu

236 nce, our results suggest that LNK suppresses IL-7R/JAK/STAT signaling to restrict pro-/pre-B progenit

237 pha on T cells, we determined that sustained IL-7R expression in IL-23R-deficient mice could not driv

238 ll development was compatible with sustained IL-7R expression; however, we observed a near complete b

239 Overall, we conclude that IL-7R alpha is not required for the development of DCs/L

240 We conclude that IL-7R signals down-regulate transcription factors requir

241 Moreover, we demonstrate that IL-7R expression is an early functional biomarker of T-A

242 In addition, we demonstrate that IL-7R signals also inhibit TCF-1 and LEF-1 expression in

243 We now demonstrate that IL-7R signals inhibit expression of transcription factor

244 nt mice, thus providing formal evidence that IL-7R function is essential for Notch1-induced T-cell le

245 We found that IL-7R blockade alone induced indefinite pancreatic islet

246 sion of functional IL-7Ralpha, we found that IL-7R signaling was not required for maintenance of Treg

247 Thus, we hypothesized that IL-7R signaling through ERK5 could drive the expression

248 These findings indicate that IL-7R signal transduction is competent to promote Treg c

249 Collectively, these data indicate that IL-7R signaling contributes to Treg cell development and

250 In this study, we show that IL-7R-dependent innate lymphoid cells (ILCs) block LIP o

251 Notably, we show that IL-7R-dependent LIC activity and leukemia progression ca

252 Our data suggest that IL-7R blockade following T cell depletion has potential

253 TSLP-specific receptor chain (TSLPR) and the IL-7R alpha-chain.

254 urvival of naive and memory T cells, and the IL-7R is expressed on the surface of these cells.

255 were equally well reconstituted by both the IL-7R alpha KO and WT donor cells.

256 Ebf1 expression is driven by the IL-7R downstream effector Stat5, providing a link betwee

257 In developing B cells, the IL-7R and precursor B cell Ag receptor (pre-BCR) synergi

258 Here we demonstrate that in pre-B cells, the IL-7R but not the pre-BCR was coupled to phosphatidylino

259 it is produced by resting stromal cells, the IL-7R is present on most T cells, and IL-7 down-regulate

260 ferential, in particular, those encoding the IL-7R and transcription factors Id2/3 and Gfi1, upregula

261 cells emerged, of which 25-50% expressed the IL-7R.

262 ment of CD19+ B-lineage cells expressing the IL-7R.

263 Signals from the IL-7R are uniquely required for T cell development and m

264 paper, we show that cyclical changes in the IL-7R signaling pathway functionally segregate pro-B cel

265 Following viral infection, the IL-7R is expressed on only a subset of effector CD8 T ce

266 immunization controls the expression of the IL-7R (CD127), which has been shown to be necessary for

267 cells expressing high and low levels of the IL-7R alpha-chain (IL-7Ralpha) that is essential for mem

268 sisted of the extracytoplasmic domain of the IL-7R alpha-chain and the cytoplasmic domain of IL-2R be

269 fferential gene expression downstream of the IL-7R are not fully elucidated.

270 l in vivo was also reduced after loss of the IL-7R in a T cell-intrinsic manner.

271 quired player in signaling downstream of the IL-7R in early B cells.

272 propose that the observed expression of the IL-7R on common lymphoid progenitors, but not ETPs, resu

273 Preblocking of the IL-7R on the Tregs also restored suppressor function, in

274 a major signaling molecule downstream of the IL-7R signaling pathway.

275 ursors do not express abundant levels of the IL-7R, and require costimulation with Flt3 ligand and IL

276 ing their survival via downregulation of the IL-7R.

277 s reversible with targeted inhibition of the IL-7R/JAK/STAT5/BCL-2 axis.

278 We propose that this activity of the IL-7R/STAT5 pathway plays a critical protective role in

279 tor in adult B lymphopoiesis and suggest the IL-7R/STAT5 module to be causally involved in mediating

280 IL-7R or IL-7, or it could indicate that the IL-7R delivers unique signals.

281 espite intact proximal signaling through the IL-7R-coupled JAK3/STAT5 pathway.

282 Thus, the IL-7R signals required in the alphabeta T cell lineage (

283 To determine whether the IL-7R provided unique signals, we exchanged its intracel

284 Thus, IL-7R signaling on Treg supports the functional activity

285 isease activity and that ligation of IL-7 to IL-7R contributes to monocyte homing, differentiation of

286 To determine whether ligation of IL-7 to IL-7R is a potential target for RA treatment and to iden

287 pressed IL-7R signaling pathway and point to IL-7R as a relevant therapeutic target and potential bio

288 region of the IL-2R beta cytoplasmic tail to IL-7R alpha enables IL-7 to initiate myeloid differentia

289 when they express high levels of transgenic IL-7R on their surface, because IL-7R signal transductio

290 P = .026), whereas high expression of tumor IL-7R was associated with worse outcome (5-year RFP, 76%

291 Expression of transgenic wild-type IL-7R or a chimeric receptor that consisted of the extra

292 Unlike IL-7R(hi) MPECs, KLRG1(hi) IL-7R(lo) SLECs relied on IL-

293 in IL-2Rbeta-/- mice appears to depend upon IL-7R signaling.

294 7R alpha for DC development in vivo, we used IL-7R alpha knockout (KO) donor cells to reconstitute DC

295 There were more T cells that were IL-7R(hi) and, correspondingly, the IFN-lambdaR-deficien

296 Whereas IL-7R(-/-) thymocytes are arrested at the double-negativ

297 To directly explore whether IL-7R targeting may be therapeutically efficient against

298 n (IL-7Ralpha) transgenic (Tg) mice in which IL-7R is expressed throughout ontogeny.

299 ed and unremitting contraction compared with IL-7R-expressing control cells and were unable to develo

300 r data indicate that pre-BCR cooperates with IL-7R in expanding the pre-B cell pool, but it is also c