ライフサイエンスコーパス: CD4 T-cell

1 c-5p in response to TCR stimulation in naive CD4 T cells.

2 sis-specific IFN-gamma(+)IL-2(-)TNF-alpha(+) CD4 T cells.

3 tential as targets of antigen recognition by CD4 T cells.

4 he presence of IL-27-responsive conventional CD4 T cells.

5 ranscriptionally silent in latently infected CD4+ T cells.

6 ockout), with antibody-mediated depletion of CD4+ T cells.

7 body required the adaptive immune system and CD4+ T cells.

8 ls in both sample sources when compared with CD4+ T cells.

9 plaque development in mice with and without CD4+ T cells.

10 ke altered the cytokine profile of activated CD4+ T cells.

11 lp explain the preferential infection of gut CD4(+) T cells.

12 rther differentiate into IFN-gamma-producing CD4(+) T cells.

13 vement of HLA-DQ2-restricted gluten-specific CD4(+) T cells.

14 in neonatal mice, characterized by a loss of CD4(+) T cells.

15 ggestive of tissue residency, such as CD69(+)CD4(+) T cells.

16 latory regions in immune cells, particularly CD4(+) T cells.

17 ral levels and massive ablation of pulmonary CD4(+) T cells.

18 es recognition of human and MCM SIV-infected CD4(+) T cells.

19 gher ratio of effector T cells to regulatory CD4(+) T cells.

20 ial to induce IL-22 expression by intestinal CD4(+) T cells.

21 ced frequency of IL-17- and GM-CSF-producing CD4(+) T cells.

22 ges in the number or function of circulating CD4(+) T cells.

23 tely suppressed by Stat3 deficiency in donor CD4(+) T cells.

24 along with a decreased TH17 phenotype within CD4(+) T-cells.

25 ations between integrated HIV DNA with PD-1+ CD4+ T-cells (1.44 fold-change in integrated HIV DNA per

26 te function of the class I-restricted TCR in CD4(+) T cells; (3) an inducible caspase 9 safety switch

27 grated HIV DNA per 10-unit increase in PD-1+ CD4+ T cells; 95% CI = 1.01-2.05; P = .045) and CD38+HLA

28 In human CD4(+) T cells, a 5-d exposure to BET inhibitors was acc

29 e that permitted sampling of more than 10(7) CD4+ T cells, a requirement for detecting exceedingly ra

30 ificantly enhanced tumor necrosis, extensive CD4 T cell accumulation, and high levels of the proinfla

31 -deficient CD4(+) T cells, as well as murine CD4(+) T cells activated in the presence of rapamycin, a

32 frequency within circulating gluten-specific CD4(+) T cells after oral gluten challenge of patients w

33 Unlike effector CD4(+) T cells, an MHC class II tetramer reagent specifi

34 ted in CXCR5 induction (mRNA and protein) in CD4 T cells and IL21 gene induction in pTfh cells that w

35 specific effector functions, but its role on CD4 T cells and in HIV-infected children is poorly under

36 anced in mice lacking expression of IL-6R by CD4(+) T cells and by treatment of wild-type mice with n

37 terferon- and tumor necrosis factor-positive CD4(+) T cells and CD8(+) T cells.

38 (+) type 2 innate lymphoid cells and IL-13(+)CD4(+) T cells and IL-5 and IL-13 production by lymph no

39 ta expression in mesenteric lymph node (MLN) CD4(+) T cells and jejunum were monitored.

40 Arterial wall dendritic cells attract CD4(+) T cells and macrophages to form prototypic granul

41 ession, including CD8(+) T cells for age and CD4(+) T cells and monocytes for sex, we detected a dire

42 ppressed TH2 responses from Bet v 1-specific CD4(+) T cells and prevented allergic sensitization in a

43 er ligation) reduced cardiac infiltration of CD4(+) T cells and prevented progressive left ventricula

44 ntly dephosphorylated in both Rheb-deficient CD4(+) T cells and T cells treated with rapamycin, sugge

45 esponse that was dominated by polyfunctional CD4(+) T cells and that targeted multiple antigenic regi

46 pathway, TSCM -->Central -->Effector memory CD4(+) T cells and the innate pathway consisting of the

47 TCR) with specificity for ovalbumin (OVA) on CD4(+)-T cells and cMy-mOVA mice expressing OVA on cardi

48 ne expression in stimulated peripheral blood CD4+ T cells and ex vivo human skin, and impacts barrier

49 Absolute counts and % of CD4+ T cells and Treg cells (CD4 + CD25 + FOXP3 + CD127d

50 inant IL-32gamma blocked HIV reactivation in CD4+ T-cells and was associated with an increase in RUNX

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

52 cytokine-producing M. tuberculosis-specific CD4 T cells, and preferential depletion of a discrete su

53 ysis identifies changes in neutrophil, naive CD4(+) T cell, and macrophage populations during peanut

54 production by autologous, NTHi-specific lung CD4(+) T cells, and cytokine production was inhibited by

55 extensive proliferation of transferred naive CD4(+) T cells, and significant uveoretinitis.

56 lure was associated with increased senescent CD4+ T cells, and reduced naive and effector and central

57 on between CCR5 CRPA and both CD4 counts and CD4 T cell apoptosis.

58 We have shown that CTLA-4(+)PD-1(-) memory CD4(+) T cells are a previously unrecognized component o

59 he mechanisms leading to IL-10 expression by CD4(+) T cells are being elucidated, with several cytoki

60 CD4(+) T cells are central mediators of autoimmune patho

61 that effector-to-memory transitioning (EMT) CD4(+) T cells are particularly permissive for the estab

62 Stat3 is constitutively acetylated and naive CD4(+) T cells are potentiated in Th17/Treg cell differe

63 t not Foxp3(-) effector T-cells (Teff), when CD4(+) T-cells are co-cultured with GM-CSF derived bone

64 15, Mx1; each P < .0001) were upregulated in CD4+ T cells as demonstrated by RNA sequencing.

65 ctivated murine wild-type and Rheb-deficient CD4(+) T cells, as well as murine CD4(+) T cells activat

66 effectively promoted reactivation of resting CD4+ T-cell, as indicated by an increased viral transcri

67 Notably, increased functional CD4 T cell avidity improved antiviral efficacy of CD8 T

68 ive-transfer approach, we show that naive Tg CD4 T cells become activated, proliferate, migrate to th

69 roportion of all circulating gluten-specific CD4(+) T cells but had impaired suppressive function, in

70 has been reported to detect live Ag-specific CD4(+) T cells, but this approach remains underexplored

71 CD4 T cells can differentiate into multiple effector sub

72 ass IA PI3K isoforms in these two subsets of CD4(+) T cells can be exploited to target Treg while lea

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

74 s, and slower interaction of these HRVs with CD4+ T cells, CD8+ T cells, and CD19+ B cells.

75 nation, the proportion of influenza-specific CD4(+) T cells coexpressing CD161 was significantly high

76 nd Foxp3(-)FR4(hi)CD73(hi) anergic phenotype CD4(+) T cells compared with Bim(-/-) mice, suggesting t

77 patients with T1D have increased tetramer(+) CD4(+) T cells compared with HLA-matched control subject

78 hese markers to recapitulate the whole CD3(+)CD4(+) T cell compartment remains questionable.

79 An emergent population of peripheral CD4 T cells conferred protection against new tumors and

80 Activated CD4 T cells connect to airway smooth muscle cells (ASMCs

81 hat were derived from such clonally expanded CD4+ T cells constituted 62% of all analyzed genome-inta

82 easing evidence suggests that virus-specific CD4(+) T cells contribute to the immune-mediated control

83 deficiency virus-infected patients who had a CD4 T-cell count <100 cells/microL and negative serum cr

84 , or not receiving antiretrovirals and had a CD4 T-cell count of greater than 500 cells per muL.

85 aluated in patients who do not regain normal CD4 T cell counts after virologically successful antiret

86 CRP levels were correlated with increases in CD4 T-cell counts.

87 th eosinophil counts and not associated with CD4 T-cell counts.

88 uals termed elite controllers (ECs) maintain CD4(+) T cell counts and control viral replication in th

89 Since the reduced number of CD4(+) T cell counts in patients' peripheral blood corre

90 l therapy (ART) correlated with HIV viremia, CD4(+) T-cell counts, and immune activation markers, sug

91 retroviral therapy, HIV-1 persists in memory CD4(+) T cells, creating a barrier to cure.

92 These data provide evidence implicating CD4(+) T-cell cytokines in the pathogenesis of RCDII.

93 or CD137 with an agonistic antibody enhanced CD4+ T cell cytotoxicity.

94 ed with increased M. tuberculosis Ag-induced CD4 T cell death ex vivo, indicating a possible mechanis

95 HIV-1-controllers from those who experience CD4(+)T-cell decline.

96 lls to determine (1) intrinsic and extrinsic CD4(+) T-cell defects and (2) how defects account for th

97 tion of the H3K27 demethylase JMJD3 in naive CD4 T cells demonstrates how critically important molecu

98 n important mechanism underlying progressive CD4(+) T cell depletion in vivo.

99 Antibody-mediated CD4(+) T-cell depletion in HF mice (starting 4 weeks aft

100 ine models of GVHD to evaluate the effect of CD4+ T cell depletion on GVL versus GVHD and revealed th

101 ion factor Thpok is required for intrathymic CD4(+) T cell differentiation and, together with its hom

102 , therefore, examined cytokine signaling and CD4(+) T cell differentiation in these cohorts to charac

103 e Akt/mTOR pathway is a key driver of murine CD4(+) T cell differentiation, and induction of regulato

104 (+) (TH1/17) and IFN-gamma(-)IL-17(+) (TH17) CD4(+) T cells display distinct transcriptional profiles

105 ory T (T reg) cell deficiency causes lethal, CD4(+) T cell-driven autoimmune diseases.

106 Associations between thymic function and CD4 T-cell dynamics and combination antiretroviral thera

107 d, resulting in enhanced PD-1 expression and CD4(+) T cell dysfunction.

108 monstrated that temporary depletion of donor CD4+ T cells early after hematopoietic cell transplantat

109 ke of exosomes, derived from IL-2 stimulated CD4+ T cells, effectively promoted reactivation of resti

110 we were able to identify a MHCII-restricted CD4 T cell epitope, corresponding to amino acids 37-47 i

111 MHC class II alleles for immunodominant Gag CD4(+) T cell epitopes in clade C virus infection, const

112 The use of A2aR-deficient CD4 T cells established that this CGS effect was T cell

113 r ability to re-stimulate influenza-specific CD4 T cells ex vivo.

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

115 Jejunal CCR5(+) CD4(+) T cells exhibited the highest levels of SIV RNA,

116 , implicating this molecule as a trigger for CD4(+) T cell expansion.

117 tory T cells (Treg cells) as well as CD25(+) CD4(+) T cells expressing the inhibitory receptor CTLA4.

118 Transcriptional regulation during CD4(+) T cell fate decisions enables their differentiati

119 e also found differences in functionality of CD4 T cells following blocking of different inhibitory r

120 Endogenous myelin peptide presentation to CD4(+) T cells following phagocytosis of injured, phosph

121 Conversely, ROS were highly elevated in CD4 T cells from mice ectopically expressing PLZF.

122 p24 in phytohemagglutinin-L (PHA)-stimulated CD4(+) T cells from individuals under effective cART.

123 ndogenous lipids, a subpopulation of primary CD4(+) T cells from multiple donors was consistently act

124 CD4(+) T cells from patients with ALF had a reduced prol

125 mpared to cells from controls; incubation of CD4(+) T cells from patients with ALF with an antibody a

126 HIV/SIV restriction factors was analyzed in CD4(+) T cells from peripheral blood and the jejunum in

127 and putative restriction factors in primary CD4(+) T cells from rhesus macaques under various condit

128 Although CD4(+) T-cells from PKC-(-/-) mice were also defective i

129 CD4+ T cells from rectal tissue had a higher frequency o

130 e are not caused primarily by impairments in CD4 T cell function but result from defects in innate im

131 ibitory receptor expression depending on the CD4 T cell function.

132 rs; however, its role as a dual modulator of CD4(+) T cell function and metabolism has not been defin

133 (hyh/hyh) mice harbor significant defects in CD4 T cell gene expression and Foxp3 regulatory T cell (

134 To determine the functional capacity of CD4 T cells generated by chronic infection upon reexposu

135 entical, consistent with clonal expansion of CD4+ T cells harboring intact HIV-1.

136 t the mechanisms by which they interact with CD4(+) T cells has been controversial.

137 phenomena implicate the potential of altered CD4(+) T-cell help.

138 and, together with its homolog LRF, supports CD4(+) T cell helper effector responses.

139 h17 differentiation pathways in autoreactive CD4 T cells, highlighting its potential as a therapeutic

140 In contrast, NOD.Tnfrsf9(-/-) CD4 T cells highly promoted T1D development.

141 n of high- or low-affinity InsB9-23-reactive CD4(+) T cells; however, we observe an increase in the p

142 ry S. venezuelensis infection is as follows: CD4(+) T cells/ILC2 cells, IgG, and FcRgamma>mast cells>

143 ponds to the progression of HIV disease, our CD4(+) T cell-immunosensor provides a simple and low-cos

144 ctional capacity of M. tuberculosis-specific CD4 T cells in HIV-infected and HIV-uninfected adults wi

145 M. tuberculosis-specific CD4 T cells in HIV-infected individuals expressed signif

146 erative capacity of M. tuberculosis-specific CD4 T cells in HIV-infected individuals.

147 the antigens to autologous antigen-specific CD4(+) T cells in a major histocompatibility complex cla

148 view captures recent knowledge on pathogenic CD4(+) T cells in asthmatic patients by drawing on obser

149 YV (DYS) epitope to characterize circulating CD4(+) T cells in coinfected HLA-DR7(+) long-term nonpro

150 P = 0.0001), and these expanded Gag-specific CD4(+) T cells in HIV controllers showed higher levels o

151 requencies of MHC class II tetramer-positive CD4(+) T cells in HIV controllers than progressors (P =

152 Activated memory CD4(+) T cells in intestinal tissues are major primary t

153 2B4 expression is increased on CD4(+) T cells in septic animals and human patients at e

154 y of data regarding the role of HIV-specific CD4(+) T cells in shaping adaptive immune responses in i

155 kedly expanded population of PD-1(hi)CXCR5(-)CD4(+) T cells in synovium of patients with rheumatoid a

156 ed interactions between Il27ra (-/-) APC and CD4(+) T cells in the aortic wall contribute to T cells

157 nmental triggers of the aberrant presence of CD4(+) T cells in the CNS are not known.

158 perimental data suggest that the majority of CD4(+) T cells in tissue die through abortive infection,

159 etion of Mycobacterium tuberculosis-specific CD4+ T cells in blood during early HIV infection, but li

160 major activated reservoir cells were memory CD4+ T cells in vivo.

161 i-CD20 Ab had a major effect on alloreactive CD4(+) T cells, increasing the expansion of this populat

162 ble in both cell lysates and supernatants in CD4+ T cells infected in vitro at frequencies as low as

163 ional keratinocytes associated with a marked CD4+ T cell infiltration, which peaked on days 10-11 aft

164 f pathogens through differentiation of naive CD4 T cells into functionally distinct subsets of effect

165 ALK is capable of transforming primary human CD4(+) T cells into immortalized cell lines indistinguis

166 n I-A(12%) mice, transfer of I-A(12%) CD25(-)CD4(+) T cells into RAG-knockout hosts revealed increase

167 in macrophages drives the differentiation of CD4(+) T cells into tumor-promoting T helper type 2 cell

168 that expression of TSLP receptor (TSLPR) on CD4 T cells is required for OVA-induced lung inflammatio

169 Expansion of PSGL-1(lo)CD4(+) T cells is also prevented by BCL6 or Stat3 defici

170 The inhibition of CD4(+) T cells is dependent on TGF-beta, whereas inhibit

171 our evidence indicates that the presence of CD4(+) T cells is of critical importance but mast cells,

172 that the major effector function of neonatal CD4(+) T cells is to produce CXCL8, a prototypic cytokin

173 f long-lived reservoirs of latently infected CD4+ T cells is the major barrier to curing HIV, and has

174 ed similar effects on the differentiation of CD4+ T cells isolated from human peripheral blood mononu

175 T cell polarization was analysed in CD4+ T cells isolated from spleens and lymph nodes of ar

176 CD4 T cells lacking Atg3 or Atg5 have increased interleu

177 L versus GVHD and revealed that depletion of CD4+ T cells leads to the upregulation of PD-L1 by recip

178 nimals, whereas B cell-deficient mice showed CD4(+) T cell loss but recovered from infection without

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

180 s, CD4(+)CD8(-) T cells, regulatory T cells, CD4(+) T cell marker expression, lifespan, and Th/regula

181 Expansion of HIV-infected CMV/EBV-specific CD4 + T cells may contribute to maintenance of the HIV D

182 Alloreactive CD4 T cell-mediated MVEC death involves TNFalpha, Fas li

183 CD4(+) T cell-mediated tissue damage and subsequent IL-3

184 and 5-FU treatment in optimally activating a CD4+ T cell-mediated immunity against actinic keratoses

185 cterise the kinetics and structure of murine CD4 T cell memory subsets by measuring the rates of infl

186 To determine whether HCMV epitope-specific CD4(+) T cell memory inflation occurs during HIV infecti

187 ction factors substantially increased in all CD4(+) T cell memory subsets at the peak of acute infect

188 ncy events in patients with greater than 500 CD4(+) T cells/muL.

189 However, cervical CD4+ T-cell number was associated with HSV-2 infection a

190 an abnormal distribution of memory and naive CD4 T cells occurred, and peripheral CD4 and CD8 T cells

191 Importantly, CD4 T cells of higher functional avidity induced by low-

192 omal targeting and reduced surface levels on CD4(+) T cells of EHD1/3/4 knockout mice.

193 spected of extracellular release by infected CD4+ T cells on protein quality control and autophagy in

194 -specific T-cell responses were dominated by CD4(+) T cells (P < 0.001 compared to CD8(+) T cells) th

195 charide of Aspergillus fumigatus and ensuing CD4+ T-cell polarization are poorly characterized.

196 lly differentiated T cells contribute to the CD4(+) T-cell pool in the atherosclerotic aorta.

197 We also observed changes in CD4+ T-cell population diversity and clonal viral sequen

198 Last, PD-1+ CD4 T cells predict impaired proliferative potential yet

199 These activated CD4(+) T cells preferentially expressed TRBV4-1(+) TCRs.

200 In addition, CD4 T cells produced less interferon-gamma in response t

201 Upon infection, an activated CD4(+) T cell produces terminally differentiated effecto

202 ved (but not Th1/Th17-derived) EVs inhibited CD4(+) T cell proliferation and suppressed two relevant

203 nic Tregs from IL233-treated mice suppressed CD4(+) T cell proliferation better than Tregs from salin

204 immunomonitoring to assess allergen-specific CD4 T-cell properties in parallel with analysis of local

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

206 Investigations into the DOCK8-deficient CD4(+) T cells provided an explanation for some of the c

207 RT is not curative due to the persistence of CD4+ T-cell proviral reservoirs that chronically resuppl

208 uld be related to a loss of circulating Th1* CD4(+) T cells rather than major changes in the number o

209 y and clonal viral sequence expansion during CD4+ T-cell reconstitution following chemotherapy cessat

210 Despite success in viral inhibition and CD4 T cell recovery by highly active antiretroviral trea

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

212 es of IFN-gamma-, IL-5-, and IL-13-producing CD4(+) T cells, reduced expression of Th1 and Th2 associ

213 l bacteria is a normal property of the human CD4(+) T-cell repertoire, and does not necessarily indic

214 lls to eliminate the HIV-1 latently infected CD4+ T-cell reservoir.

215 The Chlamydia-specific CD4 T cell response is characterized by the production o

216 no acids in length can accurately identify a CD4 T cell response to ovalbumin against a background re

217 VS is important for boosting optimal primary CD4(+) T cell response during NS4B-P38G vaccination.

218 ction of antiviral cytokines and an impaired CD4(+) T cell response in peripheral organs.

219 The HCMV-specific CD4(+) T cell response to pp65, IE1, IE2, and gB was pre

220 disease was associated with the induction of CD4 T cell responses and the epitope preferentially bind

221 a specific inhibitor of mTOR, on B cell and CD4 T cell responses during acute infection with lymphoc

222 nses by differentially regulating B cell and CD4 T cell responses during acute viral infection and th

223 ) glycoprotein (GP) and examined GP-specific CD4 T cell responses elicited by Ad5 vectors and compare

224 mice displayed markedly reduced Ag-specific CD4 T cell responses within the local draining iliac lym

225 Here we show blood central memory CD4 T-cell responses specific to Mtb dormancy related (D

226 is (TB) is that the attributes of protective CD4(+) T cell responses are still elusive for human TB.

227 d relation to the viral load of HIV-specific CD4(+) T cell responses in a cohort of untreated HIV cla

228 sorbent spot assay to interrogate CD8(+) and CD4(+) T cell responses in healthy volunteers infected w

229 lass II tetramers in evaluating HIV-specific CD4(+) T cell responses in natural infections.IMPORTANCE

230 Importantly, CD4(+) T cell responses in vaccinees were similar in mag

231 ers develop particularly efficient antiviral CD4(+) T cell responses mediated by shared high-affinity

232 s to ensure proper programming of CD8(+) and CD4(+) T cell responses to viral infection.

233 , but not the MVAgp140 boost, increased peak CD4(+) T cell responses.

234 boosts, may be further impacted by increased CD4(+) T cell responses.IMPORTANCE Prior immune correlat

235 Furthermore, depletion of CD8 and CD4 T cells resulted in loss of early control of virus r

236 l deficiency of the master regulator Bcl6 in CD4(+) T cells resulted in a marked reduction in TFH cel

237 Adoptive transfer of allospecific transgenic CD4 T cells revealed a "split tolerance" status in mAAQ(

238 n of endogenous memory-like I-A(12%) CD44(hi)CD4(+) T cells revealed highly elevated production of mu

239 We isolated circulating CD4(+) T cells specific for immunoglobulin-derived neoan

240 CD4(+) T cells specific to the HCMV proteins studied wer

241 At T0, the frequencies of CD4 T cell subsets, including peripheral T follicular he

242 NAs specifically released by different human CD4(+) T cell subsets and started to unveil the potentia

243 sponses against tumor, but the role of human CD4(+) T cell subsets in cancer immunotherapy remains il

244 lated mutant Delta5G virus infected distinct CD4(+) T cell subsets in SLOs and the small intestine, r

245 Collectively, these findings identify CD4(+) T cell subsets with properties critical for impro

246 , lymph nodes, bone marrow, CSF, circulating CD4+ T cell subsets, and plasma.

247 mited in their ability to present antigen to CD4+ T cells suggesting that other mechanism of antigen

248 , IL-2 reduces this threshold in CD8 but not CD4 T cells, suggesting that integration of multiple mit

249 involved pathways were validated in primary CD4(+) T cells, target cells for HIV-1.

250 Infected follicular helper CD4 T cells, TFH, present inside B-cell follicles repres

251 developing a TCR-transgenic (Tg) mouse with CD4 T cells that respond to a common Ag in Chlamydia mur

252 bit HIV replication, especially in activated CD4(+) T cells that are the preferred target cells for t

253 displayed a phenotypic organization of CD3(+)CD4(+) T cells that confirmed their diversity but showed

254 tokine activin-A instructs the generation of CD4(+) T cells that express the Tr1-cell-associated mole

255 tions of Mycobacterium tuberculosis-specific CD4(+) T cells that leads to failed host resistance may

256 ticle, we report that murine and human naive CD4(+) T cells that sequester Pam3Cys4 (CD4(+) T(Pam3))

257 incurable disease due to its persistence in CD4+ T cells that contain replication-competent provirus

258 allows EBV-infected B cells to interact with CD4 T cells (the major source of CD40 ligand).

259 monstrated that these cytokines can activate CD4(+) T cells, the target cells for HIV infection.

260 cells depends on the presence or absence of CD4+ T cells, the nature of the interacting receptor exp

261 uated the safety and efficacy of an adoptive CD4(+) T-cell therapy using an MHC class II-restricted,

262 We validated these pathways in primary human CD4(+) T cells through Cas9-mediated knockout and antibo

263 V-1 transmission from infected to uninfected CD4(+) T cells through virological synapses (VS) has bee

264 nhibition leads the most self-reactive naive CD4 T cells to adopt the phenotype of their less self-re

265 he phenotype and function of DOCK8-deficient CD4(+) T cells to determine (1) intrinsic and extrinsic

266 However, the contribution of defects in CD4(+) T cells to disease pathogenesis in these patients

267 ribute to the differential susceptibility of CD4(+) T cells to SIV infection.

268 apacity of human innate-like CXCL8-producing CD4(+) T cells to transition directly into Th1 cells.

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

270 We compared the CD4(+) T-cell transcriptome in obese children with asthm

271 increase UBASH3A expression in human primary CD4(+) T cells upon TCR stimulation, inhibiting NF-kappa

272 ex vivo M. tuberculosis-specific tetramer(+)CD4(+) T cells using flow cytometry.

273 ce for the functional roles of Pn3P-specific CD4(+) T cells utilizing mouse immunization schemes that

274 was driven by IL-17-producing gammadelta and CD4(+) T cells via direct IL-36R signaling in the T cell

275 oth follicular and extrafollicular FOXP3(hi) CD4 T cells was found in the vaccine group compared with

276 erative capacity of M. tuberculosis-specific CD4 T cells was markedly impaired in HIV-infected indivi

277 Trauma-induced expansion of Th17-type CD4 T cells was seen with increased expression of interl

278 . tuberculosis infection, Il10 expression in CD4(+) T cells was partially regulated by both IL-27 and

279 criptome, methylome, and pathway analyses in CD4+ T cells, we show that vitamin D affects multiple si

280 ntage of splenic monocytes, neutrophils, and CD4 T cells were examined.

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

282 DOCK8-deficient memory CD4(+) T cells were biased toward a TH2 type, and this w

283 lucose transport and glycolysis in activated CD4(+) T cells were compromised in the absence of the IN

284 (+) Tfh cells, SIV-enriched CTLA-4(+)PD-1(-) CD4(+) T cells were found outside the B cell follicle of

285 Naive human CD4(+) T cells were short-term activated in the presence

286 ic interleukin-21 (IL-21)-secreting CXCR5(+) CD4(+) T cells were significantly associated with gp120-

287 While CXCR5(+) CD4(+) T cells were significantly diminished in HIV prog

288 ity despite the fact that their OVA-specific CD4(+)-T cells were not anergic.

289 Over 500 million CD4+ T cells were assayed from both participants in a hu

290 l analyzed genome-intact sequences in memory CD4 T cells, were preferentially observed in Th1-polariz

291 induced rapid sodium influx in Napa(hyh/hyh) CD4 T cells, which reduced intracellular ATP, [ATP]i.

292 caques, we show that CTLA-4(+)PD-1(-) memory CD4(+) T cells, which share phenotypic markers with regu

293 Furthermore, CD4 T cells with a TRM cell phenotype (CD44(+)CD62L(-)CD

294 Transduction of CD4(+) T cells with BIV Vif blocked HIV-1 replication.

295 lective capture and linear quantification of CD4(+) T cells with greater dynamic range.

296 Interestingly, pretreatment of CD4(+) T cells with IFNbeta, but not IFNalpha2, selected

297 Systemically, the proportion of activated CD4(+)-T cells with a Th1 and Th17 cytokine profile was

298 dant tumour infiltration of effector CD8(+), CD4(+) T cells, with increased IFN-gamma, ICOS, granzyme

299 evented by BCL6 or Stat3 deficiency in donor CD4(+) T cells, with the induction of cGVHD ameliorated

300 Pathogenic CD4(+) T cells within affected tissues may be identified