ライフサイエンスコーパス: iTreg

1 iTreg cell-mediated immunosuppressive effects were abrog

2 iTreg cells demonstrate advantages over natural Treg (nT

3 iTreg cells, similar to nTreg cells, exhibit functional

4 iTreg induction occurs through suppression of IL-4/STAT6

5 iTreg-treated DCs are markedly defective in their capaci

6 iTreg-treated DCs expressed high levels of MARCH1, an E3

7 iTregs could be induced in large numbers from convention

8 iTregs from CTLA-4-deficient mice failed to induce downr

9 iTregs induced under TIM-4 blockade have equivalent pote

10 ry T cells generated by CD83(high) IL-10DCs (iTreg(+)) exhibited a significantly higher suppressive c

11 ory T cells generated by CD83(low) IL-10DCs (iTreg(-)).

12 Administration of Act-A-iTreg cell-modified DCs ameliorated cardinal asthma mani

13 Act-A-iTreg cell-modified DCs exhibited a significantly impair

14 DCs conditioned by Act-A-iTreg cells (Act-A-iTreg cell-modified DCs) to protect against experimental

15 The ability of DCs conditioned by Act-A-iTreg cells (Act-A-iTreg cell-modified DCs) to protect a

16 Here we investigated whether Act-A-iTreg cells can modulate DC responses and endow them wit

17 Gene-profiling studies revealed that Act-A-iTreg cells dampened crucial TH2-skewing transcriptional

18 Our studies reveal that Act-A-iTreg cells instruct the generation of a highly effectiv

19 ay disease, we examined the effects of Act-A-iTreg cells on DC phenotype, maturation status, and TH2

20 of DCs with tolerogenic properties by Act-A-iTreg cells.

21 networks induced in tolerogenic DCs by Act-A-iTreg cells.

22 cts of activin-A-induced regulatory T (Act-A-iTreg) cells on the regulation of dendritic cell (DC)-dr

23 g on induction and stability of alloreactive iTreg.

24 ntation, increased induction of allospecific iTregs and a reduction in T effector responses were obse

25 Also, iTregs display elevated Dlgh1 overall and Dlgh1-dependen

26 25 in shifting the immune response toward an iTreg(-) controlled tolerance reaction.

27 tigated the role of iTreg-produced IL-10 and iTreg fate in a treatment model of inflammatory bowel di

28 D4(+)CD25(+)) were isolated from WT mice and iTreg cells were generated from WT CD4(+)CD25(-) T cells

29 allergic responses by transferred nTreg and iTreg cells differed.

30 ion, however, the function of both nTreg and iTreg was independent on robust NFAT levels, reflected b

31 We compared the abilities of nTreg and iTreg, both from OVA-TCR-transgenic OTII mice, to mediat

32 reflected by less nuclear NFAT in nTreg and iTreg.

33 g of Foxp3-expressing IL-17A(+), ex-Th17 and iTreg cells demonstrates the dissociation between the me

34 a) in modulating plasticity between Th17 and iTreg cells.

35 l by regulating the balance between TH17 and iTreg cells.

36 also plays a major role controlling Th17 and iTreg plasticity in the gut mucosa.

37 mma gene, as DNMT3a-deficient Th2, Th17, and iTreg cells produced significant levels of IFNgamma foll

38 3a, however, DNMT3a-deficient Th2, Th17, and iTreg completely failed to methylate the ifngamma promot

39 hylated in naive T cells, but Th2, Th17, and iTreg differentiation is accompanied by substantial de n

40 d for overproduction of IFN-gamma in Th2 and iTreg and IL-10 in Th2 cells.

41 trate that glucosamine impedes Th1, Th2, and iTreg but promotes Th17 differentiation through down-reg

42 r results demonstrate that CD25(lo) Treg and iTreg instability occurs during a viral immunoinflammato

43 Thus, Th9 cells and iTregs are developmentally linked and GITR can subvert t

44 ertook a systematic comparison of eTregs and iTregs to recommend the most suitable for clinical imple

45 lity to differentiate tTregs from pTregs and iTregs.

46 17 cells undergo phenotype switch and become iTreg cells.

47 d out to investigate the interaction between iTreg cells in murine or human MCs by using both direct

48 ith animals that were competent to make both iTreg populations.

49 However, unlike nTregs, both iTreg populations lost Foxp3 expression within 3 wk in v

50 The suppressive function of both iTreg and nTreg, however, is not affected by the loss of

51 The absence of both iTreg populations was associated with significantly grea

52 of weight loss, mice were treated with both iTregs and nTregs where one marked subset was selectivel

53 ot anti-IL-13, attenuated the enhancement by iTreg cells.

54 ajor suppressive mechanism of DC function by iTregs is secondary to the effects of IL-10 on MARCH1 an

55 ignificantly improved Foxp3 stability in CD4 iTregs (and, to a lesser extent, CD8 iTregs), such that

56 These data demonstrate that CD4 iTregs can be produced rapidly in large, clinically rele

57 d the ability to make both CD8(+) and CD4(+) iTregs had accelerated GVHD mortality compared with anim

58 raft-versus-host disease (GVHD), CD4 and CD8 iTregs suppressed the proliferation of effector T cells

59 in CD4 iTregs (and, to a lesser extent, CD8 iTregs), such that they remained detectable 12 wk after

60 ), CD4(+) induced Tregs (iTregs), and CD8(+) iTregs, and was more potent than temporally concordant b

61 Strikingly, CD4, but not CD8, iTregs could then suppress Teff proliferation and proinf

62 oxp3 epigenetically, which marks mother cell iTreg lineage choice within the genome of differentiatin

63 ceptors differently to control the TH17 cell-iTreg cell developmental fate.

64 rom peripheral effector CD4CD25FOXP3T cells (iTreg) cells is still debated.In vitro studies of antige

65 ls) and CD4(+) inducible regulatory T cells (iTreg cells) emerge from an overlapping developmental pr

66 hly expressed by induced regulatory T cells (iTreg) and was crucial for the generation and function o

67 induced CD25(+)Foxp3(+) regulatory T cells (iTreg) both contribute to tolerance in mouse models of c

68 ), Th2, Th17 and induced regulatory T cells (iTreg).

69 l for the development of induced Treg cells (iTreg cells) by repression of the T helper type 2 (TH2)

70 CD4(+) Tconv cells into induced Treg cells (iTreg cells).

71 ve T cells to Foxp3(+) inducible Treg cells (iTreg) with a significant decrease of iTreg in lymphoid

72 uced levels of inducible regulatory T cells (iTregs) due to a T cell-intrinsic requirement for STIM1

73 of using murine-induced regulatory T cells (iTregs) for the induction of tolerance after bone marrow

74 sed induction of induced regulatory T cells (iTregs) from naive CD4(+) T cells, both in vitro and in

75 In vitro induced human regulatory T cells (iTregs) have demonstrated in vivo therapeutic utility, b

76 Extrathymically derived regulatory T cells (iTregs) protect against autoimmunity to tissue-specific

77 generation of inducible regulatory T cells (iTregs) remains incompletely defined.

78 nducible, CD4(+)Foxp3(+) regulatory T cells (iTregs) remains incompletely defined.

79 ferentiate into Foxp3(+) regulatory T cells (iTregs) upon suboptimal T cell receptor (TCR) stimulus o

80 ific inducible regulatory-type CD4+ T cells (iTregs), were measured in healthy older people, using a

81 CD4(+)CD25(+) inducible regulatory T cells (iTregs).

82 e frequencies of induced regulatory T cells (iTregs: CD4(+)CD25(-)Fopx3(+)) and CD4(+) and CD8(+) T c

83 ic regulatory T cells (inducible Treg cells [iTreg cells]) that express Foxp3 are also critical.

84 nsfer studies showing an increase of colonic iTreg and a decrease of Th17 cells in the gut mucosa of

85 responses by 41-56%, whereas the comparator iTreg reduced these responses by 72-86%.

86 erate CD4(+)CD25(+)Foxp3(-) cells containing iTreg precursors.

87 In this context, iTreg(+) displayed a more activated phenotype (prolifera

88 is lesions more effectively than did control iTregs.

89 l sites (pTreg), or induced in cell culture (iTreg) in the presence of transforming growth factor bet

90 nges in metabolism, DMOG treatment decreased iTreg mitochondrial respiration and increased their glyc

91 ion to decreased production, PD-1H deficient iTreg could also rapidly convert to CD4(+) T helper 1 or

92 reversed by anti-IL-10, and IL-10-deficient iTregs failed to downregulate DC function.

93 /CD86, but DCs treated with CTLA-4-deficient iTregs still exhibited impaired capacity to activate nai

94 hen nTregs were present but IL-10 deficient, iTreg-produced IL-10 was necessary and sufficient for th

95 the retina is capable of local, "on-demand" iTreg generation that is independent of circulating Treg

96 nt and function of both peripherally derived iTregs and in vitro-induced Tregs.

97 Notably, 10 days after the transfer of donor iTreg cells, predominance was shifted from Th17 cells to

98 s iTreg cell induction by rendering emerging iTreg cells refractory to signals mediated by effector-d

99 cts synergistically with TGF-beta to enforce iTreg cell differentiation and maintenance.

100 proteolysis during T-cell activation enhance iTreg development.

101 transferred iTregs lost Foxp3 expression (ex-iTregs) but retained a portion of the iTreg transcriptom

102 ted, which promotes a large population of ex-iTregs with pathogenic potential during immunotherapy.

103 Helios expression identifies Ag-experienced iTregs that should express memory markers.

104 R and C5a/C5aR interactions could facilitate iTreg-mediated tolerance to alloantigens in humans.

105 ctivity, suggesting that they were bona fide iTregs.

106 quence of STAT3 signaling may be greater for iTreg rather than nTreg cells during GvHD.

107 We also found that moesin is required for iTreg conversion in the tumor microenvironment, and the

108 This effect of PD-1H is highly specific for iTreg because both naturally generated iTreg in gut-rela

109 This is specific for iTreg development, because frequency of nTreg remained u

110 poietic compartment alone was sufficient for iTregs to prevent GVHD.

111 ing HIF-1alpha could be a strategy to foster iTreg differentiation in an inflammatory milieu.

112 that SOCS2 may prevent IL-4-induced Foxp3(+) iTreg instability.

113 the BDC12-4.1 clone to convert into Foxp3(+) iTreg cells.

114 directly promote the development of Foxp3(+) iTreg cells is unclear.

115 d that in vitro polarization toward Foxp3(+) iTreg was effective with a majority (>70%) of expanded c

116 Foxp3(+) iTregs are key regulators of immune responses at mucosal

117 dual role of SOCS2 in both Th2 and Foxp3(+) iTregs reinforces SOCS2 as a potential therapeutic targe

118 g IL-4 stimulation, SOCS2-deficient Foxp3(+) iTregs secreted elevated IFN-gamma and IL-13 levels and

119 ta, leads to increased expansion of Foxp3(+) iTregs with enhanced CTLA-4 expression and suppressive c

120 und that the frequency and number of Foxp3(+)iTreg cells and Th17 cells were significantly reduced in

121 nduction in peripheral CD4(+)CD25(+)Foxp3(-) iTreg precursors.

122 lergens suppressed their ability to generate iTreg cells coincident with blocking airway tolerance.

123 e were impaired in their ability to generate iTreg in the GALT when exposed to oral Ag, and 4-1BB-def

124 c for iTreg because both naturally generated iTreg in gut-related tissues and in vitro induced iTreg

125 IL-2 signaling upon T cell priming generates iTreg precursors, subsequent activation of IL-2 signalin

126 Here we review how iTreg cells develop and how they participate in immunolo

127 3aR/C5aR signaling augments murine and human iTreg generation, stabilizes Foxp3 expression, resists i

128 usly unrecognized function of IL-10 in human iTreg generation, with potential therapeutic implication

129 The therapeutic potential of human iTreg cells in subjects with chronic, immune-mediated in

130 the effects exerted by inflammation on human iTreg differentiation have not been extensively studied.

131 pendent activation of MCs by murine or human iTreg cells.

132 pression does not exclusively identify human iTregs, and, to our knowledge, the data provide the firs

133 Here, we report that human iTregs generated in vitro from naive cord blood cells pr

134 Furthermore, HY-iTregs expanded extensively in male but not female recip

135 We generated HY-specific iTregs (HY-iTregs) from resting CD4 T cells derived from TCR transg

136 We found that HY-iTregs were highly effective in preventing GVHD in male

137 We found that HY-iTregs were more stable in male than in female recipient

138 Furthermore, treatment with HY-iTregs still preserved the GVL effect even against pre-e

139 ylglycine (DMOG) also significantly impaired iTreg differentiation.

140 Thus, Helios expression in iTreg may reflect the context of stimulation during Foxp

141 -mediated enhancement, it was ineffective in iTreg cell-mediated enhancement; conversely, anti-IL-17,

142 , the robust Helios expression we observe in iTreg precludes its use as a marker of thymic Treg.

143 o exogenous IL-6-induced IL-17 production in iTreg cells, and in vivo conversion of transferred iTreg

144 a T cell-intrinsic requirement for STIM1 in iTreg differentiation and excessive production of IFN-ga

145 nt or function, SOCS2 is highly expressed in iTregs and required for the stable expression of Foxp3 i

146 The loss of Foxp3 in iTregs followed homeostatic and/or alloantigen-driven pr

147 quired for the stable expression of Foxp3 in iTregs in vitro and in vivo.

148 Galectin-9 increased iTreg cell stability and function by directly binding to

149 ously activated DCs still leads to increased iTreg induction.

150 and acts as an important cofactor to induce iTreg cell development while potently inhibiting TH17 ce

151 C-SIGN(+) and CD14(+)DC-SIGN(-) APCs induced iTreg cells poorly.

152 the expression of Foxp3 in TGF-beta-induced iTreg depends on the threshold value of NFAT rather than

153 TGF-beta-induced iTreg differentiation was enhanced in PKC-theta(-/-) T c

154 de evidence that transferred TGFbeta-induced iTreg cells are more stable and functional than nTreg ce

155 in gut-related tissues and in vitro induced iTreg by TGF-beta were decreased whereas the genesis of

156 (+) APCs from healthy pregnant women induced iTreg cells significantly more efficiently than CD14(+)D

157 -/-) T cells restored the ability to inhibit iTreg differentiation.

158 cells might directly cause vascular injury, iTregs may attenuate this response.

159 D4 T cells can be efficiently converted into iTreg, and that Delta-like 1 (DL1)-mediated Notch signal

160 tor RORgammat and promoted polarization into iTreg cells.

161 conventional T cells were not converted into iTregs under polarizing conditions and produced large am

162 irect evidence of the presence of intragraft iTreg suggests a possible role of iTreg in the regulatio

163 Mechanistically, iTreg cells suppressed proinflammatory cytokine levels b

164 Such GITR-mediated iTreg to Th9 induction enhances anti-tumour immunity in

165 MSC-deficient (Msc(-/-)) iTreg cells were unable to suppress TH2 responses, and M

166 f PPARgamma in CD4+ T cells impaired mucosal iTreg and enhanced colitogenic Th17 responses in mice wi

167 ta, eliminated the suppressive activities of iTreg but not nTreg.

168 model of colitis to compare the capacity of iTreg and Th17 cells to develop in situ following the tr

169 cells (iTreg) with a significant decrease of iTreg in lymphoid organs.

170 define the role of IL-2 in the formation of iTreg precursors as well as their subsequent Foxp3 expre

171 s crucial for the generation and function of iTreg cells, but not natural regulatory T (nTreg) cells.

172 approach to boost the in vitro generation of iTreg and ex vivo Treg expansion, thus facilitating the

173 es, dramatically increased the generation of iTreg and Th17 cells.

174 and promoted the unidirectional induction of iTreg cells by repressing the TH2 developmental program.

175 small intestine and diminished induction of iTreg cells in response to model antigen.

176 pathway is responsible for the inhibition of iTreg differentiation of iTregs downstream of PKC-theta.

177 Injection of iTreg cells but not natural CD4(+)CD25(+) regulatory T c

178 eg cell expansion, associated with a lack of iTreg cell overrepresentation in the decidua.

179 te that PD-1H is required for maintenance of iTreg pool size by promoting its differentiation and pre

180 ness or IgE levels, whereas equal numbers of iTreg of identical TCR specificity reduced all airway re

181 re rejection, which suggests the presence of iTreg in the EMB of nonrejectors.

182 l mechanisms contribute to the regulation of iTreg differentiation, but the timing and respective req

183 erived CCL22 contributes to the retention of iTreg cells.

184 intragraft iTreg suggests a possible role of iTreg in the regulation of alloreactivity.

185 We investigated the role of iTreg-produced IL-10 and iTreg fate in a treatment model

186 We sought to explore the roles of iTreg cells on MC function and the established MC-driven

187 required for the formation and stability of iTreg cells.

188 lung allergic responses, as did transfer of iTreg cells.

189 These findings advance the understanding of iTreg differentiation and may facilitate the therapeutic

190 transferred into Rag1(-/-) mice, with 95% of iTregs converting into ex-Tregs in the cornea.

191 and Dlgh1 silencing decreases the ability of iTregs to suppress interferon-gamma production by CD4(+)

192 HDAC3 also regulated the development of iTregs, as HDAC3-deficient conventional T cells were not

193 aling that promotes efficient development of iTregs.

194 r the inhibition of iTreg differentiation of iTregs downstream of PKC-theta.

195 The inhibitory effects of iTregs are blocked by preventing direct cellular contact

196 demonstrate that Cbl-b regulates the fate of iTregs via controlling the threshold for T cell activati

197 2 (KLF2) is necessary for the generation of iTregs but not tTregs.

198 Moreover, in vivo generation of iTregs following OVA feeding was impaired in the absence

199 in facilitating the efficient generation of iTregs.

200 mTOR signaling is essential for induction of iTregs from naive CD4(+) T cells, and the mTORC2 compone

201 hese significantly enhanced the induction of iTregs in Dicer(-/-) CD4(+) T cells.

202 macological inhibition restored induction of iTregs.

203 two-step method generated a large number of iTregs with relatively stable expression of Foxp3, which

204 maintain the anti-inflammatory phenotype of iTregs by preventing the secretion of proinflammatory cy

205 This plasticity of iTregs could be prevented when they were generated in th

206 on and may facilitate the therapeutic use of iTregs in immune disorders.

207 es also reduced the generation of pathogenic iTreg cells that lost Foxp3 expression, suggesting that

208 ing them from Treg induced in the periphery (iTreg).

209 gical tolerance, contrasting, when possible, iTreg cells with nTreg cells.

210 eutralizing IL-6-specific antibody prevented iTreg cell reprogramming into TH17-like cells and protec

211 1 and Foxo3a was found to inhibit or promote iTreg differentiation in PKC-theta(-/-) T cells accordin

212 ak RALDH activity and were poor at promoting iTreg development.

213 Recovered iTreg cells from the lungs of CD8(-/-) recipients were c

214 in-9 signaling was further found to regulate iTreg cell induction by dominantly acting through the CN

215 derson et al. (2015) show that CD5 regulates iTreg cell induction by rendering emerging iTreg cells r

216 Therefore, we propose that SOCS2 regulates iTreg stability by downregulating IL-4 signaling.

217 (Th1, Th2, and Th17) and induced regulatory (iTreg) T cells requires lineage-specifying transcription

218 tiation and stimulated induced T regulatory (iTreg) cells.

219 r 1 (Th1), Th17, and inducible T regulatory (iTreg) cells.

220 over anti-inflammatory-induced T regulatory (iTreg) differentiation, the latter by promoting endocyti

221 lopment of Th17 versus induced T-regulatory (iTreg) cells.

222 ration, stabilizes Foxp3 expression, resists iTreg conversion to IFN-gamma/TNF-alpha-producing efffec

223 However, whether Ag-specific iTreg generation and function is limited to secondary ly

224 These data confirm that allergen-specific iTreg and nTreg have active roles in asthma tolerance an

225 depends on the function of local Ag-specific iTregs and that the retina is capable of local, "on-dema

226 the suppressive function of antigen-specific iTregs by controlling the expression of MARCH1 and CD83

227 to the target organ, while antigen-specific iTregs primarily prevent T-cell priming by acting on ant

228 ic depletion (i.p. DTx), of betagal-specific iTregs enhanced experimental autoimmune uveoretinitis in

229 produced similar numbers of betagal-specific iTregs in the retina whether the mouse was depleted of p

230 Frequencies of CMV-specific iTregs and CD8+ T cells (summated response) were signifi

231 CMV-specific iTregs recognized the same antigens as conventional CD4+

232 We generated HY-specific iTregs (HY-iTregs) from resting CD4 T cells derived from

233 ls and point to interventions that stabilize iTreg cells as potentially effective therapeutic strateg

234 antly, adoptive transfer of these stabilized iTregs to HSV-1-infected mice prevented the development

235 The niche supporting stable iTregs is limited and readily saturated, which promotes

236 ent Foxp3 expression, we designed a two-step iTreg differentiation model.

237 ction of IFN-gamma and IL-12, which suppress iTreg differentiation and maintenance.

238 lampsia, however, there is impaired systemic iTreg cell expansion, associated with a lack of iTreg ce

239 Induced regulatory T (iTreg) and Th17 cells promote mucosal homeostasis.

240 to induce autoantigen-specific regulatory T (iTreg) cell conversion.

241 orkhead box protein 3-positive regulatory T (iTreg) cells are a promising source for cell-based thera

242 While induced regulatory T (iTreg) cells are required for chronic colonization witho

243 Adaptive CD4(+)Foxp3(+) regulatory T (iTreg) cells develop outside the thymus under a variety

244 T (nTreg) cells and inducible regulatory T (iTreg) cells exhibiting suppressive activity.

245 7 (TH17) cells towards induced regulatory T (iTreg) cells, we show that increased transamination, mai

246 ent overlapped that of induced regulatory T (iTreg) cells.

247 Induced regulatory T (iTreg) lymphocytes show promise for application in the t

248 ve active roles in asthma tolerance and that iTreg are substantially more tolerogenic in this setting

249 Our data demonstrate that iTreg can be efficiently induced from memory CD4 cells,

250 Our study demonstrates that iTreg cells suppress MC function and attenuate establish

251 ded Teffs from the same donors indicate that iTreg are intermediate between expanded CD4(+)CD25(hi) t

252 This study demonstrates that iTregs specific for HY miHAgs are highly effective in co

253 The iTreg generated in the presence of DL1 featured higher l

254 The iTreg were differentiated from Th2 effector T cells by e

255 The iTreg-induced defect in DC function could be completely

256 on (ex-iTregs) but retained a portion of the iTreg transcriptome, which failed to limit their pathoge

257 a directionally concordant expansion of the iTreg-Th17 cell axis and can be exploited as a therapeut

258 ablish phenotypic dominance of Th17 over the iTreg pathway.

259 CD83 were mediated by IL-10 produced by the iTregs.

260 Importantly, these iTreg displayed a stable phenotype in long-term cultures

261 cytokine to induce Foxp3 expression in these iTreg precursors.

262 regarding the suppressive capacity of these iTregs in humans, especially those generated in vitro in

263 tional features of Th17 cells in relation to iTreg cells, Th1 cells, and Th22 cells, as a basis for u

264 In contrast, transferred iTreg cells were more numerous, retained FoxP3 expressio

265 cells, and in vivo conversion of transferred iTreg cells was dependent on recipient IL-6.

266 riably, approximately 85% of the transferred iTregs lost Foxp3 expression (ex-iTregs) but retained a

267 Regardless of the treatment, iTregs acquired suppressive function and FOXP3 expressio

268 Moreover, in vitro-inducible CD25(+) Treg (iTreg) cell development is inhibited in Il2rgamma(-/-)/c

269 to generate bona fide in vitro-induced Treg (iTreg) are critical.

270 (R576)) promotes conversion of induced Treg (iTreg) cells toward a T helper 17 (TH17) cell fate.

271 bly express Foxp3, adaptive or induced Treg (iTreg) generated from peripheral CD4 T cells are suscept

272 d the in vitro generation of inducible Treg (iTreg) cells from naive CD4(+) human T cells.

273 Although polarization of inducible Treg (iTreg) often occurs in an inflammatory environment, the

274 fic T cells into functional and stable Treg (iTreg) cells has proved challenging.

275 from non-Treg CD4(+) T cells (induced Treg [iTreg] cells) by TCR triggering, IL-2, and TGF-beta or r

276 factor beta (TGFbeta) ex vivo (induced Treg [iTreg] cells) to the effects of equivalent expanded thym

277 aches to generate Ag-specific induced Tregs (iTregs) and tested their efficacy and selectivity in the

278 a model in which Ag-specific, induced Tregs (iTregs) are cocultured with DCs in the absence of T effe

279 than that observed for CD4(+)-induced Tregs (iTregs) in nearly all tissue sites.

280 ed the production of in vitro-induced Tregs (iTregs) in overexpression and blocking experiments.

281 ng the generation of TGF-beta-induced Tregs (iTregs) is unknown.

282 easing evidence suggests that induced Tregs (iTregs) may be generated in the periphery from naive cel

283 at develop in the thymus, and induced Tregs (iTregs) that differentiate in peripheral tissues upon ex

284 Lastly, in vitro-generated induced Tregs (iTregs) were shown to be highly plastic and capable of i

285 tory T cells (nTregs), CD4(+) induced Tregs (iTregs), and CD8(+) iTregs, and was more potent than tem

286 group of regulatory T cells, induced Tregs (iTregs), effectively suppress the production of ILC2-dri

287 ets, thymus-derived Tregs and induced Tregs (iTregs).

288 vivo generated counterparts, induced Tregs (iTregs)] offer particular therapeutic potential because

289 ulatory T cells (Tregs) and inducible Tregs (iTregs); however, the role of SOCS2 in Foxp3(+) Treg fun

290 Altogether, these new findings uncover iTregs as potent regulators of ILC2 activation and impli

291 uced the frequency of FOXP3(+) T cells under iTreg-polarizing conditions.

292 3 and induced TH2 differentiation even under iTreg-cell-differentiation conditions.

293 h is essential for inhibitory function of VD-iTreg cells.

294 with Cbl-b deficiency, we show that in vivo iTreg development is also controlled by Cbl-b via tuning

295 mmunosuppressive effects were abrogated when iTreg cells were pretreated with TGF-beta1 small interfe

296 athway vary depending on the milieu in which iTreg differentiate.

297 feration, cytokine production) compared with iTreg(-) In contrast to CD83(low) IL-10DCs, CD83(high) I

298 antly induced and negatively correlated with iTreg frequencies and tumor weight.

299 y after immunization, mice were treated with iTreg or nTreg cells that were generated or expanded in

300 Galectin-9 expression within iTreg cells was driven by the transcription factor Smad3