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 hat iTregs induced in the presence of 3C (3C-iTregs) are stable, even after exposure to inflammatory

13 on, adoptive transfer of antigen-specific 3C-iTregs prevented the induction of experimental autoimmun

14 In the presence of IL-6, iTreg cells converted to T(H)17 cells, mediating a neutr

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

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

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

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

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

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

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

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

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

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

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

26 g on induction and stability of alloreactive iTreg.

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

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

29 25 in shifting the immune response toward an iTreg(-) controlled tolerance reaction.

30 fications of Rorgammat; Foxp3 expression and iTreg cell-mediated suppression remained intact.

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

32 allergic responses by transferred nTreg and iTreg cells differed.

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

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

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

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

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

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

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

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

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

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

43 lity to differentiate tTregs from pTregs and iTregs.

44 17 cells undergo phenotype switch and become iTreg cells.

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

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

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

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

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

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

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

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

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

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

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

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

57 lls also promoted induced regulatory T cell (iTreg) differentiation and inhibited interferon-gamma pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 is lesions more effectively than did control iTregs.

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

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

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

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

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

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

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

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

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

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

94 proteolysis during T-cell activation enhance iTreg development.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 feres with differentiation of human FOXP3(+) iTregs and to disclose some of the molecular pathways in

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

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

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

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

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

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

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

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

120 3aR/C5aR signaling augments murine and human iTreg generation, stabilizes Foxp3 expression, resists i

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

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

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

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

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

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

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

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

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

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

131 ylglycine (DMOG) also significantly impaired iTreg differentiation.

132 h to cultures of naive human CD4+ T cells in iTreg culture conditions increased FOXP3 expression.

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

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

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

136 Sirt-1 deletion in iTregs increased Foxp3 stability and restrained iTreg co

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

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

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

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

141 ously activated DCs still leads to increased iTreg induction.

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

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

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

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

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

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

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

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

150 nsion of Vbeta5(+) conventional T cells into iTreg cells.

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

152 tor RORgammat and promoted polarization into iTreg cells.

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

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

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

156 In wild-type mice, iTreg cells suppressed lung allergic responses linked to

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

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

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

160 ne the suppressor or enhancing activities of iTreg cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 erived CCL22 contributes to the retention of iTreg cells.

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

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

178 required for the formation and stability of iTreg cells.

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

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

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

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

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

184 aling that promotes efficient development of iTregs.

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

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

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

188 2 (KLF2) is necessary for the generation of iTregs but not tTregs.

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

190 in facilitating the efficient generation of iTregs.

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

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

193 macological inhibition restored induction of iTregs.

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

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

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

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

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

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

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

201 1 and Foxo3a was found to inhibit or promote iTreg differentiation in PKC-theta(-/-) T cells accordin

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

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

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

205 TGF-beta regulates iTreg cell outcomes through 2 distinct signal transducti

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

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

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

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

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

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

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

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

214 egs increased Foxp3 stability and restrained iTreg conversion into pathogenic T cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 To generate suppressor iTreg cells, cells were then differentiated in the prese

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

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

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

234 Inducible CD4(+)CD25(+) regulatory T (iTreg) cells can become pathogenic effector cells, enhan

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

236 7 (TH17) cells towards induced regulatory T (iTreg) cells, we show that increased transamination, mai

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

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

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

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

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

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

243 We found that iTregs induced in the presence of 3C (3C-iTregs) are sta

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

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

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

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

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

249 ablish phenotypic dominance of Th17 over the iTreg pathway.

250 1 and inhibiting MAPK pathways, shifting the iTreg polarization in favor of Th1 and Th17 subsets.

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

252 dited ex vivo to generate stable therapeutic iTregs.

253 edited ex vivo to produce stable therapeutic iTregs.

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

255 cytokine to induce Foxp3 expression in these iTreg precursors.

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

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

258 acquire a Th17-like phenotype in response to iTreg polarization.

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

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

261 analysis revealed that pembrolizumab-treated iTregs showed upregulation of genes promoting DNA repair

262 However, pembrolizumab-treated iTregs were relatively less suppressive in higher Treg r

263 at both nontreated and pembrolizumab-treated iTregs were suppressive.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 of pembrolizumab on in vitro-induced Tregs (iTregs).

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

285 Here we focused on the inducible Tregs (iTregs) and studied whether the Foxp3 locus can be epige

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

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

288 Under iTreg-inducing condition where activated CD4(+) T effect

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

290 3 and induced TH2 differentiation even under iTreg-cell-differentiation conditions.

291 deficient mice, we show that these Vbeta5(+) iTreg cells are dispensable for limiting anti-viral immu

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

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

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

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

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

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

298 rk showed that PD-1 blockade interferes with iTreg differentiation and has no potential effect on the

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