ライフサイエンスコーパス: T cell

1 t), with antibody-mediated depletion of CD4+ T cells.

2 nd reduced production of IFN-gamma by CD8(+) T cells.

3 bited a faster development and maturation of T cells.

4 nique subset of innate-like CD1d-independent T cells.

5 type 1 diabetes-relevant autoreactive CD8(+) T cells.

6 nt epitopes for gluten-specific CD4-positive T cells.

7 expressed on circulating HSV-2-specific CD8 T cells.

8 d naive and effector and central memory CD8+ T cells.

9 s, and this regulation is conserved in human T cells.

10 prevent induction of capsid-specific CD8(+) T cells.

11 d progenitor cells (HSPCs) through to mature T cells.

12 ens directly activated CD1b-autoreactive HJ1 T cells.

13 environment via type 2 cytokines from innate T cells.

14 tional lymphocytes, including virus-specific T cells.

15 of thymic and peripheral Foxp3(+) regulatory T cells.

16 ubsets, that is, naive, effector, and memory T cells.

17 l cells to recruit and activate alloreactive T cells.

18 n suppress activation of diabetogenic CD8(+) T cells.

19 When regulatory T cells (2 x 106/mouse) were intravenously administered

20 also demonstrate that a norovirus can infect T cells, a previously unrecognized target, in vitro.

21 t permitted sampling of more than 10(7) CD4+ T cells, a requirement for detecting exceedingly rare la

22 r RNA-electroporated CART (RNA-CART123); (2) T-cell ablation with alemtuzumab after treatment with le

23 123-4-1BB-CD3zeta T cells (CART123); and (3) T-cell ablation with rituximab after treatment with CD20

24 Reductions in CXCL10 and T cell accumulation were reversed by IDH-C35, a specific

25 in the Treg population, intratumoral CD8(+) T cells acquired a more functional phenotype characteriz

26 Here, we report that T cells activated in such a context are mainly IFN-gamma

27 ent CD4(+) T cells, as well as murine CD4(+) T cells activated in the presence of rapamycin, a pharma

28 ility of using rapamycin in conjunction with T cell-activating agents in HIV-1 cure strategies.

29 s with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically distributed in lymp

30 The cell surface receptor CD6 regulates T cell activation in both activating and inhibitory mann

31 not affect HIV-1 gene expression induced by T cell activation in these rCD4s.

32 ling, costimulatory pathways are involved in T cell activation.

33 vent of pAg sensing that ultimately leads to T cell activation.

34 timulates the CD27 pathway, which results in T-cell activation and antitumor activity in tumor models

35 We undertook translatome analysis of CD8 T-cell activation, combining polysome profiling and micr

36 spite maraviroc prophylaxis showed increased T-cell activation, naive T-cell skewing, and elevated se

37 T-cell acute lymphoblastic leukemia (T-ALL) is a highly

38 cytes prior to treatment or among peripheral T cells after treatment would be associated with effecti

39 few PD-1+ (programmed cell death 1-positive) T cells, an immunophenotypic pattern also observed in ot

40 evealed the presence of H-2L(d)/AH1-specific T cells and an expansion of sequence diversity in treate

41 d that a discrete proportion of infiltrating T cells and B cells underwent proliferation within the p

42 imulatory molecules such as ICOS, regulatory T cells and by compounds such as nicotine.

43 Additionally, both CD8(+) T cells and CD8(+) dendritic cells were identified in th

44 d for sufficient suppression of autoreactive T cells and helps to understand how MSCs ameliorate symp

45 ific effector functions, but its role on CD4 T cells and in HIV-infected children is poorly understoo

46 including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex, we detected a direct effe

47 ated" DCs stimulated the activation of naive T cells and polarized a subset of these cells into CD4+C

48 tion) reduced cardiac infiltration of CD4(+) T cells and prevented progressive left ventricular dilat

49 reduction in the frequency of self-reactive T cells and resistance to autoimmunity.

50 phosphorylated in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting m

51 ights into the nature of neoantigen-specific T cells and the effects of checkpoint blockade immunothe

52 f interferon-gamma (IFN-gamma) expression in T cells and to generate pathogenic TH17 cells in vivo.

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

54 nd -independent activation of Vgamma9Vdelta2 T cells and, importantly, strongly reduced the productio

55 whereas adoptive transfer of splenic CD4(+) T cells (and, to a lesser extent, cardiac CD3(+) T cells

56 al that IFN-gamma induces CD70 expression in T cells, and CD70 limits T cell expansion via a regulato

57 was associated with increased senescent CD4+ T cells, and reduced naive and effector and central memo

58 microbial products by Toll-like receptors on T cells, and this regulation is conserved in human T cel

59 The interaction between the T cell antigen receptor (TCR) expressed by natural kille

60 Unlike B cell depletion, pan-T cell aplasia is prohibitively toxic.

61 nt mechanism that involves caspase-dependent T cell apoptosis and upregulation of inhibitory immune c

62 anisms leading to IL-10 expression by CD4(+) T cells are being elucidated, with several cytokines imp

63 tumor cells, and mice with NFATc1-deficient T cells are defective in controlling Listeria infection.

64 vity assays, we predict that tumour reactive T cells are frequently present in NSCLC.

65 elements of the cytokine genes in the memory T cells are marked by activating histone modifications e

66 s constitutively acetylated and naive CD4(+) T cells are potentiated in Th17/Treg cell differentiatio

67 d murine wild-type and Rheb-deficient CD4(+) T cells, as well as murine CD4(+) T cells activated in t

68 tively promoted reactivation of resting CD4+ T-cell, as indicated by an increased viral transcription

69 ng human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombinant chem

70 that it showed not only a mechanism by which T cells become pathogenic before entering the CNS, but a

71 e E-selectin binding among CD4(+) and CD8(+) T cells but no binding by B cells.

72 oint therapies target tumor antigen-specific T cells, but less is known about their effects on natura

73 Determination of HCMV-specific T cells by cultured ELISPOT, in pregnant women with prim

74 in thymic negative selection of autoreactive T cells by promoting the ectopic expression of tissue-sp

75 IFN-gamma-primed MCs guide activation of T cells by Staphylococcus aureus superantigen and, when

76 the inhibitory microenvironment and how CAR T cells can be further engineered to maintain efficacy.

77 CD4 T cells can differentiate into multiple effector subsets

78 ivirally transduced anti-CD123-4-1BB-CD3zeta T cells (CART123); and (3) T-cell ablation with rituxima

79 purified immune subsets including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK

80 subsets including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49

81 sion of MYC signaling and an increase in the T cell chemoattractant CCL5.

82 In resting T cells cholesterol keeps TCRs in the resting conformati

83 n elevated mutation load in combination with T cell clonal dominance among intratumoral lymphocytes p

84 actor 6 mRNAs, whereas concentrations of the T-cell co-activators CD80 and CD86 increased in parallel

85 igands and receptors play important roles in T-cell co-stimulation and co-inhibition.

86 ed that soluble CD137 produced by regulatory T cells contributed to their autoimmune-suppressive func

87 1-cell-associated molecules IL-10, inducible T-Cell costimulator (ICOS), lymphocyte activation gene 3

88 py (ART) correlated with HIV viremia, CD4(+) T-cell counts, and immune activation markers, suggesting

89 In our in vitro T cell culture system, MART1-specific CD8 T cells were e

90 -controllers from those who experience CD4(+)T-cell decline.

91 Combined immunodeficiency (CID) is a T-cell defect frequently presenting with recurrent infec

92 ansferred polyclonal cancer antigen-reactive T cells deficient in the regulator diacylglycerol kinase

93 gammadelta-T-cell-deficient mice developed profound RPE and retinal

94 lation of infiltrated MAC387(+) macrophages, T cells, dendritic cells (DCs), and residential macropha

95 ricted high-avidity epitope provided strong, T cell-dependent protection against viruses or tumors.

96 Antibody-mediated CD4(+) T-cell depletion in HF mice (starting 4 weeks after liga

97 nclear how RICD sensitivity is calibrated in T cells derived from different individuals or subsets.

98 Studies of human T cell development require robust model systems that rec

99 has a crucial role in positive selection and T cell development.

100 (SCID) is characterized by severely impaired T-cell development and is fatal without treatment.

101 Furthermore, T-cell diapedesis became equivalent between control and

102 fferentiation was significantly reduced, and T cells did not express CXCR3.

103 TH1, TH17, and CD8(+) memory T-cell differentiation was significantly reduced, and T

104 fter ischemia, little is known about whether T cells directly impact cardiac fibroblasts (CFBs) to pr

105 lets and suggest that therapeutic regulatory T cells directly or indirectly regulate their influx by

106 of clinical phenotypes that involve distinct T cell-driven inflammatory processes.

107 uperfamily (TNFRSF) are key costimulators of T cells during infection, and there has been an increasi

108 exosomes, derived from IL-2 stimulated CD4+ T cells, effectively promoted reactivation of resting CD

109 Adoptive transfer of T cells engineered to express a hepatitis B virus-specif

110 nity by regulating natural killer and CD8(+) T cells, epigenetic downregulation of HLA-E by high-risk

111 ted T cells were determined by a novel CD154 T cell epitope mapping assay.

112 After identification of T cell epitope-containing parts on each of the 3 parenta

113 Thus, sequence homology between T cell epitopes of 2 self-proteins and a related order o

114 This phenotype, known as T cell exhaustion, occurs during chronic infections caus

115 tern of chromatin accessibility specific for T-cell exhaustion, characterized by enrichment for conse

116 disease, chronic immune activation leads to T-cell exhaustion.

117 Furthermore, OVA-exposed lung Ptx3(-/-) CD4 T cells exhibit an increased production of IL-17A, an ef

118 CD70 expression in T cells, and CD70 limits T cell expansion via a regulatory T cell-independent mec

119 ANTES and activation of p38/Stat pathways in T-cells exposed to exosomes derived from HIV-1 infected

120 ciated with Wnt-responsive enhancers through T cell factors (TCF) and kept silent by Groucho/TLE co-r

121 and sex on gene expression, including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex

122 and positive selection of conventional human T cells from all sources of HSPCs.

123 vivo antiviral inhibitory activity of CD8(+) T cells from elite controllers than from HIV-1 progresso

124 47, is a tegument antigen targeted by CD8(+) T cells from HSV-seropositive individuals.

125 ced significantly more IL-17 than gammadelta T cells from infected unprimed mice.

126 D57 was significantly up-regulated in CD8(+) T cells from patients with hepatitis delta.

127 tative restriction factors in primary CD4(+) T cells from rhesus macaques under various conditions, f

128 Furthermore, gammadelta T cells from the lungs of mice reinfected with B. pertus

129 lls (and, to a lesser extent, cardiac CD3(+) T cells) from donor mice with HF induced long-term left

130 sion of CD200 (OX2), a negative regulator of T-cell function that binds CD200 receptor (CD200R), is c

131 )alpha4beta7(high) subsets enhanced Th1/Th17 T cell generation and accumulation in the intestine, and

132 ade (ICB)-mediated rejuvenation of exhausted T cells has emerged as a promising approach for treating

133 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as a therapeutic tar

134 Virus-specific CD8 T cells home to the site of recurrent infection and part

135 on the role of cell death in maintenance of T-cell homeostasis and outline novel therapeutic strateg

136 gh- or low-affinity InsB9-23-reactive CD4(+) T cells; however, we observe an increase in the proporti

137 Blockade of ICOSL rescues T cell ICOS surface expression and rescues, at least in

138 acted in synergy in the thymus to establish T cell identity and to suppress the aberrant development

139 current helminth infection potently inhibits T cell immunity; however, whether helminthes prevent T c

140 n-2 inducible T cell kinase (Itk) results in T cell immunodeficiency in mice and humans.

141 des a proof of principle that suboptimal CD8 T cell in old organisms can be optimized by manipulating

142 d CCR10, are upregulated on HSV-specific CD8 T cells in blood.

143 We measured the abundance of T cells in circulation and intestinal tissues that respo

144 rucial role of effective HIV-specific CD8(+) T cells in controlling HIV-1 replication.

145 ed antiviral capacity of HIV-specific CD8(+) T cells in elite controllers to inhibit HIV infection.IM

146 udy is to explore the role of natural killer T cells in impaired liver regeneration.

147 Pathogenic T cells in individuals with rheumatoid arthritis (RA) in

148 engraftment (TME), the presence of maternal T cells in peripheral blood before transplantation, is d

149 Despite emerging data indicating a role for T cells in profibrotic cardiac repair and healing after

150 In this study, we focused on the role of T cells in the maintenance/survival of the mature naive

151 ity of H1N1- and H3N2-specific memory CD8(+) T cells, including tissue-resident cells, compared with

152 ShRNA knockdown of La in HEK 293 T cells increased Sendai virus infection efficiency, dec

153 D70 limits T cell expansion via a regulatory T cell-independent mechanism that involves caspase-depen

154 is is an autoimmune disease characterized by T-cell infiltration in the skin that leads to fibrosis,

155 Invariant natural killer T cells (iNKT cells) are innate-like lymphocytes that pr

156 nstrates that CCL2 enables the prolonged MSC-T cell interactions needed for sufficient suppression of

157 The differentiation of naive CD8 T cells into effector cytotoxic T lymphocytes upon antig

158 capable of transforming primary human CD4(+) T cells into immortalized cell lines indistinguishable f

159 Here, we demonstrated that T-cell intrinsic MyD88 signaling is required for prolife

160 ghlight the need for further analysis of the T cells involved in insulitis to elucidate their role in

161 tiviral capacity of some HIV-specific CD8(+) T cells is a consequence of factors in addition to TCR s

162 shown that the proportion of natural killer T cells is markedly elevated during liver regeneration a

163 ld type and tristetraprolin-deficient CD8(+) T-cells is comparable.

164 T cells isolated from TAC-treated hearts show enhanced p

165 he Tec family kinase Interleukin-2 inducible T cell kinase (Itk) results in T cell immunodeficiency i

166 1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/t

167 Human T-cell leukemia virus type 1 (HTLV-1) is the etiological

168 whereas B cell-deficient mice showed CD4(+) T cell loss but recovered from infection without lethali

169 utely transforming retrovirus AKT8 in rodent T-cell lymphoma/signal transducer and activator of trans

170 Activated and memory CD4 T cells, macrophages, and dendritic cell (DC) showed che

171 propose that sulfatide recognition by innate T cells may be an important pathologic feature of neuroi

172 Pdcd1 (PD-1) disruption augmented CAR T cell mediated killing of tumor cells in vitro and enha

173 eg) subset that suppresses follicular helper T cell-mediated B cell responses in the germinal center

174 sms whereby HIV infection impedes successful T cell-mediated control of M. tuberculosis have not been

175 shown that psoriasis represents a bona fide T cell-mediated disease primarily driven by pathogenic T

176 Central to CD8(+) T cell-mediated immunity is the recognition of peptide-m

177 ntDeltadriven vectorial migration, while CD8 T cell migration across LEC was not.

178 Effector T cell migration through tissues can enable control of i

179 nse rates have been reported with the use of T cells modified by chimeric antigen receptor (CAR) that

180 n receptor (TCR) expressed by natural killer T cells (NKT cells) and the antigen-presenting molecule

181 rance, but increased IL-22 in vivo decreased T cell numbers and functions in the liver and lymphoid t

182 gen-presenting capacity of DCs and increased T-cell numbers.

183 a production by blood and lymph node-derived T cells of patients with CVID with immune dysregulation

184 e characterized the DNA methylome in primary T cells of patients with systemic sclerosis.

185 ed of extracellular release by infected CD4+ T cells on protein quality control and autophagy in card

186 er percentage of CD4+CD25hiFoxP3+ regulatory T cells (P < .01), but higher proportions of IgM+CD21-/l

187 ion between IFNG-secreting and non-secreting T cells (P < 1 x 10(-5)).

188 CARs are designed with elements that augment T cell persistence and activity.

189 etection method, phenotype/genotype (B cell, T cell, Philadelphia chromosome), and EFS and OS.

190 de of Aspergillus fumigatus and ensuing CD4+ T-cell polarization are poorly characterized.

191 Furthermore, antibody-mediated depletion of T cells prevented nasopharyngeal infection by S. pyogene

192 Indeed, absence of CD8(+) T cells prevented recovery from MRV infection and led to

193 pe mice, and adoptive transfer of gammadelta T cells prevented sensitization.

194 mmunity; however, whether helminthes prevent T cell priming or skew clonal recruitment and effector d

195 In addition, CD4 T cells produced less interferon-gamma in response to T-

196 egative regulator of IL-7R-STAT signaling in T cell progenitors, contributing to both the quantitativ

197 results from the transformation of immature T-cell progenitors.

198 ly shown to be involved in the regulation of T cell proliferation and function.

199 ophages is one pathway that suppresses local T cell proliferation.

200 nomonitoring to assess allergen-specific CD4 T-cell properties in parallel with analysis of local muc

201 Here, we have identified T cell protein tyrosine phosphatase (TC-PTP), also known

202 functional studies define landscapes of the T cell proteome and phosphoproteome and reveal signaling

203 The TCR repertoire of Gag293-specific CD4(+) T cells proved highly biased, with a predominant usage o

204 ur findings demonstrate that lung gammadelta T cells provide an early source of innate IL-17, which p

205 a hepatitis B virus-specific (HBV-specific) T cell receptor (TCR) may supplement HBV-specific immune

206 Defects in T cell receptor (TCR) repertoire are proposed to predisp

207 ic monoclonal antibodies (mAb) targeting the T-cell receptor coregulatory molecule GITR exert potent

208 We revealed that altering T-cell receptor stimulation influenced recruitment of mR

209 Using T-cell receptor-beta sequencing and tumour reactivity as

210 Sequence analysis of T-cell receptors of CD8(+) T cells revealed the presence

211 activity has been correlated with activated T-cell recognition of neoantigens, which are tumour-spec

212 FN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expression of Th1 and Th2 associated tr

213 trauma, including induction of Th17-type CD4 T cells, reduced T-bet expression by natural killer cell

214 n CD4(+)CD8(+) thymocytes resulted in skewed T cell repertoire, contributing to a reduction in the fr

215 CD8(+) T cells require sustained Ca(2+) signaling for inflammat

216 Detailed knowledge of the T cell response may further contribute to the identifica

217 se (ROCK)2 downregulates the proinflammatory T cell response while increasing the regulatory arm of t

218 is infection contribute significantly to its T cell response.

219 Although the effector T-cell response in patients with celiac disease has been

220 This study aimed to determine the T-cell response to Phl p 12 in profilin-sensitized patie

221 the cultured ELISPOT assay detected a higher T-cell response to pp65 than to IE-1 or IE-2, whereas in

222 The immune system can mount T cell responses against tumors; however, the antigen sp

223 key transcriptional determinant controlling T cell responses during transplantation.

224 were successful in the induction of NAbs and T cell responses in guinea pigs.

225 s that induce strong peptide-specific CD8(+) T cell responses in vivo by incorporating an NKT cell-ac

226 Moreover, IL-22 deficiency enhanced T cell responses to promote viral clearance, but increas

227 Fibroblasts possess the capacity to suppress T cell responses, although the molecular mechanisms of t

228 that share cross-reactivity in antibody and T cell responses, and co-circulate in increasing numbers

229 esponses in preclinical models, particularly T cell responses, remain sparse.

230 itizing cytokines and promotion of antitumor T cell responses.

231 n and the subsequent development of effector T cell responses.

232 escribe the appearance of transgene-specific T-cell responses in two subjects that were part of the p

233 tabolism and function to limit DC-stimulated T-cell responses.

234 kade (ICB) therapies can unleash anti-tumour T-cell responses.

235 iency of the master regulator Bcl6 in CD4(+) T cells resulted in a marked reduction in TFH cell numbe

236 We find that EZH2 deficiency in FOXP3(+) T cells results in lethal multiorgan autoimmunity.

237 uence analysis of T-cell receptors of CD8(+) T cells revealed the presence of H-2L(d)/AH1-specific T

238 tic cells and macrophages as well as resting T-cells, SAMHD1 blocks HIV-1 infection through this dNTP

239 lying dermis, predominantly composed of CD3+ T cells, scattered CD20+ B cells, and relatively few PD-

240 is showed increased T-cell activation, naive T-cell skewing, and elevated serum CXCL9 and CXCL10 leve

241 to proliferation, is common in newly arising T cells (so-called "recent thymic emigrants") in adults,

242 ever, the fratricide conferred by SLAMF7-CAR T cells spares the SLAMF7(-/low) fraction in each cell s

243 t & Microbe, Moguche et al. (2017) show that T cells specific for different immunodominant vaccine an

244 T cell-specific deletion of talin in Tln1(fl/fl)Cd4(Cre)

245 THEMIS, a T cell-specific protein with high expression in CD4(+)CD

246 CD8(+) T cell specificity depends on the recognition of MHC cla

247 roduced less interferon-gamma in response to T-cell stimulation.

248 metabolic programs of functionally distinct T cell subsets are tailored to their immunologic activit

249 Collectively, these findings identify CD4(+) T cell subsets with properties critical for improving ca

250 At T0, the frequencies of CD4 T cell subsets, including peripheral T follicular helper

251 eously study the responsiveness of different T cell subsets, that is, naive, effector, and memory T c

252 T cells subsets in blood, spleen and lymph nodes were de

253 here, integrates the activities of distinct T-cell subsets and by definition is dynamic and responsi

254 tumor-infiltrating, miR-155-deficient CD8(+) T cells, suggesting that miR-155 and ICB regulate overla

255 s tailored to manipulate cell death to limit T-cell survival (eg, autoimmunity and transplantation) o

256 autoimmunity and transplantation) or enhance T-cell survival (eg, vaccination and immune deficiency).

257 d the frequency of IFN-gamma secreting total T cells, T-helper and CTLs against both H1N2 and H1N1 Sw

258 (OXPHOS) for energy production, and effector T cells (Teffs) rely on glycolysis for proliferation, th

259 s and steps controlling postinfection CD8(+) T cell terminal effector versus memory differentiation a

260 To test this hypothesis, we compared 3 CAR T-cell termination strategies: (1) transiently active an

261 l rates result in near-optimal production of T cells that are capable of surviving selection and reco

262 ent a small subset of glycolipid-recognizing T cells that are heavily implicated in human allergic, a

263 neration of CD4 effector and effector memory T cells that contribute to protection.

264 activin-A instructs the generation of CD4(+) T cells that express the Tr1-cell-associated molecules I

265 In dysfunctional T cells that have a decreased cytotoxic capacity, 4-1BB

266 iated disease primarily driven by pathogenic T cells that produce high levels of IL-17 in response to

267 Here, we show that in developing T cells, the Bcl11b enhancer repositioned from the lamin

268 Efforts to improve the efficacy of adoptive T-cell therapies and immune checkpoint therapies in myel

269 ed from PD-1(+) TILs can be used in adoptive T-cell therapy (ACT).

270 tate safer application of effective CD19 CAR T-cell therapy.

271 ed by HLA-DQ2/8-restricted responses of CD4+ T cells to cereal gluten proteins.

272 and chemotaxis of previously activated human T cells to CXCL11, but not CXCL10 or CXCL12.

273 egs and M2-like macrophages and reduces CD8+ T cells to promote lung tumor growth.

274 ression of the transcription factor Foxp3 in T cells, trans-presentation of IL-6 by DC-bound IL-6Ralp

275 cursor effector subset of virus-specific CD8 T cells transferred into antigen-free mice revealed that

276 ed in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, suggesting mTORC1 signal

277 T (TFR) cells are a newly defined regulatory T cell (Treg) subset that suppresses follicular helper T

278 he distinct metabolic features of regulatory T cells (Tregs) are less well established.

279 Regulatory T cells (Tregs) in skin preferentially localize to hair

280 these cells into CD4+CD25+FoxP3+ regulatory T cells (Tregs).

281 ibitory receptor blockade partially reversed T cell unresponsiveness.

282 equivalent between control and EVL/VASP dKO T cells upon alpha4 integrin blockade.

283 While quiescent T cells use oxidative phosphorylation (OXPHOS) for energ

284 n resting naive, central and effector memory T cells using ChIP-Seq and found that unlike the naive c

285 ncy of Pf-specific polyfunctional CD4 memory T cells was associated with protection.

286 patients, the frequency of CD1b-autoreactive T cells was increased compared with that in healthy cont

287 ive capacity of M. tuberculosis-specific CD4 T cells was markedly impaired in HIV-infected individual

288 Mitochondrial flux from ASMCs to T cells was partially FGF2b and FGFR1 dependent.

289 Trauma-induced expansion of Th17-type CD4 T cells was seen with increased expression of interleuki

290 sted TILs and in acutely restimulated CD8(+) T cells, we define a pattern of chromatin accessibility

291 5) Finally, SERCA2a 971-990-sensitized T cells were able to transfer disease to naive recipient

292 eads in the inner chamber produced ET-1 when T cells were activated with antigen or anti-CD3 antibody

293 te infection pp65-, IE-1-, and IE-2-specific T cells were detected at comparable levels.

294 The Ag specificities of these activated T cells were determined by a novel CD154 T cell epitope

295 ro T cell culture system, MART1-specific CD8 T cells were expanded from healthy donors using artifici

296 The OVA-specific CD4 T cells were then analyzed for IL-13 and IFN-gamma expre

297 These properties license CD26(high) T cells with a natural capacity to traffic to, regress a

298 a recently discovered, innate-like subset of T cells with cytotoxic function, the role of which in lu

299 PD-1 identifies "exhausted" CD8 T cells with impaired HIV-specific effector functions, b

300 LP2A retention was driven by macrophages and T cells, with less contribution from neutrophils and B c