ライフサイエンスコーパス: IL-7

1 IL-7 administration in vivo failed to boost B cell devel

2 IL-7 and TSLP abrogated this inhibition and induced ster

3 IL-7 increased tumor sphere formation and expression of

4 IL-7 increases total circulating CD4 and CD8 T cell coun

5 IL-7 inhibited the differentiation of Th17 cells, but pr

6 IL-7 is a key factor in T cell immunity and common varia

7 IL-7 is a key homeostatic cytokine that provides signals

8 IL-7 is one such cytokine capable of augmenting the func

9 IL-7 production from IECs in response to C. rodentium wa

10 IL-7 restored ex vivo IFN-gamma production in septic pat

11 IL-7 therapy did not reduce TCR diversity of the memory

12 IL-7 therapy has been evaluated in patients who do not r

13 IL-7 treatment improved mTOR activation, GLUT1 expressio

14 IL-7 treatment increased levels of phospho-ribosomal pro

15 IL-7(+) cells expressed CXCL12 and the cytokine SCF, wer

16 IL-7, IL-7R, and IFN-gamma protein expression was signif

17 IL-7-induced phosphorylation of STAT5 as well as Bcl-2 a

18 BOS IL-1beta (P<0.001), IL-1Ralpha (P<0.01), IL-7 (P<0.05), IL-8/CXCL8 (P<0.001), MCP-3/CXCCL7 (P<0.0

19 IL-12 p70, IL-17A, GM-CSF, IL-12 p40, IL-10, IL-7, IL-1alpha, and IL-5) subject-to-subject variation.

20 3 (n=77; IL [interleukin]-12, IL-17, IL-10, IL-7, VEGF [vascular endothelial growth factor]), and cl

21 o-inflammatory cytokines (Eotaxin, IL-1beta, IL-7, IL-8, IL-12/IL-23p40, IL-12p70, IL-13, IL-16, IP-1

22 in vitro by anti-CD3, interleukin-2 (IL-2), IL-7, or IL-15 but not by Toll-like receptor ligands.

23 -4, IL-9, IL-10, fibroblast growth factor 2, IL-7, IL-15, and transforming growth factor alpha) but l

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

25 Finally, we show that the cytokines IL-2, IL-7, and IL-15, which induce homeostatic T cell prolife

26 ious cytokines known to activate ILCs (IL-2, IL-7, IL-12, thymic stromal lymphopoietin (TSLP), IL-25,

27 ls, whereas exposure of CD8 T cells to IL-2, IL-7, IL-15, and IL-21 increased granzyme B production.

28 n metabolites inhibited interleukin (IL)-2-, IL-7-, and IL-15-dependent expansion of CARTs; diminishe

29 icellulose, xylose value was high in IL 6-3, IL 7-2 and IL 6-2, whereas arabinose showed a low conten

30 e interleukin (IL) receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21.

31 he receptors for interleukin-2 (IL-2), IL-4, IL-7, IL-9, IL-15, and IL-21.

32 pha), CXCL10 (IP-10), IFN-gamma, IL-4, IL-5, IL-7, IL-12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LI

33 Plasma interleukin (IL) 2, IL-4, IL-5, IL-7, IL-17, interferon-gamma, and tumor necrosis factor

34 DR-induced quiescence of HSCs, whereas IL-6/IL-7 substitutions rescued the impairment of B lymphopoi

35 Interleukin 7 (IL-7) and its alpha-receptor, IL-7Ralpha, serving as ess

36 Interleukin 7 (IL-7) promotes the survival of TCRbeta(-) DN thymocytes

37 velopmental downregulation of interleukin 7 (IL-7)-receptor signaling in small pre-B cells induced ex

38 component of the receptor for interleukin-7 (IL-7) and the transcription factor c-myc.

39 nase-3 (Flt3) ligand (FL) and Interleukin-7 (IL-7) are cytokines pivotal for B-cell development, as m

40 Interleukin-7 (IL-7) availability determines the size and proliferative

41 nt protein-1 (MCP-1) and peak interleukin-7 (IL-7) concentrations above the median, were associated w

42 Interleukin-7 (IL-7) engages multiple mechanisms to overcome chronic vi

43 ed by cytokines, particularly interleukin-7 (IL-7) for murine developing B cells.

44 The cytokine interleukin-7 (IL-7) functions to enhance lymphocyte proliferation, sur

45 Interleukin-7 (IL-7) is fundamental for thymopoiesis, T-cell homeostasi

46 feration of infected cells by interleukin-7 (IL-7) or antigenic stimulation, as well as new rounds of

47 aused a downregulation of the interleukin-7 (IL-7) receptor, needed for survival of conventional T ce

48 ainst reinfection and require interleukin-7 (IL-7), but the mechanisms by which IL-7 controls memory

49 engagement in the presence of interleukin-7 (IL-7), IL-21, and the glycogen synthase-3beta inhibitor

50 (RABV) that expressed murine interleukin-7 (IL-7), referred to here as rLBNSE-IL-7, was constructed,

51 ain cytokines (CGCC), such as interleukin-7 (IL-7), render resting CD4 T cells permissible to HIV-1 i

52 Precise mechanisms underlying interleukin-7 (IL-7)-mediated tumor invasion remain unclear.

53 iple hematopoietic cytokines (interleukin-7 [IL-7], Flt3L, stem cell factor [SCF], ThPO, and IL-6) fr

54 d for CLP positioning near Interleukin-7(+) (IL-7) cells and for optimal IL-7 receptor signaling.

55 gression; however, the significance of IL-7R/IL-7 signaling in T-ALL pathogenesis and its contributio

56 Accordingly, IL-7-deficient DN4 cells lacked trophic receptors and di

57 In addition, IL-7 or thymic stromal lymphopoietin were able to replac

58 In addition, IL-7-stimulated pro-B cell cultures revealed a reduced d

59 s proliferation and did so without affecting IL-7 levels.

60 On the other hand, a JAK inhibitor and an IL-7-blocking antibody decreased the invasiveness of PC-

61 using a Janus kinase (JAK) inhibitor and an IL-7-blocking antibody.

62 r than 70 days in the lung and airways in an IL-7 dependent fashion.

63 ence interval {CI}, .77-43.0]; P = .088) and IL-7 (HR, 9.30 [95% CI, 1.96-44.0]; P = .005) were predi

64 MCP-1 and IL-7 concentrations increased after lymphodepletion, and

65 nd a novel mechanism through which IL-12 and IL-7 synergistically control granzyme B through upregula

66 We found that IL-1alpha and IL-7 secreted from keratinocytes work in tandem to expan

67 al interleukin receptors, including IL-2 and IL-7 receptors.

68 IL-8, IL-10, fibroblast growth factor 2, and IL-7 remained higher.

69 address the contribution of IL-23/IL-23R and IL-7/IL-7R signaling in Th17 and Th1 cell dynamics durin

70 y of gp41, and inhibited the IL-2, IL-4, and IL-7 responses, as well as TCR-mediated activation and p

71 High plasma IL-5 and IL-7 levels pre-ART were associated with increased risk

72 red to controls (all P < .05), with IL-5 and IL-7 significant after Bonferroni-Holm correction.

73 ); interferon gamma, interleukin (IL)-6, and IL-7 in CC group compared to Ctrl; and IL-8 in both UC a

74 F, VEGF, MIP-1beta, TNF-beta, IFN-alpha2 and IL-7 in response to an LPS challenge.

75 en-binding integrin alpha2beta1 (CD49b), and IL-7 increases their adhesion to collagen via alpha2beta

76 between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previously been proposed, but h

77 IL-15 was required for CD8(+) TRM cells, and IL-7 for CD8(+) and CD4(+) TRM cells, to exert epidermot

78 -7 transgenic mice suggests that both FL and IL-7 regulate B-cell commitment in a permissive manner:

79 e interplay between IFN-gamma/IFN-gammaR and IL-7/IL-7R pathways.

80 th increased surface expression of c-Kit and IL-7 receptors on the IL-18-treated cells.

81 resumably via interaction with the c-Kit and IL-7 signaling axis.

82 ng experimental lymphopenic mouse models and IL-7-induced homeostatic proliferation to measure IL-7 a

83 6D(+)CD135(+)CD127(+)CD19(-) progenitors and IL-7 by providing survival signals to these progenitors.

84 eplication stress by integrating pre-TCR and IL-7 signaling with DNA damage and cell cycle control.

85 L-4, renders DCs responsive to both TSLP and IL-7.

86 Thymic stromal lymphopoietin (TSLP) and IL-7 are related cytokines that mediate growth and diffe

87 complex, a heterodimer composed of TSLPR and IL-7 receptor alpha (CD127).

88 associated with lymphocyte count in vivo and IL-7 secretion levels in vitro.

89 In vivo IL-7/anti-IL-7 mAb complexes selectively expanded and enhanced the

90 reaction and developed non-neutralizing anti-IL-7 antibodies.

91 Although not as critical as IL-7, based on our studies, IL-21 plays an important com

92 Importantly, we found that cytokines such as IL-7 and IL-4, which are particularly active in sites of

93 ith heterodimeric cytokine receptors such as IL-7 receptor or IL-9 receptor, in which JAK1 is appende

94 pro-B progenitor homeostasis by attenuating IL-7-stimuated JAK/STAT5 signaling via a direct interact

95 ole is in the proper folding of Wnt3a, BAFF, IL-7, and perhaps other factors produced by the extra-he

96 Because IL-7 was shown to interfere with T cell functionality, w

97 herapy relies on the interdependence between IL-7 and IFN-gamma signalling in T cells, as lack of eit

98 Blocking IL-7 signaling reduced the Th17 autoimmune compartment b

99 Here, we investigated whether blocking IL-7 signaling with a mAb that targets IL-7 receptor alp

100 PLCgamma pathway inhibition blocks IL-7-induced activation of mTOR, but not Stat5.

101 th prostate cancers that highly express both IL-7 and IL-7Ralpha.

102 apoptosis, proliferation, and activation by IL-7, IL-23, and IL-12 by cell culture, flow cytometry,

103 transplantation and appeared to be driven by IL-7-mediated homeostatic T cell proliferation.

104 lls before antigen recognition is ensured by IL-7, which drives expression of the prosurvival factor

105 17 T(RM) cells are maintained in the lung by IL-7, produced by lymphatic endothelial cells.

106 dant to its role in suppressing signaling by IL-7, a critical gammac cytokine in early thymopoiesis.

107 HGF), T-cell development/activation (CD40L, IL-7, CCL25, IL-2RB, IL-15RA, CD6) and angiogenesis (VEG

108 recursors failed to undergo a characteristic IL-7-dependent proliferative burst.

109 plantation and other lymphopenic conditions, IL-7 plays an important role in the reconstitution, surv

110 of FRC-derived chemokine CCL21 and cytokine IL-7 were accompanied by altered composition and aberran

111 d by the stroma-derived homeostatic cytokine IL-7, and priming diminishes if Il7r is subsequently del

112 Because the lymphotropic cytokine IL-7 plays crucial roles in both development of TN in th

113 The cytokine IL-7 and its receptor, IL-7R, are critical for T cell an

114 optosis in response to homeostatic cytokines IL-7 and IL-15.

115 cal trials include KGF, use of the cytokines IL-7 and IL-22, and hormonal modulation including growth

116 clude keratinocyte growth factor, cytokines (IL-7 and IL-22), and hormonal modulation including sex s

117 ded on the presence of hair follicle-derived IL-7.

118 However, whether host-derived IL-7 plays a role in driving the proper function of CD4+

119 l development does not result from disrupted IL-7 signaling.

120 demethylation was heritably preserved during IL-7- and IL-15-mediated in vitro cell proliferation.

121 m depleted patients showed markedly elevated IL-7 levels posttransplantation.

122 to increased availability of the endogenous IL-7 in mice.

123 suggest caution in relying on the endogenous IL-7 to enhance donor T cell expansion and persistence a

124 ) on CD4(+) and CD8(+) T cells and evaluated IL-7-dependent signaling events in patients at different

125 consumption of the lymphocyte growth factor IL-7 before motor onset of HD.

126 Serum was analyzed for IL-7.

127 These data support a novel role for IL-7 in the repression of the TFH gene program and evoke

128 te physiological receptors, such as that for IL-7.

129 hile conditional Cxcl12 or Scf deletion from IL-7(+) cells reduced HSC and MPP numbers.

130 s had higher levels of cord blood IFN-gamma, IL-7, sTNFR1, and sTNFR2 compared with neonates with no

131 tein [MIP]-1alpha, MIP-1beta), hematopoietic IL-7, and granulocyte macrophage colony-stimulating fact

132 Importantly, high IL-7 expression was detected in the CNS during EAE and c

133 impaired clearance of cryptococci while high IL-7 levels may reflect IL-7/IL-7R pathway dysfunction i

134 of 3 subcutaneous doses of recombinant human IL-7 (rhIL-7) per week in patients with ICL who were at

135 esized that treatment with recombinant human IL-7 (rhIL-7) would augment host defense against Pneumoc

136 metabolism in sepsis with recombinant human IL-7 as a treatment option.

137 d the beneficial effect of recombinant human IL-7.

138 stemic inflammation, we found that in humans IL-7 also controlled alpha4beta7 integrin expression and

139 PLCgamma/PKC-induced mTOR activation impairs IL-7-mediated B cell development.

140 ient mice overexpressing Bcl2, as well as in IL-7 transgenic mice suggests that both FL and IL-7 regu

141 sion of PDPN resulted in profound defects in IL-7-mediated T cell expansion and survival.

142 Consistently, deficiency in IL-7 receptor alone, a common gamma chain-containing rec

143 These data suggest that differences in IL-7-dependent proliferation is one exploitable mechanis

144 CD3/28-activated T cells expanded in IL-7 and IL-15 produced greater expansion of memory stem

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

146 usly unappreciated function for monocytes in IL-7 biology and IL7R-associated diseases.

147 ha Tyr(449) cytoplasmic SH2-binding motif in IL-7-mediated B cell development using a knock-in mouse

148 in T-cell development caused by mutations in IL-7 receptor alpha (IL7RA) and IL-2 receptor gamma (IL2

149 tained demonstrate that FL overexpression in IL-7-deficient mice rescues B-cell commitment, resulting

150 y6D(+)CD135(+)CD127(+)CD19(-) progenitors in IL-7- or FL-deficient mice overexpressing Bcl2, as well

151 The defect was not due to a reduction in IL-7 expression, but from a combination of changes in th

152 Other pathways, including IL-7 signaling and B cell development were affected only

153 in gut immunity and tissue repair, including IL-7, Ccl2, Ptgs2, and Amphiregulin.

154 Increased IL-7 availability enhanced Treg survival, stabilized Tre

155 C. rodentium infection induced IL-7 production from intestinal epithelial cells (IECs).

156 lymphopenia in conjunction with its induced IL-7 receptor defects.

157 SOCS family activity consequently inhibited IL-7-mediated STAT5 activation and T cell homeostatic pr

158 1 integrin with a neutralizing mAb inhibited IL-7-induced bone loss and osteoclast numbers by reducin

159 However, despite intact IL-7 signaling, GON4L-deficient pro-B cell stage precurs

160 Intriguingly, IL-7 diminished the suppressive activity of DN T cells t

161 rescue of B-cell commitment in mice lacking IL-7 but simultaneously overexpressing FL.

162 T cells, and prevent early and increase late IL-7 induction by lymph node stromal cells.

163 gamma-chain (gammac) receptor but that, like IL-7 and IL-15, induced expression of the lineage-specif

164 of other homeostatic regulators, most likely IL-7.

165 L-7, were primarily responsible for limiting IL-7 availability via their expression of IL-7R.

166 pression of genes related to B cell lineage, IL-7 signaling, and cell cycle.

167 ation of the zebrafish ortholog of mammalian IL-7 based on chromosomal localization, deduced protein

168 induced homeostatic proliferation to measure IL-7 availability in vivo, we found that radioresistant

169 Mechanistically, IL-7-dependent activation of STAT5 contributes to Bcl-6

170 While in mice IL-7 is known to play a role in systemic inflammation, w

171 Our studies indicate that endogenous murine IL-7 is part of the normal host response to Pneumocystis

172 a novel rabies vaccine that expressed murine IL-7 was developed.

173 sthmatic patients had increased TSLP but not IL-7 levels.

174 self-renewal of DN4 cells in the absence of IL-7, but overexpression of BCL2 did not.

175 he several potential mechanisms of action of IL-7 is unknown.

176 xtent to which therapeutic administration of IL-7 could reverse TN deficiency in aging rhesus macaque

177 least in part, to additional availability of IL-7.

178 revealed to be the C-terminus of helix B of IL-7, highlighting the value of solution-based character

179 ecific CD8 T cells 10 wk after completion of IL-7 treatment.

180 that TAG synthesis is a central component of IL-7-mediated survival of human and mouse memory CD8+T c

181 ne marrow as well as serum concentrations of IL-7, Flt3L, SCF, and ThPO to the levels displayed by sp

182 itizes Treg cell to the biological effect of IL-7, possibly rendering more common gammac-chain availa

183 naive T cells to the prosurvival effects of IL-7 and allowing T-cell persistence in vivo.

184 strated that the immune-enhancing effects of IL-7 were also applicable to donor CD4+ T cells pre-acti

185 These results suggest that the expression of IL-7 is beneficial for induction of potent and long-last

186 dexamethasone upregulated ILC2 expression of IL-7 receptor alpha, which augmented and sustained signa

187 Protein secretion and gene expression of IL-7, IL-7R, IFN-gamma, MC1R, NF-kappaB, phosphorylated

188 urvival molecule Bcl-2, but the functions of IL-7 during beta-selection have remained unclear.

189 , and appeared to be limited by induction of IL-7 nonresponsiveness.

190 The serum levels of IL-7 were also increased in chronic chagasic patients.

191 c stromal lymphopoietin (TSLP), 2 ligands of IL-7 receptor alpha.

192 ata suggest that a compensatory mechanism of IL-7-mediated homeostatic proliferation can restore the

193 Despite of a paucity of IL-7 in the immune milieu, CTX preconditioning allowed a

194 e derivatives, and assessed the potential of IL-7 as a clinical target using a Janus kinase (JAK) inh

195 when cells were cultured in the presence of IL-7, a cytokine that is critical for normal T cell func

196 In the presence of IL-7, this augmented downstream signal transduction, res

197 rosine kinase (BTK), a negative regulator of IL-7 signaling, was reduced in preleukemic and leukemic

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

199 me chronic viral infections, but the role of IL-7 in bacterial infections, especially enteric bacteri

200 ver, there is little known about the role of IL-7 in PCP or its potential use as an immunotherapeutic

201 racterized the previously unexplored role of IL-7 in the innate immune response to the attaching and

202 Thus, we investigated the role of IL-7 in tumor invasiveness using metastatic prostate can

203 Here we assessed the role of IL-7, a key cytokine regulating T-cell homeostasis, in s

204 Sequestration of IL-7 or impairment of IL-7R signaling after allograft tr

205 that radioresistant cells were the source of IL-7 for both CD4(+) and CD8(+) T cells.

206 ge cells, although irrelevant as a source of IL-7, were primarily responsible for limiting IL-7 avail

207 ys an important role in the transcription of IL-7 receptor alpha-subunit (CD127), enabling responsive

208 own resistance by promoting upregulation of IL-7 receptor (IL-7R) expression.

209 ence, the inhibitory effects of IFN-alpha on IL-7-induced proliferation of CD4(+) T cells are unlikel

210 The first wave of expansion is dependent on IL-7.

211 lls were found to have a potent influence on IL-7 amounts in the primary and secondary lymphoid tissu

212 t that PU.1 and Spi-B activate Btk to oppose IL-7 responsiveness in developing B cells.

213 nterleukin-7(+) (IL-7) cells and for optimal IL-7 receptor signaling.

214 s in the presence or absence of IL-18 and/or IL-7.

215 verall, our data suggest that overexpressing IL-7 improved the induction of long-lasting primary and

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

217 Treg cells can control physiological IL-7 production that is indispensable for normal B-cell

218 IEC-produced IL-7 was only essential for protective immunity against

219 ly, supplementation of exogenous recombinant IL-7 markedly amplified and sustained polyfunctional CD4

220 and highlight the usefulness of recombinant IL-7 as an adjuvant for adoptive immunotherapy.

221 ndicate that the ability of cells to recycle IL-7 is dependent on IL-7R alpha-chain (CD127) and endoc

222 absence of intracellular TCRbeta and reduced IL-7 signaling.

223 BC antibodies, lower hematocrit, and reduced IL-7 signaling.

224 yptococci while high IL-7 levels may reflect IL-7/IL-7R pathway dysfunction in T cells, both of which

225 Their persistence in skin required IL-7 and thymic stromal lymphopoietin, and localization

226 rLBNSE-IL-7 induced higher rates of T follicular helper (Tfh) c

227 rleukin-7 (IL-7), referred to here as rLBNSE-IL-7, was constructed, and its effectiveness was evaluat

228 Interestingly, rLBNSE-IL-7 improved the percentages of long-lived memory B cel

229 em and PCs after a boost with rLBNSE, rLBNSE-IL-7-immunized mice promptly produced a more potent seco

230 he IL-7-expressing recombinant virus (rLBNSE-IL-7) were able to sustain VNA levels much longer than t

231 higher numbers for up to 360 dpi with rLBNSE-IL-7 compared to rLBNSE, could differentiate into antibo

232 ) and old (>20 y) RM with recombinant simian IL-7 (rsIL-7) results in only transient increases in per

233 r, the mechanisms that regulate steady-state IL-7 amounts are unclear.

234 cking IL-7 signaling with a mAb that targets IL-7 receptor alpha (IL-7Ralpha) alone or following T ce

235 These results demonstrate that IL-7 homeostasis is achieved through consumption by mult

236 Collectively, these data demonstrate that IL-7 is produced by IECs in response to C. rodentium inf

237 Furthermore, we determined that IL-7 signaling is important for the homeostasis of these

238 We discover that IL-7 induces expression of the glycerol channel aquapori

239 In this article, we provide evidence that IL-7 utilization is enhanced by a novel mechanism of cyt

240 Here we found that IL-7 signaled TCRbeta(+) DN3 and DN4 thymocytes to upreg

241 We found that IL-7 stimulated wound-healing migration and invasion of

242 These findings indicate that IL-7 and Akt/mTOR signaling are critical factors for the

243 -cell progenitors, therefore indicating that IL-7 can be dispensable for commitment to the B-cell lin

244 Of interest, our studies revealed that IL-7 activates the Akt/mechanistic target of rapamycin (

245 Here we show that IL-7 receptor (IL-7R) is not strictly required for the d

246 In this article, we show that IL-7 therapy in humans increases the number of circulati

247 Previous results showed that IL-7 can restore TRAF1 expression in virus-specific CD8

248 Taken together, we showed that IL-7 mediates an intrinsic and physiologic mechanism of

249 We also showed that IL-7-induced bone loss in vivo is associated with Th17 c

250 Collectively, these data suggest that IL-7 and/or IL-7Ralpha are promising targets of inhibiti

251 Taken together, our data support that IL-7 drives cellular turnover non-cell autonomously, whi

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

253 ngenital deficiencies in genes affecting the IL-7 signaling pathway.

254 1), recent thymic emigration (CD31), and the IL-7 receptor-alpha (IL-7Ralpha).

255 ified the silencing of the IL7R gene and the IL-7 signaling pathway genes as potential biomarkers.

256 the long-lived PCs that were elicited by the IL-7-expressing recombinant virus (rLBNSE-IL-7) were abl

257 trols, we report that key transcripts of the IL-7 receptor (IL-7R) pathway are accumulated in inflame

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

259 we generated a high-confidence model of the IL-7/IL-7Ralpha complex.

260 T cell development critically depends on the IL-7 cytokine signaling pathway.

261 the protein kinases Akt or mTOR reversed the IL-7 effect, thereby restoring the functionality of DN T

262 Further analyses suggest that the IL-7/Akt/mTOR signaling cascade downregulates anergy-ass

263 D4+, and CD8+ T cells were affected in their IL-7-dependent phosphorylation of STAT5 (pSTAT5) which w

264 uced cytotoxicity of TECs and restored their IL-7 and IL-15 secretion.

265 g a lack of homeostatic cell control through IL-7 signalling.

266 Thus, IL-7 critically acts cooperatively with signaling via th

267 Thus, IL-7 receptor controls early B lymphopoiesis through act

268 Thus, IL-7 therapy in antiretroviral therapy-treated patients

269 e-negative 3 stage, similar in efficiency to IL-7.

270 -/- pro-B progenitors were hypersensitive to IL-7, exhibited marked self-renewal in vitro and in vivo

271 -deficient pro-B cells are hyporesponsive to IL-7, a key cytokine required for early B cell developme

272 sed lower levels of IL-7R, responded less to IL-7, IL-12, or IL-23 cytokines, and were more prone to

273 ble degradation of Socs mRNAs in response to IL-7 signalling in order to reprogram naive T cells for

274 nstrated robust proliferation in response to IL-7, whereas more differentiated cells proliferated poo

275 ent RORgammat(+) ILCs are less responsive to IL-7 mediated signalling, more prone to apoptosis and pr

276 DeltaPB mice had increased responsiveness to IL-7 and could proliferate indefinitely in response to t

277 over and diminished T-cell responsiveness to IL-7 by IL-1beta and IL-6 exposure may contribute to the

278 7R and concomitant limited responsiveness to IL-7 signals as a common mechanism resulting in reduced

279 ory T-cell development and responsiveness to IL-7-dependent signals.

280 regain IL-7Ralpha expression, giving rise to IL-7-responsive polyfunctional CD4+ effector cells.

281 n, TEM became increasingly more sensitive to IL-7 stimulation in vivo, and transcriptional analysis o

282 Also, similar to IL-7, IL-21 seems to be involved in the positive selecti

283 rly pro-B-like stage that is unresponsive to IL-7 receptor signaling and unable to efficiently comple

284 d renders B cell progenitors unresponsive to IL-7.

285 re and the first year after transplantation, IL-7 and IL-2 induced STAT5 phosphorylation, and the exp

286 Unlike IL-7, which is known to be critical for T cell thymic de

287 echanism that enables cells to optimally use IL-7.

288 In vivo IL-7/anti-IL-7 mAb complexes selectively expanded and en

289 cell development in HNF1A(-/-) mice, whereas IL-7 stimulation of HNF1A(-/-) B cell progenitors in vit

290 o IL-6 favours the TFH gene program, whereas IL-7 signalling represses TFH-associated genes including

291 endocytosis, consistent with a model whereby IL-7 is internalized via receptor interactions before re

292 with T cell functionality, we asked whether IL-7 affects the functionality of human DN T cells.

293 leukin-7 (IL-7), but the mechanisms by which IL-7 controls memory T cell survival, particularly metab

294 y uncovers the metabolic mechanisms by which IL-7 tailors the metabolism of memory T cells to promote

295 at combining immune checkpoint blockade with IL-7 signalling could be an effective modality to improv

296 e transcriptional profile that overlaps with IL-7-induced gene sets.

297 id not do so when ILC2s were stimulated with IL-7 and thymic stromal lymphopoietin (TSLP), 2 ligands

298 bility, further enhanced by stimulation with IL-7.

299 IL-18 showed synergy with IL-7 and enhanced proliferation of both the thymus-deriv

300 Treatment with IL-7/mAb complexes can restore naive T cell homeostatic