ライフサイエンスコーパス: Treg cell

1 and functional facets of regulatory T cells (Treg cells).

2 nction to porcine-NICC xenografts that naive Treg cell.

3 l of memory CD4(+)CD25(+)CD127(low)CD45RO(+) Treg cells.

4 evated mTORC1 signalling in Ndfip1-deficient Treg cells.

5 Treg cells were found to be CD45RA(+) naive Treg cells.

6 PDAC especially combined with high levels of Treg cells.

7 c-Rel was decreased in A20-deficient thymic Treg cells.

8 on of gastrointestinal-homing LAP(+)Foxp3(-) Treg cells.

9 ted to the FOXP3 promoter and its targets in Treg cells.

10 CCR8 ligands, CCL1 is unique in potentiating Treg cells.

11 in the peripheral lymphoid tissues, induced Treg cells.

12 n of strongly suppressive forkhead box P3(+) Treg cells.

13 activity-had reduced numbers of circulating Treg cells.

14 uppressive function compared with polyclonal Treg cells.

15 atory cytokine TGF-beta and Foxp3-expressing Treg cells.

16 tors required for PGRN induction of IL-10 in Treg cells.

17 eventing pathological secretion of IL-4 from Treg cells.

18 of functional CD8(+)CD28(-)CD127(lo)CD39(+) Treg cells.

19 eptors and inducing mouse and human Foxp3(+) Treg cells.

20 otent regulatory function in vivo than naive Treg cells.

21 that beta-cells are prone to attract CCR2(+) Treg cells.

22 tiation and the inducible differentiation of Treg cells.

23 epended on forkhead-box-protein-P3(foxp3)(+) Treg cells.

24 cells and asthma pathogenesis by activating Treg cells.

25 n-specific forkhead box protein 3 (FOXP3)(+) Treg cells.

26 lls, as well as similarity of Th2 cells with Treg cells.

27 tion of host immunosuppressive regulatory T (Treg) cells.

28 the differentiation of Foxp3(+) regulatory (Treg) cells.

29 d IL-35-producing regulatory B (Breg) and T (Treg) cells.

30 stimulation of Th1, Th17, and T regulatory (Treg) cells.

31 cells undergo apoptosis, and such apoptotic Treg cells abolish spontaneous and PD-L1-blockade-mediat

32 Depletion of Treg cells abolished these effects of SEA and IL-13 expr

33 Cancer-FOXP3 was positively correlated with Treg cells accumulation in tumor tissues derived from PD

34 ral Treg cells in check, A20 thus integrates Treg cell activity and increased effector T cell surviva

35 signaling as an upstream factor controlling Treg cell activity in specific tissue environments.

36 th early failure of chimerism, regardless of Treg cell administration.

37 ne tolerance by an increase in regulatory T (Treg) cells after extracorporeal photopheresis (ECP) is

38 in Th17-like effector phenotype in Foxp3(+) Treg cells and a decrease in granzyme B expression after

39 ighly proliferative and metabolically active Treg cells and by preventing pathological secretion of I

40 therapeutically amenable functional role for Treg cells and CTLA-4 in limiting antimalarial immunity.

41 integrin LFA-1-mediated interactions between Treg cells and dendritic cells.

42 mbers p65 and c-Rel in developing and mature Treg cells and found they have unique but partially redu

43 IL-33 dysregulated lung Treg cells and impaired immunologic tolerance to inhaled

44 expressed on IFN-g-producing T cells, FoxP3+ Treg cells and innate immune cells (macrophages and dend

45 ered metabolic signature of Ndfip1-deficient Treg cells and metabolic profiling reveals elevated glyc

46 y that underlies IL-10 production by PGRN in Treg cells and present new insights into the mechanisms

47 of PTEN is highly expressed in normal human Treg cells and provides complementary phosphatase activi

48 tatistically significant association between Treg cells and skin or steroid response, whereas a large

49 for TAZ in regulating the differentiation of Treg cells and TH17 cells.

50 invariant natural killer T and regulatory T (Treg) cells and altered composition of gammadelta T-cell

51 mes responses characterized by regulatory T (Treg) cells and immunosuppression.

52 Foxp3(+) regulatory T (Treg) cells and induction of anergy, an acquired state o

53 f immune cell types, including regulatory T (Treg) cells and the emerging type 2 innate lymphoid cell

54 is expressed at high levels on regulatory T (Treg) cells and was initially proposed as a target for c

55 CD4 T cells, including T regulatory cells (Treg cells) and effector T helper cells (Th cells), and

56 mised the development of regulatory T cells (Treg cells) and resulted in a substantial decrease in mo

57 ges of immunosuppressive regulatory T cells (Treg cells) and the inflammatory TH17 subset of helper T

58 rom spleens of treated BALB/c mice (tolerant Treg cell), and splenocytes were cotransferred into isle

59 conditional deletion of HDAC11 within Foxp3+ Treg cells, and their use, along with small molecule HDA

60 ssed in both effector (Teff) and regulatory (Treg) cells, and mice with T cell-specific deletion of B

61 roliferation and activation of regulatory T (Treg) cells, and resulted in chronic arthritis with exce

62 D3(+)CD4(+) Th cells, FOXP3(+) T regulatory (Treg) cells, and T regulatory type 1 (Tr1) cells are ess

63 a generalizable strategy for identifying the Treg cell antigens relevant to human autoimmunity.

64 Ndfip1-deficient Treg cells are highly proliferative and are more likely

65 Our study demonstrates that Treg cells are important for B-cell differentiation from

66 However, whether TGF-beta and Treg cells are part of the same regulatory module, or ex

67 Regulatory T (Treg) cells are well known to modulate inflammatory resp

68 Current interest in Foxp3+ T-regulatory (Treg) cells as therapeutic targets in transplantation is

69 study identifies CCR8(+) regulatory T cells (Treg cells) as drivers of immunosuppression.

70 CD4(+) CD25(+) FOXP3(+) regulatory T cells (Treg cells) as well as CD25(+) CD4(+) T cells expressing

71 Whether expression of these factors in Treg cells-as in effector T cells-is indicative of heter

72 -feeding mechanism by which CCL1 produced by Treg cells at an autoimmune site up-regulates the expres

73 CD4+ or Treg cells at baseline to 12 months post-ECP were compar

74 hway as a metabolic checkpoint that controls Treg cell behavior and affects the efficacy of therapeut

75 pact of long term fingolimod use on Th17 and Treg cell biology and general health in MS patients.

76 udy the impact of S1P1 signaling on Th17 and Treg cell biology, we specifically deleted S1P1 in Th17

77 days without immunosuppression, whereas non-Treg cell BMT recipients rejected delayed donor kidneys

78 In contrast, 2 of 5 recipients of Treg cell BMT that were evaluable displayed chimerism in

79 function or elimination of T-bet-expressing Treg cells-but not of T-bet expression in Treg cells-res

80 osuppressive microenvironment via recruiting Treg cells by directly trans-activating CCL5.

81 radical resection to detect cancer-FOXP3 and Treg cells by immunohistochemistry and evaluated clinica

82 he activation and expansion of regulatory T (Treg) cells by multiple mechanisms via antigen-presentin

83 , CRIg stabilized the expression of Foxp3 in Treg cells, by enhancing their responsiveness to interle

84 Treg cells can control physiological IL-7 production tha

85 suggest that peripheral expansion of induced Treg cells can serve as a promising therapeutic target a

86 Compared to CCR6(-) naive or memory Treg cells, CCR6(+) Treg cells exhibit stronger suppress

87 Absolute counts and % of CD4+ T cells and Treg cells (CD4 + CD25 + FOXP3 + CD127dim/-) were evalua

88 We found that two recurrent Treg cell clones, one prevalent in prostate tumors and t

89 4, a receptor for lysophosphatidylserine, on Treg cells, collectively supporting the accumulation and

90 cyte population toward greater regulatory T (Treg) cell commitment, resulting in a more tolerogenic T

91 ge cells, we show that thymic and peripheral Treg cell compartments are quantitatively enlarged becau

92 FOXP3(+)CD39(+) Treg cells comprised a major proportion of all circulati

93 HLA-DR1-induced Treg cells confer resistance to disease in HLA-DR15/DR1

94 Tumour-associated Th17-to-Treg cell conversion identified here provides insights f

95 Treg cells currently used in clinical trials are either

96 re genes, causing severe autoimmunity due to Treg cell deficiency.

97 ngeneic mice but not in immunocompromised or Treg cell-depleted mice.

98 Mice were also subject to transient Treg cell depletion before sensitization with OVA plus S

99 Ib at the tumor site prevented intra-tumoral Treg cell depletion, which may underlie the lack of anti

100 Most Foxp3(+) regulatory T (Treg) cells develop in the thymus as a functionally matu

101 e non-redundant, critical roles in promoting Treg cell development and function.

102 ndant key regulator of BIC/miR-155-dependent Treg cell development and homeostasis.

103 In addition, TAZ attenuated Treg cell development by decreasing acetylation of the T

104 scription factors is critically required for Treg cell development, partly via initiating Foxp3 expre

105 hose stimulation is closely linked to thymic Treg cell development.

106 While metabolic reprogramming during Treg cell differentiation has been extensively studied,

107 In vitro, D-mannose stimulated Treg cell differentiation in human and mouse cells by pr

108 resent study, we outline the role of Dll4 in Treg cell differentiation, stability, and function in RS

109 munosuppressive state to cancer by promoting Treg cell differentiation, thus offering a potential the

110 cy in TAZ or overexpression of TEAD1 induced Treg cell differentiation, whereas expression of a trans

111 the T cell enhancer landscape and affecting Treg cell differentiation.

112 ription factors RORgammat and Foxp3 promoted Treg cell differentiation.

113 naive CD4(+) T cells are potentiated in Th17/Treg cell differentiation.

114 Despite evidence of increased Treg cell division, Foxp3 expression was not stably main

115 ver, once the immune response resolved, some Treg cells downregulated CD25, upregulated Bcl-6 and dif

116 paired suppressive function, indicating that Treg cell dysfunction might be a key contributor to dise

117 A20-deficient Treg cells efficiently suppressed effector T cell-mediat

118 Regulatory T (Treg) cells establish tolerance, prevent inflammation at

119 l blood Treg cells express CCR6, and CCR6(+) Treg cells exhibit an activated effector/memory phenotyp

120 A20-deficient thymic Treg cells exhibit reduced dependence on IL-2 but unchan

121 CCR6(-) naive or memory Treg cells, CCR6(+) Treg cells exhibit stronger suppressive activity and dis

122 pansion, the gluten-specific FOXP3(+)CD39(+) Treg cells exhibited significantly reduced suppressive f

123 Here we show that Treg cells expand in both humans and mice in blood-stage

124 , most ( approximately 60%) peripheral blood Treg cells express CCR6, and CCR6(+) Treg cells exhibit

125 Paradoxically, some activated Treg cells express the aforementioned effector CD4 T cel

126 SEA-activated Treg cells expressed IL-4, upregulated CD69, and downreg

127 Regulatory T (Treg) cells expressing the transcription factor Foxp3 ar

128 Regulatory T (Treg) cells expressing the transcription factor FOXP3 pl

129 ominantly CD4(+)Foxp3(+) regulatory T cells (Treg cells) expressing tolerogenic cytokines.

130 enerated mice that lack EZH2 specifically in Treg cells (EZH2(Delta/Delta)FOXP3(+)).

131 Strategies to improve and tailor Treg cells for cell therapy to induce transplantation to

132 rkhead box P3 (FOXP3)(+)CD4(+) regulatory T (Treg) cells form a part of these responses, their influe

133 ides the first estimation of FOXP3(+)CD39(+) Treg cell frequency within circulating gluten-specific C

134 Detailed analyses of Treg cells from Foxp3(Cre)xT-bet(fl/fl) mice revealed un

135 uppressive function in peripheral polyclonal Treg cells from patients with celiac disease, after a sh

136 cancer-FOXP3 and promoted the recruitment of Treg cells from peripheral blood to the tumor site in vi

137 ated pathways that modulate context-specific Treg cell function and stability.

138 Inhibiting Treg cell function in tumors is an attractive strategy t

139 Mechanistically, Treg cells function in a critical temporal window to imp

140 immunosuppressive function and indicate that Treg cell functional heterogeneity is a critical feature

141 (TGF-beta) signals in safe-guarding specific Treg cell functions.

142 CD4CD127CD25CD45RA Treg cells had a stable TSDR demethylated FOXP3 phenotyp

143 MMD patients which were enriched with FrIII Treg cells had deficient suppressive functions (P = 0.00

144 These tolerant Treg cells had the capacity to transfer dominant toleran

145 These results suggest that T-bet(+) Treg cells have an essential immunosuppressive function

146 Regulatory T cells (Treg cells) have a pivotal role in the establishment and

147 al roles of canonical NF-kappaB in Tconv and Treg cells highlight the functional plasticity of the NF

148 ummarize recent advances in knowledge of how Treg cells home to lymphoid and peripheral tissues, and

149 ntrols tTreg cell development and peripheral Treg cell homeostasis through the regulation of BIC/micr

150 known how S1P1 signaling regulates Th17 and Treg cell homeostasis.

151 Thus, unlike its effects on conventional Treg cells, IL-2 inhibits TFR cell responses.

152 oreover, sepsis-surviving patients have more Treg cells, IL-33 and IL-10 in their peripheral blood.

153 tract is deficient in de novo generation of Treg cells in allergic mice.

154 insights for targeting the dynamism of Th17-Treg cells in cancer immunotherapy.

155 summary, our data indicate a new subtype of Treg cells in cGN.

156 Holding thymic production of natural Treg cells in check, A20 thus integrates Treg cell activ

157 undance of CD62L(hi)CD44(lo)Foxp3(+) central Treg cells in draining lymph nodes.

158 is largely restricted to tumor-infiltrating Treg cells in mice and humans.

159 , we demonstrate the pivotal role of CCR8(+) Treg cells in restraining immunity and highlight the pot

160 ell, Ali et al. (2017) reveal a function for Treg cells in stem cell maintenance by showing that skin

161 Furthermore, we found that the increase in Treg cells in T cell-specific A20-deficient mice was alr

162 -type Treg cells outcompeted T-bet-deficient Treg cells in terms of population expansion and expressi

163 e frequency of CD8(+)CD28(-)CD127(lo)CD39(+) Treg cells in the circulation of HIV-infected patients.

164 supporting the accumulation and retention of Treg cells in the colon and control of colitogenic respo

165 rams the metabolic and functional fitness of Treg cells in the control of immune tolerance and homeos

166 CD4(+)Foxp3(+) Treg cells in the lungs expressed the IL-33 receptor ST2

167 nti-CD25 antibodies were observed to deplete Treg cells in the periphery, upregulation of the inhibit

168 to numerical and functional deficiencies of Treg cells in the periphery.

169 sms facilitates the functional activation of Treg cells in the prevention of diverse types of inflamm

170 estigated the metabolic demands of migrating Treg cells in vitro and in vivo.

171 spensable for the differentiation of induced Treg cells in vitro and Treg cell mitochondrial fitness.

172 ell characterized, the role of regulatory T (Treg) cells in the loss of tolerance to gluten remains p

173 es played by IL-33 in altering regulatory T (Treg) cells in the lungs and in affecting previously est

174 production of Foxp3-expressing regulatory T (Treg) cells in the thymus.

175 induce either Th17 or RORg(+) T-regulatory (Treg) cells in vivo.

176 e proportion of Foxp3(+) regulatory T cells (Treg cells) in mice.

177 to effective depletion of tumor-infiltrating Treg cells, increased effector to Treg cell ratios, and

178 SEA-activated Treg cells induced IL-13 but suppressed IFN-gamma expres

179 eviously, we demonstrated that regulatory T (Treg) cells induced by the cytokine activin-A suppress T

180 Through the use of regulatory T cells (Treg cells) induced by transforming growth factor-beta (

181 sociated transcription factor T-bet in mouse Treg cells, induced at steady state and following infect

182 s that control the PI3K pathway, we assessed Treg cell induction in vitro, mitochondrial depolarizati

183 Antigen-specific regulatory T (Treg)-cell induction was assessed by flow cytometry usin

184 ility complex mismatched BMT with or without Treg cell infusion.

185 t study, for the first time, we evaluate how Treg cells interact with pulmonary ILC2s and control the

186 other approaches, here we show that Foxp3(+) Treg cell-intrinsic expression of Blimp1 is required to

187 Apoptosis in Treg cells is attributed to their weak NRF2-associated a

188 Cellular therapy with CD4FOXP3 T regulatory (Treg) cells is a promising strategy to induce tolerance

189 roRNA expression profile was investigated in Treg cells isolated from peripheral blood (PB) and from

190 Elevated miR-125a-5p was detected in Treg cells isolated from PLN but not from PB of donors w

191 Moreover, CCR6(+) Treg cells isolated from tumor-infiltrating lymphocytes

192 eing critical for the development of induced Treg cells (iTreg cells) by repression of the T helper t

193 ation of naive T cells to Foxp3(+) inducible Treg cells (iTreg) with a significant decrease of iTreg

194 and Il17, whereas reduced expression of the Treg cell key transcription factor forkhead box p3 (Foxp

195 Additionally, T-bet-deficient Treg cells lacked expression of the Th1-characteristic t

196 mphocyte subsets, forkhead box P3 (FOXP3)(+) Treg cell levels, and phenotype.

197 Here, we have identified natural Treg cell ligands in mice.

198 lection of self-reactive thymocytes into the Treg cell lineage.

199 e after expansion whereas CD4CD127CD25CD45RA Treg cell lost the TSDR demethylated phenotype.

200 Treg cells lost their ability to suppress effector T cel

201 y effector molecules while a shift to Th1 or Treg cells mainly contributes to the efficacy of SIT by

202 How Treg cells maintain their identity is not completely und

203 Finally, Dll4-exposed induced Treg cells maintained the CD62L(hi)CD44(lo) central Treg

204 development by decreasing acetylation of the Treg cell master regulator Foxp3 mediated by the histone

205 Loss of MSC reduced expression of the Treg cell master TF Foxp3 and induced TH2 differentiatio

206 ur data suggest a critical role for talin in Treg cell-mediated maintenance of immune homeostasis.

207 , IL-35, and IL-10, contributes to apoptotic Treg-cell-mediated immunosuppression.

208 Ndfip1 restricts Treg cell metabolism and IL-4 production via distinct me

209 Thus, GCK-dependent glycolysis regulates Treg cell migration.

210 entiation of induced Treg cells in vitro and Treg cell mitochondrial fitness.

211 Foxp3(+) regulatory T cells (Treg cells) modulate the immune system and maintain self

212 onversion, a significant increase in FOXP3 + Treg cell numbers and tumor-specific T cell responses we

213 Although total CD4(+)FOXP3(+) Treg cell numbers are reduced, frequencies are maintaine

214 After challenge, symptoms, Treg cell numbers, and forkhead box protein 3 (Foxp3), T

215 of forkhead box protein (FOX)3 regulatory T (Treg) cells offers a promising strategy to reduce damage

216 Targeting Treg cells or CTLA-4 in this precise window accelerated

217 It remains unclear how Treg cells orchestrate their homeostasis and interplay w

218 d that S1P1 not only regulated the egress of Treg cells out of lymphoid organs and subsequent non-lym

219 ompetitive cotransfer experiments, wild-type Treg cells outcompeted T-bet-deficient Treg cells in ter

220 Regulatory T cells (Treg cells) perform suppressive functions in disparate t

221 the tissue-enriched factor(s) that influence Treg cell phenotype and function remain largely unknown.

222 activation during differentiation sustained Treg cell phenotype and function to control RSV infectio

223 lls maintained the CD62L(hi)CD44(lo) central Treg cell phenotype, had increased Foxp3 expression, bec

224 ext- and partner-dependent manner, to govern Treg cell phenotypes.

225 ed with tolerance induction, indicating that Treg cells play an important role in the regulation of p

226 Regulatory T (Treg) cells play an essential role in the maintenance of

227 fective immune regulation with regulatory T (Treg) cells playing a fundamental role in this process.

228 omeostasis and survival of the regulatory T (Treg) cell pool.

229 rophages, thereby enhancing expansion of the Treg cell population via IL-10.

230 emia elevated the intrahepatic regulatory T (Treg) cell population and increased the expression of tr

231 unction, with expansion of the regulatory T (Treg) cell population.

232 Treg cell precursors expressed high levels of the tumor

233 nance by showing that skin-resident Foxp3(+) Treg cells preferentially localize to the hair follicle

234 LPR) signaling specifically in regulatory T (Treg) cells prevented their activation and permitted rap

235 Tolerant Treg cell produced high levels of IL-10 and had diverse

236 gle-positive CD25(+) GITR(+) Foxp3(-) thymic Treg cell progenitors.

237 However, how Treg cells proliferate in these patients is not clear.

238 -5p resulted specifically hyper-expressed in Treg cells purified from PLN of T1D patients.

239 filtrating Treg cells, increased effector to Treg cell ratios, and improved control of established tu

240 been further reinforced by the evidence that Treg cells recruitment by cancer-FOXP3 was impaired by n

241 Mechanistically, apoptotic Treg cells release and convert a large amount of ATP to

242 evealed that intrahepatically differentiated Treg cells relocated to the inflamed aorta in atheroscle

243 However, Treg cells require TGF-beta signals to appropriately dam

244 these findings, we propose a model in which Treg cell responses at peripheral sites converge on thos

245 kin 2 (IL-2) promotes Foxp3(+) regulatory T (Treg) cell responses, but inhibits T follicular helper (

246 he other hand, permanent deletion of S1P1 in Treg cells resulted in autoimmunity and acute deletion r

247 ng Treg cells-but not of T-bet expression in Treg cells-resulted in severe TH1 autoimmunity.

248 Ndfip1 deletion in Treg cells results in autoinflammatory disease.

249 ferentiation, and induction of regulatory T (Treg) cells results from low TCR signal strength and low

250 Anergic CD4(+) T cells and Treg cells share a number of phenotypic and mechanistic

251 , which were associated with Foxp3 and other Treg cell signature genes, began to be activated in Treg

252 ceptor 4, and the epigenetic modification of Treg cell signature genes-and an interesting relationshi

253 In contrast, under Treg cell-skewing conditions, TEAD1 expression and seque

254 Using mice with Foxp3(+) Treg-cell specific deletion of Blimp1 and other approach

255 We found that Treg cell-specific super-enhancers (Treg-SEs), which wer

256 family E3 ubiquitin ligases, is required for Treg cell stability and function.

257 the suppressive function of Foxp3-expressing Treg cell subsets.

258 oach, we then demonstrate that human induced Treg cells suppress syngeneic human ILC2s through ICOSL

259 Foxp3(+) T regulatory (Treg) cells suppress immune cell activation and establis

260 Treg cell suppression was shown to be antigen specific.

261 a novel pathway of direct TGF-beta-dependent Treg-cell suppression of mast cell activation, in the ab

262 LKB1 deficiency disrupted Treg cell survival and mitochondrial fitness and metabol

263 Thus, the data support a model wherein tumor Treg cells sustain and amplify their suppressor capacity

264 ssing tolerogenic DCs and forkhead box P3(+) Treg cells that could be targeted for the design of nove

265 n addition to natural (n)Treg and induced (i)Treg cells that develop from naive precursors, suppressi

266 relative abundance of self-epitope specific Treg cells that leads to protection or causation of auto

267 ed numbers of invariant natural killer T and Treg cells that likely contribute to the patients' immun

268 e analyzed CD4(+) forkhead box P3 (Foxp3)(+) Treg cells that were isolated from the lungs of naive BA

269 CD4 CD25 Treg cells that were polyclonally expanded in culture we

270 e recruitment and retention of regulatory T (Treg) cells that express the CCL20 receptor, CCR6.

271 e expansion of CD8(+)CD28(-)CD127(lo)CD39(+) Treg cells, the frequency of which correlates with both

272 Conversely, following depletion of T-bet(-) Treg cells, the remaining T-bet(+) cells specifically in

273 able the long term interactions of pDCs with Treg cells, thereby enhancing suppression of Th1 anti-tu

274 actor T-bet optimizes Foxp3(+) regulatory T (Treg) cells to counteract Th1-type inflammation.

275 ctivating allergen-nonspecific regulatory T (Treg) cells to create a TH2-polarizing cytokine milieu.

276 Migration of activated regulatory T (Treg) cells to inflamed tissue is crucial for their immu

277 en extensively studied, the bioenergetics of Treg cell trafficking remains undefined.

278 1, Il1rl1, Itgae, TIGIT and ICOS are Th17-to-Treg cell transdifferentiation-associated markers.

279 Here we show that tumor Treg cells undergo apoptosis, and such apoptotic Treg ce

280 When exposed to IL-33, Treg cells upregulated their expression of the canonical

281 gy, we specifically deleted S1P1 in Th17 and Treg cells using IL-17A (Cre) and Foxp3 (Cre) mice, resp

282 This predominance of CCR6(+) Treg cells was also found in the draining lymph nodes an

283 of circulating CD8(+)CD28(-)CD127(lo)CD39(+) Treg cells was analyzed and correlated with viral load a

284 in maintaining high IL-2Ralpha expression by Treg cells was due, in part, to integrin LFA-1-mediated

285 The critical role of the CCL1-CCR8 axis in Treg cells was further dissected through adoptive transf

286 Unexpectedly, LKB1 function in Treg cells was independent of conventional AMPK signalli

287 transcription factor for regulatory T cells (Treg cells), was also expressed in many tumors including

288 Also, human ILC2s and Treg cells were adoptively transferred into NOD SCID gam

289 SEA-activated Treg cells were analyzed for the expression of the TH2-p

290 ILC2s and Treg cells were evaluated by using in vitro suppression

291 ast, a significant portion (>30%) of CCR6(-) Treg cells were found to be CD45RA(+) naive Treg cells.

292 CC, and intratumoral and circulating FOXP3 + Treg cells were higher in KT-mTORi-SCC (P < 0.05).

293 Peripheral talin-deficient Treg cells were unable to maintain high expression of IL

294 in reporter mice revealed that regulatory T (Treg) cells were the predominant source of IL-10 in resp

295 Tregs cells were found to induce alternate activation of

296 , CD20 + B, CD56 + NK, FOXP3 + regulatory T [Treg] cells) were explored in a cross-sectional analysis

297 lving increased expression of miR-125a-5p on Treg cells which results into reduced expression of CCR2

298 specific CD4(+) T cells were FOXP3(+)CD39(+) Treg cells, which reside within the pool of memory CD4(+

299 Dysregulated Foxp3(+) Treg cells with distinct characteristics of TH2 cells in

300 actors, which have been suggested to provide Treg cells with enhanced suppressive capacity.