ライフサイエンスコーパス: teff

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

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

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

4 mediated by CD4(+)CD25(-) effector T cells (Teffs).

5 and compromising Treg inhibitory effects on Teff.

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

7 MPEC compared with terminally differentiated Teff.

8 ression and glucose metabolism essential for Teff.

9 a) regulates metabolic pathways critical for Teff.

10 hile boosting immunoregulatory properties in Teff.

11 d Tfh cell fate trajectories toward those of Teff.

12 erative capacity that was vastly superior to TEFF.

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

14 ved peptides, with a restricted expansion of Teffs.

15 le dramatically reducing IL-21 production by Teffs.

16 imilar to that observed in rapamycin-treated Teffs.

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

18 olves a resistance of truly naive Cbl-b(-/-) Teffs.

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

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

21 along with a lesser but significant role in Teff activation and suggest a strategy of pharmacologic

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

23 e immunological synapse is required for full Teff activation.

24 of genes than ones involved in counteracting Teff activation.

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

26 T cells (Teffs), but less is known about how Teffs affect Tregs.

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

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

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

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

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

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

33 neous dendritic cell antigen presentation to Teff and Treg cells.

34 immune tolerance in vivo via its effects on Teff and Treg cells.

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

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

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

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

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

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

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

42 ction from diabetes by Tregs is dependent on Teffs and partially dependent on TNF-alpha, a cytokine t

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

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

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

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

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

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

49 Effector (Teff) and regulatory (Treg) T cells produce cytokines th

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

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

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

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

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

55 chanisms mediated by effector T lymphocytes (Teff), and regulatory mechanisms mediated by FOXP3(+) re

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

57 oimmune disease, we now show that Cbl-b(-/-) Teffs are resistant to suppression by Tregs in vivo and

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

59 t Cbl-b(-/-) CD4(+)CD25(-) effector T cells (Teffs) are resistant to CD4(+)CD25(+) regulatory T cell

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

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

62 er levels of infection in Treg compared with Teff at both early and late time points.

63 gher levels of infection in Treg compared to Teff at early time points, but this difference disappear

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

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

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

67 cytokine that has been shown to affect Treg/Teff balance.

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 une responses triggered by effector T cells (Teffs), but less is known about how Teffs affect Tregs.

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

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

74 1 (PD-1) and inhibition of effector T cells (Teffs) by CD4+Foxp3+Tregs are among the many described m

75 iferation of CD4(+)CD25(-) effector T cells (Teffs) by mechanisms that are not well understood.

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

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

78 epleted Stat5b-CA TG versus WT CD4(+)CD25(-) Teffs caused less GVHD lethality associated with diminis

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

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

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

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

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

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

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

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

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

88 the intricate mechanisms regulating Treg and Teff cell function.

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

90 How TEFF cell identity is established and maintained is not

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

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

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

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

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

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

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

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

99 Activation of Teff cells also up-regulated TRPC5 channels which mediat

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

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

102 ll-established model of RA, the interplay of Teff cells and Treg cells in K/BxN mice recapitulated ma

103 rt hairpin RNA (shRNA) knockdown of TRPC5 in Teff cells blocked contact-dependent proliferation inhib

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

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

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

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

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

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

110 Here, we show that Treg and Teff cells specific for the same foreign peptide:major h

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

112 Our results thus indicate GM1 in Teff cells to be the primary target of Gal-1 expressed b

113 eff cells were more resistant than wild-type Teff cells to suppression by Tregs, suggesting BTLA expr

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

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

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

117 sion by Tregs, suggesting BTLA expression by Teff cells was required for their suppression by Tregs.

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

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

120 rmal suppressive activity, whereas BTLA(-/-) Teff cells were more resistant than wild-type Teff cells

121 injection, whereas a similar fraction of the Teff cells were producing IFN-gamma.

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

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

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

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

126 expression was comparable in naive Tregs vs Teff cells, but after stimulation HVEM expression was qu

127 ncreased the fraction of IFN-gamma-producing Teff cells, indicating that Teff function was limited by

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

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

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

131 VEM expression was quickly down-regulated by Teff cells, whereas HVEM was further up-regulated by Tre

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

133 aired upregulation of cytotoxic molecules in TEFF cells.

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

135 s together with suppression and depletion of Teff cells.

136 production via Tfh cells or inflammation by Teff cells.

137 ptosis, thereby maintaining equilibrium with Teff cells.

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

139 or the proliferative expansion of pathogenic Teff cells.

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

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

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

143 amma-producing CD4(+) and CD8(+) T effector (Teff) cells and expanded T regulatory (Treg) cells in re

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

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

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

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

148 tion of murine CD4(+) and CD8(+) effector T (Teff) cells resulted in significant elevation of GM1 and

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

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

151 inhibitory signaling cascade in effector T (Teff) cells, but we now report that the HVEM-BTLA pathwa

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

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

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

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

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

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

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

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

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

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

162 Reduced GVHD by Stat5b-CA TG versus WT Teffs could not be explained by conversion into Tregs in

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

164 the present results suggest that Cbl-b(-/-) Teffs demonstrate a context-dependent sensitivity to TGF

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

166 n be manipulated in vivo to control Treg and Teff development in inflammatory diseases.

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

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

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

170 to the oxidation product (sulfate), whereas Teffs divert more of the cysteine pool toward protein an

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

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

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

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

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

176 The fraction of tumor-infiltrating Teffs expressing CTLA-4 and PD-1 increases, reflecting t

177 Whole grain teff flour becomes increasingly important in healthy foo

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

179 In parallel, Teff from discordant asthmatic twins demonstrated increa

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

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

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

183 Although the signals that contribute to Teff function are well understood, less is known about t

184 -gamma-producing Teff cells, indicating that Teff function was limited by the Treg cells.

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

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

187 rasitemia, which is consistent with improved Teff function.

188 ll (Treg) activity controls effector T cell (Teff) function and is inhibited by the inflammatory cyto

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

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

191 uppression, which is rectified by increasing Teff GM1.

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

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

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

195 As Cbl-b(-/-) Teffs have been shown to be insensitive to the suppressi

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

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

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

199 activity that inhibits the proliferation of Teffs in vivo.

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

201 ected with HIV compared to effector T cells (Teff) in vivo.

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

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

204 d CTLA-4 blockade increases effector T-cell (Teff) infiltration, resulting in highly advantageous Tef

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

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

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

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

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

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

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

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

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

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

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

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

217 Teffs, natural killer cells, and eosinophils also respon

218 in Cbl-b(-/-) mice are related to defects in Teff, not Treg, function.

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

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

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

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

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

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

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

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

227 ss GVHD lethality associated with diminished Teff proinflammatory and increased Th2 anti-inflammatory

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

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

230 Suppression of Teff proliferation was determined by application of GM1

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

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

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

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

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

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

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

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

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

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

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

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

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

244 In addition, Stat5b-CA TG Teffs retained a graft-versus-leukemia response.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 tion blockade also synergistically increases Teff-to-myeloid-derived suppressor cell ratios within B1

275 filtration, resulting in highly advantageous Teff-to-regulatory T-cell ratios with the tumor.

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

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

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

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

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

281 0% CD4(+)Foxp3(-) T cells (effector T cells [Teffs]) upregulated SnL.

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

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

284 ibility of Treg to HIV infection compared to Teff varies, depending on both viral and host factors.

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

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

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

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

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

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

291 Stat5b-CA TG Tregs added to WT CD4(+)CD25(-) Teffs were superior on a per-cell basis for inhibiting G

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

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

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

295 ibution from the nucleus to the cytoplasm in Teffs, which is abrogated by the addition of exogenous c

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