ライフサイエンスコーパス: teff

1 so causes proliferation of effector T-cells (Teff).

2 rentiated effector phenotype CD8(+) T cells (TEFF).

3 okine production in CD4(+) T effector cells (Teff).

4 buckwheat, corn, quinoa, millet, oat, rice, teff).

5 roduction by CD4(+)CD25(-) effector T cells (Teff).

6 cells (Tregs) and suppress effector T cells (Teffs).

7 a control of self-reactive effector T cells (Teffs).

8 erative capacity that was vastly superior to TEFF.

9 and compromising Treg inhibitory effects on Teff.

10 mbers in the lung relative to the numbers of Teff.

11 ression and glucose metabolism essential for Teff.

12 a) regulates metabolic pathways critical for Teff.

13 MPEC compared with terminally differentiated Teff.

14 hile boosting immunoregulatory properties in Teff.

15 d Tfh cell fate trajectories toward those of Teff.

16 ed to induce full-fledged colitis, unlike WT Teffs.

17 IL-2 and IFN-gamma than corresponding SnL(-) Teffs.

18 ved peptides, with a restricted expansion of Teffs.

19 le dramatically reducing IL-21 production by Teffs.

20 ed signaling compared with CD4(+) and CD8(+) Teffs.

21 imilar to that observed in rapamycin-treated Teffs.

22 ociated with proliferation of IL-2-producing Teffs.

23 shed capacity to suppress disease-implicated Teffs.

24 ppressive function against CD4(+) and CD8(+) Teffs.

25 ceptibility [IC(50)]: Treg [.5 muM] > CD4(+) Teff [2.0 muM] > CD8(+) Teff [6.5 muM]) and acting at th

26 eg [.5 muM] > CD4(+) Teff [2.0 muM] > CD8(+) Teff [6.5 muM]) and acting at the level of AKT and NF-ka

27 reas luteolin derivatives prevailed in brown teff (91-94%).

28 fied an unexpected function for PPARgamma in Teffs: a role in Teff proliferation and survival in lymp

29 ermore, we show that progression toward full Teff activation is promoted by increased duration of inf

30 of genes than ones involved in counteracting Teff activation.

31 Alloreactive CD8 T effector (Teff) activation and T memory (Tmem) differentiation dur

32 NOD Teffs also showed attenuated Ca(2+) influx via transient

33 (hi)CD27(+)) are less divided than CD62L(lo) Teff and express memory genes.

34 Although both TEFF and TM could protect Rag(-/-) mice, only TM persist

35 ptor CX3CR1 identifies three distinct CD8(+) Teff and Tmem subsets.

36 res a wide linear antigen response range for Teff and Treg cells under real spatiotemporal conditions

37 ling during antitumor responses acts on both Teff and Treg cells, which have opposing roles in promot

38 ic change in the balance between Ag-specific Teff and Treg from approximately 1:1 at steady state to

39 We show that Teff and Treg require distinct metabolic programs to sup

40 Importantly, Teff and Treg use distinct metabolic programs to support

41 ith glycolysis and lipid oxidation promoting Teff and Treg, respectively, Teff were selectively incre

42 OX40L/OX40 interactions between DCs and Teff and/or Treg are critical for priming effective and

43 GM1 deficiency occurs in NOD Teffs and contributes importantly to failed suppression,

44 xa-inducible ROSA-rtTA-IL-21-Tg mice expands Teffs and FoxP3(-) cells.

45 eptor (C5aR1) signaling on T cells activates Teffs and inhibits Tregs, but whether and/or how C5aR1 a

46 Ag leads to generation of cytokine-producing Teffs and peripheral Tregs.

47 both phenotypic and functional responses of Teffs and Tregs has also proven important.

48 Interestingly, both Teffs and Tregs respond to IL-6 stimulation through stro

49 r determinant of the relative frequencies of Teffs and Tregs.

50 BDC12-4.1 CD4 T cells convert into effector (Teff) and Foxp3(+)-expressing adaptive regulatory T cell

51 Frequencies of effector T cells (Teff) and graft infiltrating immune cells were measured

52 cells, Blimp1 is expressed in both effector (Teff) and regulatory (Treg) cells, and mice with T cell-

53 While abnormalities of both effector (Teff) and regulatory (Treg) T cells have been reported i

54 differential expansion of effector T cells (Teff) and regulatory T cells (Treg) were identified as c

55 of tumor antigen-specific effector T cells (Teff) and regulatory T cells (Treg).

56 file distinct from that of effector T cells (TEFF) and TMEM cells that was minimally remodeled after

57 ative capacity than effector memory T cells (TEFF) and, therefore, polarizing vaccine-induced T cells

58 balance between pathogenic effector T cells (Teffs) and protective Foxp3(+) regulatory T cells (Tregs

59 rentiated effector phenotype (TNF-alpha-only TEFF), and the level of CD27 expression on IFN-gamma-pro

60 Effector T cells (TEFF) are a barrier to booster vaccination because they

61 red with CD4(+) and CD8(+) effector T cells (Teffs) as evident from effects on anti-CD3/CD28/CD2-indu

62 rferon gamma (IFNgamma)(+) effector T cells (Teffs), as well as allosensitization in the hosts, dimin

63 ing mice contained tolerized CXCR3-deficient Teff, as well as a large increase in Treg.

64 tumoral Treg depletion is mediated by CD8(+) Teff-associated cytokines IFN-gamma and TNF-alpha.

65 ned markers of progressive activation of CD4 Teff at the peak of malaria infection, including a subse

66 sociated with modifications in both Treg and Teff at the transcriptional level among asthmatics.

67 he Tim-3 pathway appears to control Treg and Teff balance through altering cell proliferation and apo

68 been made to enhance the sensory quality of teff based products.

69 nts of pyrazines, terpenes and esters, while teff, buckwheat and rice flours presented the highest co

70 bitor, p21, was significantly upregulated in Teffs but not nTregs after treatment with AzaC.

71 only on IL-2-producing CD4(+)CD25(+)Foxp3(-) Teffs, but also on CD4(+)CD25(+)Foxp3(+) Tregs, which ac

72 The inactivation of Teffs by persistent Ag is associated with reduced ERK ph

73 amma released by activated effector T cells (Teffs), by up-regulating their Fas ligand (FasL) express

74 ithin B cell follicles in the spleen whereas TEFF cannot traffic through follicular regions, Ag produ

75 protect against GvHD and that nTregs, unlike Teffs (CD3(+)FOXP3(-)), are resistant to the antiprolife

76 onversion of alloreactive donor T effectors (Teffs; CD4(+)CD25(-)FOXP3(-)) and the direct antiprolife

77 PKC-theta plays a central role in Teff cell activation and survival, and negatively regula

78 ent toward low-affinity binding sites within Teff cell cis-regulatory elements, including those of Pr

79 ich Treg cells are highly activated by their Teff cell counterparts depends on the immune context for

80 y of this DC subpopulation to support CD8(+) Teff cell differentiation.

81 Tfh-Teff cell fate commitment is regulated by mutual antagon

82 R signaling raised Irf4 amounts and promoted Teff cell fates at the expense of Tfh ones.

83 ntrols common and unique aspects of Treg and Teff cell function by differentially regulating gene exp

84 the intricate mechanisms regulating Treg and Teff cell function.

85 erred Rag1(-/-) mice restored Mdr1-deficient Teff cell homeostasis and attenuated ileitis.

86 How TEFF cell identity is established and maintained is not

87 transporter Glut1 and aerobic glycolysis for Teff cell proliferation and inflammatory function, the m

88 ied role for CD27 in augmenting autoreactive Teff cell responses.

89 e results suggest that CD27 does not promote Teff cell survival by increasing expression of antiapopt

90 This Teff cell-dependent Treg cell boost may be crucial to li

91 In a condition of low inflammation, the Teff cell-mediated Treg cell boost involved TNF, OX40L,

92 s can be used to enhance local production of Teff cell-recruiting chemokines.

93 or (TCR)/CD28 signals leading to effector T (Teff) cell activation.

94 KC)-theta regulates conventional effector T (Teff) cell function.

95 y, we further characterized this effector T (Teff) cell-dependent Treg cell boost in vivo in mice.

96 Runx3-deficient CD8(+) TEFF cells aberrantly upregulated genes characteristic o

97 that coordinated interaction between mucosal Teff cells and CBAs in the ileum regulate intestinal imm

98 gulated during the differentiation of CD8(+) Teff cells and might have a role in fate 'decisions' inv

99 CD27 resulted in the progressive survival of Teff cells during the autoimmune response.

100 oxidative stress and enforced homeostasis in Teff cells exposed to conjugated bile acids (CBAs), a cl

101 In contrast, CD27-deficient Teff cells expressed higher levels of active caspase 8.

102 Transfer of TNFR2-deficient Teff cells failed to induce full-fledged colitis, unlike

103 This combination was only seen in tolerant Teff cells following PIT, but not in Teff that transient

104 on of Blimp1 is required to control Treg and Teff cells homeostasis but, unexpectedly, it is dispensa

105 e proliferative expansion of TNFR2-deficient Teff cells in the lymphopenic mice, as well as their red

106 Ablating Tcf7 in Runx3-deficient CD8(+) TEFF cells prevented the upregulation of TFH genes and a

107 Expression of CD27 on Ag-specific Teff cells resulted in enhanced skin inflammation when c

108 slation of those transcripts when the CD8(+) Teff cells stopped dividing just before the contraction

109 ypoproliferative response of TNFR2-deficient Teff cells to TCR stimulation was associated with an inc

110 ssion has been demonstrated in both Treg and Teff cells under inflammatory conditions, the intrinsic

111 Whereas wild-type Teff cells upregulated Mdr1 in the ileum, those lacking

112 s phenomenon was observed when both Treg and Teff cells were activated by their cognate Ag, with the

113 Large numbers of short-lived Teff cells were continuously produced via a proliferativ

114 latory T (Treg) cells persistently contacted Teff cells with or without involvement of CD11c(+) dendr

115 CD4(+) effector T cells (Teff cells) and regulatory T cells (Treg cells) undergo

116 e of virus-specific CD8(+) effector T cells (Teff cells) during acute infection of mice with lymphocy

117 ervous system-infiltrating effector T cells (Teff cells).

118 s that bolstered an autoinhibitory effect in Teff cells, and this induction appears to be governed by

119 utic implications of inhibiting PKC-theta in Teff cells, to reduce effector function, and in Treg cel

120 preferentially expressed on Tregs but not on Teff cells, was required for selective Treg proliferatio

121 Using CD4(+) autoimmune Teff cells, we demonstrate that peptide immunotherapy (P

122 ed a preserved pattern of gene expression on Teff cells, with a varying degree of genes being suppres

123 or the proliferative expansion of pathogenic Teff cells.

124 h induction of anergy in CHIKV-specific CD4+ Teff cells.

125 , there was no additional Treg cell boost by Teff cells.

126 s together with suppression and depletion of Teff cells.

127 flammation when compared with CD27-deficient Teff cells.

128 the functional role of CD27 on autoreactive Teff cells.

129 aired upregulation of cytotoxic molecules in TEFF cells.

130 f Bcl6-expressing Tfh and Blimp-1-expressing Teff cells.

131 is essential for optimum IL-2 production by Teff cells.

132 production via Tfh cells or inflammation by Teff cells.

133 roliferation of antigen-specific T-effector (Teff ) cells in vitro and in vivo via T-cell immunoglobu

134 Highly functional CD8(+) effector T (Teff) cells can persist in large numbers during controll

135 s and a greater frequency of FoxP3-negative (Teff) cells compared with patients with antibiotic-respo

136 atory receptor influences CD4(+) effector T (Teff) cells in inflamed tissues.

137 ctively suppressed CD25(-)CD4(+) effector T (Teff) cells in secondary cultures.

138 between T regulatory (Treg) and T effector (Teff) cells is likely to contribute to the induction and

139 cells differentiate into cytotoxic effector (TEFF) cells that eliminate target cells.

140 Here, we show that CD4(+) T effector (Teff) cells upregulated the xenobiotic transporter, Mdr1

141 ) memory T cells, but not CD8(+) T effector (Teff) cells, possessed substantial mitochondrial spare r

142 pported the generation of CD8(+) T effector (Teff) cells, which migrate from lymph nodes to the infec

143 B cells, as opposed to Tregs or effector T (Teff) cells, whose BTLA expression was not affected.

144 neutralizing virus-specific CD4+ effector T (Teff) cells.

145 rt a genomic footprint on target effector T (Teff) cells.

146 mal number for the regulation of T effector (Teff) cells.

147 external environment than CD8(+) effector T (Teff) cells.

148 ent recruitment of type-1 effector CD8(+) T (Teff) cells.

149 itted TRM precursor cells in the circulatory TEFF compartment.

150 uch comparisons also suggested that the Treg-Teff conversion process is not an active process at the

151 model of spontaneous lupus and SnL levels on Teffs correlated strongly with the degree of proteinuria

152 Furthermore, we demonstrate that Teffs deficient in p21 are less sensitive to the antipro

153 Additionally, T-PPAR Teffs demonstrated decreased cytokine production in infl

154 ase that is associated with effector T cell (Teff) destruction of insulin-producing pancreatic beta-i

155 ver, local environmental factors influencing Teff differentiation and migration are largely unknown.

156 SnL(+) Teffs displayed higher levels of activation markers CD25

157 mor-infiltrating Tregs and T effector cells (Teff) displayed sequence profiles in the CDR3 region tha

158 ilence antigen-experienced effector T cells (Teff) driving ongoing immune pathology.

159 Teff (Eragrostis tef) is a cereal native to Ethiopia and

160 Teff (Eragrostis tef) is a cornerstone of food security

161 n and simultaneously converts into aTreg and Teff, establishing an equilibrium that determines diabet

162 uggest a novel mechanism by which pathogenic Teffs evade regulatory suppression, thereby leading to a

163 This environment promoted CD8(+) and CD4(+) Teff expansion over that of antigen-specific Tregs, tipp

164 Whole grain teff flour becomes increasingly important in healthy foo

165 in T cells during GVHD and were not seen in Teff following acute activation.

166 In parallel, Teff from discordant asthmatic twins demonstrated increa

167 n and reduced Teff function when compared to Teff from the non-asthmatic twin.

168 D mice contained significantly less GM1 than Teffs from the other three mouse strains tested.

169 od-derived CD4(+)CD25(hi) tTreg and expanded Teffs from the same donors indicate that iTreg are inter

170 ls (Tregs) are less efficient in suppressing Teff function and they produce IFN-gamma following mitog

171 Finally, these abnormalities in T-PPAR Teff function were not elicited by lymphopenia alone but

172 s, decreased IFNgamma expression and reduced Teff function when compared to Teff from the non-asthmat

173 rasitemia, which is consistent with improved Teff function.

174 of ERRalpha reduced T-cell proliferation and Teff generation in both immunization and experimental au

175 addition selectively restored Treg--but not Teff--generation after acute ERRalpha inhibition.

176 The teff genome contains two complete sets of homoeologous c

177 uppression, which is rectified by increasing Teff GM1.

178 and this, too, was reversed by elevation of Teff GM1.

179 ty, nutritional composition and food uses of teff grain.

180 on the phenolic composition of two types of teff grains differing in their colour (white and brown).

181 s and extruded products made only from brown teff grains.

182 f lung rejection that CXCR3-deficient CD8(+) Teff have impaired migration into the lungs compared wit

183 regulates the early divergence of Tmem from Teff in chronic infection.

184 R-Valpha7.2+ MAIT T cells and CD4+CCR2+CCR5+ Teffs in paediatric-onset multiple sclerosis, compared t

185 Notably, the transcriptional signature of Teffs in the presence of leptin blockade appears similar

186 th a significant decrease in accumulation of Teffs in the spleen, lymph nodes, and tissues after adop

187 activity that inhibits the proliferation of Teffs in vivo.

188 lls (Tmem) from responding effector T cells (Teff) in chronic parasite infection.

189 (+) CD25(high) cells, an activated subset of Teff, in 32 patients with AIH and 20 with AISC and in 36

190 The attractive nutrients of teff include protein, dietary fiber, polyphenols, and ce

191 o activate tumour-specific effector T cells (Teff), inhibiting the conversion of Treg and compromisin

192 ng effects on Treg sensitivity versus CD8(+) Teff insensitivity to idelalisib could still potentially

193 of the primary response that is dominated by TEFF Interestingly, although the ablation of B cells bef

194 ent of some, but not necessarily all, CD8(+) Teff into the target organ and suggest a novel approach

195 In recent years, teff is becoming globally popular due to the attractive

196 Teff is currently being incorporated into a range of foo

197 in CD4(+) CD25(-) T cells (T effector cells [Teffs]) is actually required for development of autoimmu

198 athway has been shown to negatively regulate Teffs, its role in regulating Foxp3(+) Tregs is poorly e

199 Both CD4(+) and CD8(+) effector T (Teff) lymphocytes directly engaged target cells.

200 rine models and determined that inflammatory Teffs maintain high expression of glycolytic genes and r

201 is a selective transcriptional regulator of Teff metabolism that may provide a metabolic means to mo

202 -mTOR axis and define a potential target for Teff modulation in normal and pathologic conditions.

203 found to be more resistant to, and Foxp3(-) Teffs more sensitive to, TCR activation-induced cell apo

204 CD4(+)CD25(+) T cells promoted expansion of Teffs more substantially than Tregs through improving ST

205 White teff mostly contained apigenin-derived flavones (86-92%)

206 Teffs, natural killer cells, and eosinophils also respon

207 In turn, the implicated Teffs of multiple sclerosis patients were relatively res

208 Resting and activated CD4(+) and CD8(+) Teffs of NOD mice contained significantly less GM1 than

209 genes is already apparent in the circulating TEFF offspring of such clones.

210 , reflecting an excess abnormality in either Teff or Treg limbs of the T cell response, or a combinat

211 iferation and differentiation into effector (Teff) or inducible regulatory (Treg) subsets with specif

212 ytes can differentiate into effector T cell (Teff) or inducible regulatory T cell (Treg) subsets with

213 Cultures in which either effector T cells (Teffs) or Tregs were pretreated with Stat3 inhibitors in

214 pG-ODN or Poly(I:C) preferentially amplified Teffs over Tregs, dramatically increasing the antigen-sp

215 CD27(-)) late effector cells have a terminal Teff phenotype (PD-1(+), Fas(hi), AnnexinV(+)).

216 Treg skewing confers activated Teff phenotypic and functional properties of T regulator

217 TE analysis allows us to estimate that the teff polyploidy event occurred ~1.1 million years ago (m

218 r memory (Tem) cells and their corresponding Teff precursors were CX3CR1(-) and CX3CR1(high), respect

219 It allowed indicating amaranth and teff products as flakes with the highest impact on the r

220 CD4, but not CD8, iTregs could then suppress Teff proliferation and proinflammatory cytokine producti

221 d function for PPARgamma in Teffs: a role in Teff proliferation and survival in lymphopenia-associate

222 Suppression of Teff proliferation was determined by application of GM1

223 ective proliferation of Foxp3+Tregs (without Teff proliferation), by co-culturing CD4+ T-cells with O

224 on during priming increased effector T cell (Teff) proliferation and strongly decreased peak parasite

225 ft regulatory T cell (Treg):effector T cell (Teff) ratios can substantially reduce GVHD in cancer pat

226 show that, once in the tissue, Tregs inhibit Teff recruitment, further enabling a Teff:Treg ratio opt

227 for energy production, and effector T cells (Teffs) rely on glycolysis for proliferation, the distinc

228 ereas the number of Foxp3- effector T cells (Teffs) remained at a normal level.

229 of TLR1 on T lymphocytes and confer enhanced Teff resistance to Treg suppression in the presence of P

230 uld influence immune-related disease through Teff resistance to Treg suppression.

231 After activation, NOD Teffs resisted suppression by Tregs or GM1 cross-linking

232 d(-/-)) mice, we find that alloimmune CD4(+) Teff responses are fully competent in vivo.

233 a novel link between nutritional status and Teff responses through the leptin-mTOR axis and define a

234 onal signature that determine the outcome of Teff responses, both in vitro and in vivo.

235 es in suppressing antiviral effector T cell (Teff) responses that are essential for viral clearance.

236 to a large degree on CD4(+) effector T cell (Teff) responses, was impaired with ICOS-L blockade.

237 m influence CD4+CD25-FOXP3- effector T cell (Teff) responses.

238 Interestingly, the TNF-alpha-only TEFF signature in participants with recently acquired LT

239 The TNF-alpha-only TEFF signature was significantly higher in the group wit

240 eucalyptus wood, teff straw was derived from teff stem, and sand was obtained from indigenous crushed

241 Finally, Teffs stimulated strongly through the TCR are also resis

242 sorbent materials such as sand, biochar, and teff straw in a media.

243 Biochar was prepared from eucalyptus wood, teff straw was derived from teff stem, and sand was obta

244 The performances of biochar and teff straw were assessed based on the operation paramete

245 The two teff subgenomes have partitioned their ancestral functio

246 The earliest observed Teff subsets (CD127(-)CD62L(hi)CD27(+)) are less divided

247 at activated T cells generate three distinct Teff subsets with progressive activation phenotypes.

248 raction phase and generate the terminal late Teff subsets, whereas in uninfected recipients, they bec

249 egulatory T cell (Treg) and effector T cell (Teff) subsets were assessed for levels of cellular funct

250 d mitochondrial volume in Tmem compared with Teff, supporting previous reports in acute infection.

251 his cytokine resulted from the abrogation of Teff suppression; however, T1D-derived iNKT cells showed

252 g adoptive transfer, we show that only early Teff survive the contraction phase and generate the term

253 vidual naive CD8+ T cells to the T effector (TEFF), T circulating memory (TCIRCM), and TRM pools by l

254 CD4+ effector T cell (Teff) (Th1 and Th17) and Treg subsets are metabolically

255 olerant Teff cells following PIT, but not in Teff that transiently express PD-1.

256 at SnL is a novel marker of activated CD4(+) Teffs that are implicated in the pathogenesis of autoimm

257 ing the imbalance of Foxp3(+) Tregs/Foxp3(-) Teffs that was induced by HCV infection.

258 cell differentiation into diverse effectors (Teff) that give rise to memory (Tmem) subsets.

259 lls and differentiate into T-effector cells (Teffs) that migrate to GVHD target organs.

260 in contrast to robust suppression of Balb/c Teffs; this was reversed by preincubation of NOD Teffs w

261 FasL) expression, which enabled them to kill Teffs through apoptosis.

262 press the proliferation of effector T cells (Teffs) through a cell contact-independent mechanism.

263 oups, the biological impact of decreased CD8 Teff/Tmem activation and function in the sensitization p

264 , and IL-15Ralpha, which support/program CD8 Teff/Tmem expansion, differentiation, and survival, were

265 were important for optimal alloreactive CD8 Teff/Tmem function in the sensitization phase, the fulmi

266 There is great potential to adapt teff to the other parts of the world for healthy food an

267 that of antigen-specific Tregs, tipping the Teff to Treg balance to favor effector cells.

268 This newly defined role for the balance of Teff to Treg, together with its known key function in T

269 he inability of PPARgamma-deficient (T-PPAR) Teffs to mediate lymphopenic autoimmunity is associated

270 aintaining appropriate ratios of Ag-specific Teffs to Tregs in tissues.

271 regulate autoreactive CD4+ effector T cells (Teffs) to prevent autoimmune diseases, such as type 1 di

272 in vivo and induced CD4(+) effector T cells (Teffs) to produce interleukin-2, a key survival factor f

273 An abnormal Teff/Treg ratio at the individual child level best disti

274 oxP3(+) regulatory T cells and increased the Teff/Treg ratio.

275 inhibit Teff recruitment, further enabling a Teff:Treg ratio optimal for regulation.

276 dramatically increasing the antigen-specific Teff:Treg ratios and inducing polyfunctional effector ce

277 ntigen-specific Tregs and failed to increase Teff:Treg ratios.

278 -bearing mice, high ratios of tumor-specific Teffs:Tregs in draining lymph nodes were associated with

279 osition, some of which were dependent on the teff type.

280 In both teff types, processing changed the phenolic profiles sim

281 n 90% of the total phenolic contents in both teff types.

282 gulated on CD4(+) Foxp3(-) effector T cells (Teffs) upon TCR stimulation.

283 0% CD4(+)Foxp3(-) T cells (effector T cells [Teffs]) upregulated SnL.

284 onstrate that alloreactive effector T cells (Teff) use fatty acids (FAs) as a fuel source to support

285 that Treg requires lipid oxidation, whereas Teff uses glucose metabolism, and lipid addition selecti

286 chromosome-scale assembly of allotetraploid teff (variety Dabbi) and patterns of subgenome dynamics.

287 Induction of ligands on CD4(+)Foxp3(-) Teffs was also observed in vivo using the New Zealand Bl

288 This abnormal accumulation of T-PPAR Teffs was associated with defects in both in vivo prolif

289 Calcium influx in Teffs was quantified using fura-2.

290 ons in Treg suppression of effector T cells (Teff), we performed in vitro suppression assays in healt

291 ation promoting Teff and Treg, respectively, Teff were selectively increased in Glut1 transgenic mice

292 CD4(+) and CD8(+) Teffs were isolated from spleens of prediabetic NOD mice

293 +) Tregs, but not Foxp3(-) effector T-cells (Teff), when CD4(+) T-cells are co-cultured with GM-CSF d

294 e between expanded CD4(+)CD25(hi) tTregs and Teffs, whereas modulation of suppressive activities by P

295 ation into the lungs compared with wild-type Teff, which results in a dramatic reduction in fatal pul

296 accessibility in wheat-red sorghum (WrS) and teff-white sorghum (TwS) flour blends used in Ethiopia t

297 The influence of cereal blends, teff-white sorghum (TwS), barley-wheat (BW) and wheat-re

298 s; this was reversed by preincubation of NOD Teffs with GM1.

299 s to functional inactivation and loss of the Teffs with preservation of Tregs in the target tissue.

300 Coculture of activated Teffs with Sn(+) macrophages or Sn(+) Chinese hamster ov