ライフサイエンスコーパス: Treg cell

1 elopment and function of regulatory T cells (Treg cells).

2 (+)CD4(+)CD25(+) regulatory T cells (induced Treg cells).

3 ent but is not expressed on TGF-beta-induced Treg cells.

4 nd share features of visceral adipose tissue Treg cells.

5 n exposure altered the phenotype of expanded Treg cells.

6 ere identical, as was in vitro generation of Treg cells.

7 suppression by in vivo rapamycin-conditioned Treg cells.

8 ease in PD-1- and a decrease in PD-1+ memory Treg cells.

9 r lineage stability and effector function in Treg cells.

10 he mechanism of IL-21-mediated inhibition of Treg cells.

11 tein GPA33 is expressed on a subset of human Treg cells.

12 ion into follicular Treg and tissue-resident Treg cells.

13 4(+)Foxp3(+)RORgammat(+)IL-17A(+) cells from Treg cells.

14 t-resident and peripherally derived Foxp3(+) Treg cells.

15 diabetes showed decreased HPGD expression in Treg cells.

16 LV expression selective for CD4+CD25+FoxP3+ Treg cells.

17 errant properties of Tet2/3(fl/fl)Foxp3(Cre) Treg cells.

18 2 responses indirectly through inhibition of Treg cells.

19 to the BAFF-independent effect of B cells on Treg cells.

20 RC1 activation and functional programming of Treg cells.

21 helper T cells promotes asthma by inhibiting Treg cells.

22 n of T(H)2 cells and increased generation of Treg cells.

23 cells and decreased numbers of RORgammat(+) Treg cells.

24 the identity and effector differentiation of Treg cells.

25 suggesting that Helios also functions in non-Treg cells.

26 airing their capacity to generate functional Treg cells.

27 ne dysregulation and, in particular, loss of Treg cells.

28 ed basal Ca(2+) levels before the arrival of Treg cells.

29 ecies, which upregulated Tgfb1 expression in Treg cells.

30 o identify Foxp3 regulators in mouse primary Treg cells.

31 s of Th1 and Th17 profiles, while increasing Treg cells.

32 cular T helper (Tfh) cells, or regulatory T (Treg) cells.

33 es include dendritic cells and regulatory T (Treg) cells.

34 ne the role of TET proteins in regulatory T (Treg) cells.

35 6 also affects the function of regulatory T (Treg) cells.

36 d is thought to be produced by regulatory T (Treg) cells.

37 xpansion of T cells, including T regulatory (Treg) cells.

38 e the relationships among BAFF, B cells, and Treg cells, a panel of C57BL/6 (B6) congenic mice was te

39 Here, we demonstrate that Treg cell ablation is sufficient to trigger experimental

40 deletion of Stim1 and Stim2 genes in mature Treg cells abolishes Ca(2+) signaling and prevents their

41 Deletion of Myd88 or Rorc in Treg cells abrogated protection by bacteriotherapy.

42 The enhancing effect of 1,4-DPCA/hydrogel on Treg cell accumulation and bone regeneration was reverse

43 to investigate the role of BMP signaling in Treg-cell accumulation in psoriasis.

44 However, the factors mediating Treg-cell accumulation in psoriatic skin currently remai

45 the chromatin remodeling factor Brg1 impairs Treg cell activation and causes fatal autoimmunity in mi

46 ty of NK cells and T cells and downmodulated Treg cell activities.

47 In contrast, Treg cells adopt a confined, repetitive-scanning motilit

48 Skin-homing Treg cells also play a critical role in mitigating the r

49 ion promotes CXCR4-dependent accumulation of Treg cells and alveolar bone regeneration, suggesting a

50 We present evidence for a beneficial role of Treg cells and IL-35 in attenuating pain associated with

51 We demonstrate that spinal delivery of Treg cells and IL-35 reduces pain associated with EAE by

52 Alum impairs PM-induced functional FOXP3(+) Treg cells and promotes Th1/Th2/Th17 responses.

53 AE-induced female mice, adoptive transfer of Treg cells and spinal delivery of the Treg cell cytokine

54 elated disorders that exploits the defective Treg cells and the inflammatory environment pre-existing

55 IL-21 directly promotes apoptosis of Treg cells and therefore indirectly sustains generation

56 reduced, whereas the number of regulatory T (Treg) cells and immature B cells was increased, by IL-17

57 for the first time a role for regulatory T (Treg) cells and interleukin-35 (IL-35) in suppressing fa

58 35-55)-specific FoxP3(+) regulatory T cells (Treg cells) and type 1 regulatory T cells (Tr1 cells), c

59 eg (aTreg) cells at the expense of quiescent Treg cells, and also resulted in impaired Treg suppressi

60 a (PPARgamma)-induced HPGD expression in VAT Treg cells, and consequential Treg-cell-mediated generat

61 vored Th17 cell differentiation over that of Treg cells, and promoted a heightened pro-inflammatory g

62 d a large population of Foxp3+ T-regulatory (Treg) cells, and donor Foxp3+ Treg depletion, by diphthe

63 rsus canonical TGF-beta signaling in DCs and Treg cells; and modeling of psoriatic skin inflammation

64 e data support a model in which non-rhythmic Treg cells are driven to rhythmic activity by systemic s

65 igration to the mesenteric lymph node, where Treg cells are induced and oral tolerance is established

66 Bcl6-deficient Treg cells are more susceptible, and Blimp1-deficient Tr

67 s are more susceptible, and Blimp1-deficient Treg cells are resistant, to acquiring the ST2(+) Treg-c

68 Expanded GPA33(high) Treg cells are suppressive, unable to produce proinflamm

69 Foxp3(+) T-regulatory (Treg) cells are capable of suppressing immune responses.

70 Regulatory T (Treg) cells are critical for maintaining immune homeosta

71 Regulatory T (Treg) cells are critical mediators of immune tolerance w

72 Regulatory T (Treg) cells are crucial for immune homeostasis, but they

73 Foxp3(+) regulatory T (Treg) cells are essential for maintaining peripheral tol

74 Regulatory T cells (Treg cells) are important for preventing autoimmunity an

75 In contrast, Treg cells arrive after Th17 cells and persist during th

76 viding a physiological adaptation of colonic Treg cells as a function of the age of the cell or of th

77 nical trial with ex vivo expanded autologous Treg cells as an adoptive cellular therapy in renal tran

78 CD103(+) dendritic cells, and regulatory T (Treg) cells, as well as intestinal permeability, were ev

79 Disruption of Th17-Treg cell balance is implicated in a number of immune-me

80 ether Treg ligands can be used to manipulate Treg cell biology are unknown.

81 rectly inhibited expansion of differentiated Treg cells but was dispensable for T(H)1/T(H)17 effector

82 is important not only for the generation of Treg cells, but also for regulating their functional act

83 ns is required for the thymic development of Treg cells, but its function in mature Treg cells remain

84 Bcl6-deficient ST2(+) Treg cells, but not Bcl6-deficient ST2(+) conventional T

85 pic dermatitis had higher circulating memory Treg cells, but not higher IgE(+) B-cell numbers.

86 L-2 in mice abrogated all IL-2R signaling in Treg cells, but was well tolerated and only gradually im

87 on of forkhead box P3-positive regulatory T (Treg) cells, but the mechanism and functional relevance

88 expression profile of rapamycin-conditioned Treg cells by droplet-digital PCR.

89 whether proper function could be restored to Treg cells by ex vivo expansion in the presence of facto

90 how that TNFR2 maintains Foxp3 expression in Treg cells by restricting DNA methylation at the Foxp3 p

91 Genomic analysis of Treg cells by RNA-sequencing, Foxp3 chromatin immunoprec

92 maintaining tissue homeostasis, but whether Treg cells can adopt tissue- or immune-context-specific

93 Treg cells can be generated during thymic development (c

94 of peptides recognized by a bona fide murine Treg cell clone isolated from the visceral adipose tissu

95 link between a viral trigger and an impaired Treg cell compartment resulting in the initiation of imm

96 n impact on intestinal Th17 and RORgammat(+) Treg cell compartments emerges as a unifying feature of

97 Regulatory T (Treg) cells control self-tolerance, inflammatory respons

98 patterns in resting and activated subsets of Treg cells, conventional CD4 T cells, and cells expressi

99 Finally, IL-2/alphaIL-2 complex-expanded Treg cells could be recalled upon allergen challenge, wh

100 antigen-specific targeting of VAT-localized Treg cells could eventually be a strategy for improving

101 fer of Treg cells and spinal delivery of the Treg cell cytokine interleukin-35 (IL-35) significantly

102 Finally, Treg cell depletion increases APC numbers in the spinal

103 into lymphodepleted animals or regulatory T (Treg) cell depletion promoted GzmB expression by tumor-i

104 Treg cell-derived IL-10 is indispensable for the establi

105 These results identify a privileged role of Treg cell-derived TGF-beta1 in regulating allergy and au

106 Treg cells, twice as many ST2(+) (IL-33R(+)) Treg cells develop as are observed in wild-type mice.

107 /fl)Foxp3(Cre) mice lacking Tet2 and Tet3 in Treg cells develop inflammatory disease, and Treg cells

108 O-GlcNAc-deficient Treg cells develop normally but display modestly reduced

109 bearing RagA-RagB- or Rheb1-Rheb2-deficient Treg cells developed a fatal autoimmune disease and had

110 Mice with Foxp1-deficient Treg cells developed spontaneous inflammatory disease wi

111 ver, mice lacking PI3Kalpha and PI3Kdelta in Treg cells developed spontaneous peripheral nerve inflam

112 Treg cell development and function are dependent on the

113 DNA regions of CpG demethylation that govern Treg cell development and function.

114 hat PI3Kdelta is required to maintain normal Treg cell development and phenotype under homeostatic co

115 uction of short-chain fatty acids leading to Treg cell development, and merits study as a potential c

116 ent knowledge of the signals that coordinate Treg cell development, the antigen-presenting cell types

117 or l-arginine, on gut immunity by promoting Treg cell development.

118 adaptive immune responses and regulatory T (Treg)-cell development, while dysregulated MALT1 activit

119 The mechanisms by which regulatory T (Treg) cells differentially control allergic and autoimmu

120 Activated Treg cells differentiate into effector Treg subsets that

121 understanding of the mechanisms coordinating Treg cell differentiation is crucial for understanding n

122 ated orphan receptor gamma t (ROR-gammat)(+) Treg cell differentiation.

123 ected by its ability to induce regulatory T (Treg) cell differentiation and inhibit Th1 and Th2 respo

124 Treg cells do not seem to have intrinsic circadian oscil

125 nditions but that loss of PI3Kdelta alone in Treg cells does not lead to autoimmunity.

126 y active form of STAT5 partially ameliorates Treg cell dysfunction and systemic inflammation in O-Glc

127 Thereafter, the regulatory T (Treg) cells emerged and maintained a relatively high lev

128 y skin, a portion of inflammation-associated Treg cells exhibit constitutive-active BMP signaling.

129 The VAT-Treg cells expanded in vivo by one of the surrogate agon

130 B cells promoted BAFF-independent Treg cell expansion in vivo, as evidenced by the correla

131 inistration to DEREG donor mice whose Foxp3+ Treg cells expressed diphtheria toxin receptor, restored

132 to suppress peripheral T cells while sparing Treg cells expressing wild-type FOXP3, thereby proving b

133 se and for developing approaches to modulate Treg cells for clinical benefit.

134 lity of EVR to expand functionally competent Treg cells for their clinical use.

135 ower levels of the integrin alpha4beta7 than Treg cells from control patients.

136 ower levels of the integrin alpha4beta7 than Treg cells from control patients.

137 neous psoriatic lesions and show that unlike Treg cells from healthy skin, a portion of inflammation-

138 Treg cells from patients with CD express lower levels of

139 We found that Treg cells from patients with CD express lower levels of

140 Treg cells from patients with CD incubated with rapamyci

141 Phenotype and function of FOXP3-mutated Treg cells from rapamycin-treated patients with IPEX syn

142 Treg cells develop inflammatory disease, and Treg cells from these mice show altered expression of Tr

143 ed during treatment as compared with that of Treg cells from untreated healthy subjects.

144 s well tolerated and only gradually impacted Treg cell function and immune homeostasis.

145 Brd9 ablation compromised Treg cell function in inflammatory disease and tumor imm

146 3 that is required for the retention of full Treg cell function in the periphery.

147 led to reduced Foxp3 expression and reduced Treg cell function in vitro.

148 HD2 leads to impairment of immunosuppressive Treg cell function via a HIF2alpha-dependent mechanism,

149 as a target for therapeutic manipulation of Treg cell function.

150 g) cell identity is central to understanding Treg cell function.

151 Mutations disrupting regulatory T (Treg) cell function can cause IPEX and IPEX-related diso

152 I3Kdelta is a key regulator of regulatory T (Treg) cell function.

153 es; yet the degree of peptide specificity of Treg-cell function, and whether Treg ligands can be used

154 nity through both thymic clonal deletion and Treg cell generation.

155 ed for clonal deletion and for regulatory T (Treg) cell generation from endogenous tissue-restricted

156 mAb induced tolerance through regulatory T (Treg) cell generation.

157 ents and healthy controls; ex vivo models of Treg-cell generation in the presence or absence of Lange

158 Locally secreted BMP7 can directly promote Treg-cell generation through the BMP signaling cascade.

159 that harbors B cells, the effect of BAFF on Treg cells goes beyond its ability to expand the B cell

160 These Treg cells had increased suppressive activities in assay

161 ummary, we describe the relationship between Treg cell heterogeneity and recruitment to NLTs through

162 However, the molecular mechanisms underlying Treg cell homeostasis and suppressive function are still

163 controls effector CD4(+) cell responses and Treg cell homeostasis.

164 Thus, Foxp3 defines Treg cell identity in a largely indirect manner by fine-

165 the mechanisms that establish regulatory T (Treg) cell identity is central to understanding Treg cel

166 Regulatory T (Treg) cell identity is defined by the lineage-specifying

167 the function of thymus-derived regulatory T (Treg) cells (ie, FOXP3), resulting in impaired Treg func

168 Our findings underscore the role of Treg cells, IL-2, and Blimp-1 in controlling the differe

169 Depletion of Treg cells impaired skin-barrier regeneration and was as

170 rrelation between B cells and percentages of Treg cells in B6.Baff(-/-) mice and by the greater perce

171 (-/-) mice and by the greater percentages of Treg cells in B6.Bcl2(Tg) mice (which harbor B cells lar

172 notype, and suppressor function of long-term Treg cells in culture with EVR were similar to those wit

173 lated with decreased frequencies of CRTH2(+) Treg cells in EA patients.

174 We show that Treg cells in food allergy (FA) had decreased expression

175 GPA33 identifies Treg cells in human blood that lack the ability to produ

176 Wild-type Treg cells in mixed bone marrow chimeras and in Tet2/3(f

177 mechanisms of immunosuppression selective to Treg cells in patients with IPEX syndrome are unclear.

178 e of IL-2 in the maintenance and function of Treg cells in the adult peripheral immune system remains

179 RORgamma+ and Helios+ Treg cells in the colon are phenotypically and functiona

180 ST2(+) Treg cells in the context of allergic airway inflammatio

181 in motility characteristics between Th17 and Treg cells in the inflamed spinal cord and reveal three

182 d numbers of tolerogenic dendritic cells and Treg cells in the intestinal tract, and increased intest

183 Rather, the delayed replenishment of Treg cells in Vbeta5-deficient mice compromises suppress

184 Metabolic support for regulatory T (Treg) cells in noninflamed tumors is not well understood

185 ncreased abundance of FOXP3(+) T regulatory (Treg) cells in the periodontal tissue.

186 frequency and total numbers of regulatory T (Treg) cells in vivo.

187 study was to define the functions of Bcl6 in Treg cells, including Tfr cells, in the context of aller

188 e development and functions of regulatory T (Treg) cells, including those producing IL-10.

189 uced-3 (EBI3, an IL-35 subunit) in patients' Treg cells increased during treatment as compared with t

190 me analysis revealed increased expression of Treg-cell-inducing genes in the intestine after PA intak

191 Thus, Treg cell induction by oral anti-CD3 is a consequence of

192 inflammatory phenotype, and impairs FOXP3(+)/Treg cell infiltration in the spinal cord of hSOD1(G93A)

193 doptive transfer of naive CD4(+) T cells and Treg cells into lymphopenic mice to assess the cell-intr

194 lammatory environment, can convert defective Treg cells into powerful, super-activated Treg cells (Su

195 uncover the importance of T regulatory (Treg) cell-intrinsic Tgfb1 gene dose in the prevention o

196 n of bone marrow-infiltrating ICOShigh/PD-1- Treg cells is a highly significant independent predictor

197 e, the equilibrium between effector Th17 and Treg cells is crucial for balancing intestinal homeostas

198 while the development of Th2, Th17, Tfh, and Treg cells is dependent on transcription factors GATA3,

199 Tr1 cells, but not FOXP3-positive Treg cells, isolated from healthy individuals and patien

200 orkhead box (Foxp) subfamily member Foxp1 in Treg cells led to increased numbers of activated Treg (a

201 cell selection, and the nature of endogenous Treg cell ligands, focusing on evidence from studies in

202 y, but how interstitial motility patterns of Treg cells limit neuroinflammation is not well understoo

203 These locally confined but highly motile Treg cells limit Th17 cells from accessing APCs and supp

204 on with LCMV results in type I IFN-dependent Treg cell loss that is rapidly compensated by the conver

205 pite substantially reduced IL-2 sensitivity, Treg cells maintained selective IL-2 signaling and preve

206 ance of T helper 17 (Th17) and regulatory T (Treg) cells maintains immune tolerance and host defense.

207 on in preventing AD, by increased Gli-driven Treg cell-mediated immune suppression, paving the way fo

208 esults show a key role for PI3K signaling in Treg cell-mediated protection against CNS inflammation.

209 ression in VAT Treg cells, and consequential Treg-cell-mediated generation of 15-keto PGE(2) suppress

210 In the absence of STIM1/STIM2 in Treg cells, mice develop a broad spectrum of autoantibod

211 Furthermore, PA normalized Treg cell mitochondrial function and morphology in MS.

212 ood-allergic sensitization had higher memory Treg cell numbers 12.3% (95% CI 4.2; 21.0), (11.1% (95%

213 Regulatory T (Treg)-cell numbers strongly increase during psoriatic sk

214 demonstrated a positive correlation between Treg-cell numbers and epidermal BMP7 expression in cutan

215 otherapy induced expression by regulatory T (Treg) cells of the transcription factor ROR-gammat in a

216 Furthermore, the anti-inflammatory action of Treg cells on innate immune cells contributes to the nig

217 em to interrogate the impact of intratumoral Treg cells on the TME.

218 eckpoint blockade, suggesting that targeting Treg cells or their modulation of lipid metabolism in M2

219 oncogene-driven fatty-acid synthesis favors Treg cells over effector T cells and how this imbalance

220 lite 15-keto PGE(2), was highly expressed in Treg cells, particularly those in visceral adipose tissu

221 cells are resistant, to acquiring the ST2(+) Treg-cell phenotype in vitro and in vivo in response to

222 of T cell-driven CNS inflammation, in which Treg cells play a key protective role.

223 Regulatory T (Treg) cells play a pivotal role in suppressing auto-reac

224 Regulatory T (Treg) cells play central roles in maintaining immune hom

225 Foxp3-expressing CD4(+) regulatory T (Treg) cells play key roles in the prevention of autoimmu

226 T regulatory (Treg) cells play vital roles in modulating immunity and

227 e defect in the suppressor function of their Treg cell population, suggesting that Helios also functi

228 aled sharing of TCR clonotypes between these Treg cell populations, potentially denoting a common pro

229 normalities in naive Th, naive regulatory T (Treg) cell populations, and cytokines, and active cGVHD

230 Regulatory T (Treg) cells prevent autoimmune disorders by suppressing

231 Adoptively transferred Treg cells prevented spontaneous production of PF4/hepar

232 nd IFN-gamma, upregulated IL-10, and induced Treg cell production.

233 MARCO(+) macrophages enhanced regulatory T (Treg) cell proliferation and IL10 production and diminis

234 h PM plus alum inhibits in vivo induction of Treg cells promoted by PM without altering the capacity

235 t population of Foxp3(+)CD4(+) regulatory T (Treg) cells promotes repair of acutely or chronically in

236 ules, such as CEBPA and B2M in regulatory T (Treg) cells, providing a better understanding of the gen

237 ematopoietic cells had a high conventional T/Treg cell ratio and were protected from melanoma challen

238 f the chemokine receptor CXCR4 that mediates Treg cell recruitment.

239 three potential cellular mechanisms by which Treg cells regulate Th17 cell effector functions: reduct

240 Thus, Treg-cell regulation of localized inflammation enables H

241 nt of Treg cells, but its function in mature Treg cells remains unclear.

242 upon T cell activation, its function in non-Treg cells remains unknown.

243 In a polyclonal Treg cell replacement system, naive conventional CD4+ (T

244 Mice with Treg cell-restricted Neuropilin-1 deficiency show tumor

245 sentation, negative selection, and increased Treg cells, resulting in a diminished antitumor response

246 blockade of TNFalpha signaling, expanded VAT-Treg cells, resulting in protection from inflammation an

247 ith the efficient induction of regulatory T (Treg) cells, resulting in impaired Treg stability in mou

248 rely curtailed CD25 expression and function, Treg cells retain selective access to IL-2 that supports

249 riptional profiling of STIM1/STIM2-deficient Treg cells reveals that Ca(2+) signaling regulates trans

250 FOXP3-expressing regulatory T (Treg) cells safeguard immunological tolerance.

251 he antigen-presenting cell types that direct Treg cell selection, and the nature of endogenous Treg c

252 hat, among effector T cell subsets, Th17 and Treg cells selectively expressed multiple components of

253 his and other genetic models, we showed that Treg cells shaped the transcriptional landscape across m

254 pressing ILC2, CD4(+) and CD8(+) T cells and Treg cells showed attenuated responses to exogenous PGD2

255 Th2-like Treg cells showed increased intra-chromosomal interactio

256 ges may disrupt the generation of donor-type Treg cells so that the immunomodulatory effect of the TM

257 These changes were modeled by Treg cell-specific Tgfb1 monoallelic inactivation, which

258 ining transcription factor Foxp3 establishes Treg-cell-specific chromatin architecture indirectly, mo

259 that Foxp3-deficient mice lacking functional Treg cells spontaneously produced PF4/heparin-specific A

260 indicate that Tet2 and Tet3 are guardians of Treg cell stability and immune homeostasis.

261 instructs inflammatory DCs to gain enhanced Treg-cell-stimulatory activity.

262 n the tolerogenic RORgammat(+) regulatory T (Treg) cell subset, and susceptibility to disease in coli

263 th Brg1 re-expression in a minor fraction of Treg cells sufficient for the resolution in some cases.

264 ve Treg cells into powerful, super-activated Treg cells (SuperTreg cells) that can resolve advanced a

265 ls repress the production of IgE and Bcl6(+) Treg cells suppress the generation of type 2 cytokine-pr

266 T-regulatory (Treg) cells suppress the immune response to maintain hom

267 inal center and in the development of ST2(+) Treg cells that promote type 2 cytokine responses.

268 Cs restores development of functional FoxP3+ Treg cells that suppress T cell proliferation in vitro a

269 d differentiated into Ag-specific peripheral Treg cells that suppressed the recall response in an Ag-

270 rogram leading to the generation of Th2-like Treg cells that were unable to suppress extrinsic Th2 ce

271 e adjunctive strategy for patients receiving Treg cell therapeutics.

272 nflammatory conditions, loss of TNFR2 causes Treg cells to adopt a proinflammatory Th17-like phenotyp

273 We show that IL-21 sensitizes Treg cells to apoptosis by interfering with the expressi

274 d that TNFR2 signaling is required to enable Treg cells to promote resolution of inflammation and pre

275 tivate a MyD88/ROR-gammat pathway in nascent Treg cells to protect against FA, while dysbiosis impair

276 icantly limits the ability of ICOS-deficient Treg cells to reverse ongoing inflammation.

277 In mice with Bcl6-deficient Treg cells, twice as many ST2(+) (IL-33R(+)) Treg cells

278 GPA33(high) Treg cells universally express the transcription factor

279 l/DC to gain an enhanced capacity to promote Treg cells via BMPR-mediated CD25 induction and that thi

280 In vivo proliferation of Treg cells was greatest in B6.BTg mice, whereas in vivo

281 in B6.BTg mice, whereas in vivo survival of Treg cells was lowest in B6.Baff(-/-) mice.

282 sed frequency of TRP1-specific regulatory T (Treg) cells was present in chimeras with increased delet

283 dly increased and elevated levels of Foxp3 + Treg cells were detected in close proximity to lung meta

284 Treg cells were disproportionately expanded in mice expr

285 Tr1 and FOXP3-positive Treg cells were expanded, and phenotypes and gene expres

286 es of B6 wild-type, B6.BTg, and B6.Baff(-/-) Treg cells were identical, as was in vitro generation of

287 pressive abilities of Tr1 and FOXP3-positive Treg cells were measured.

288 among splenocytes of infected mice in which Treg cells were not depleted.

289 CD25 Treg cells were selected from leukapheresis product with

290 FOXP3-positive Treg cells were sorted as CD4(+)CD25(high)CD127(low) cel

291 nic forkhead box P3 (FOXP3)(+) regulatory T (Treg) cells were quantified.

292 CD39 is expressed by regulatory T (Treg)-cells, where it mediates immunosuppression, and by

293 ease of functionally competent regulatory T (Treg) cells, whereas Th1 and Th17 cells decreased signif

294 microbiotas led to induction of RORgammat(+) Treg cells, which was associated with an increase in the

295 lexes highly efficiently expanded peripheral Treg cells, while concomitant allergen exposure altered

296 Reduction of Treg cells with a depleting version of the same CD25 Ab

297 e been reported as a novel subset of induced Treg cells with modulatory characteristics.

298 Incubation of patients' ex vivo expanded Treg cells with rapamycin and an RARA agonist induced ex

299 dine promotes homeostatic differentiation of Treg cells within the gut and reduces pathology in a mod

300 Anti-inflammatory regulatory T (Treg) cells within the joints show diurnal variation, wi