ライフサイエンスコーパス: CD4

1 CD4 count decreased by a median of -130 cells per muL (r

2 CD4 T cells can differentiate into multiple effector sub

3 CD4 TEMRA cells have been implicated in protective immun

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

5 CD4(+)CD161(+)Rho-effluxing T cells proliferated vigorou

6 ls (P < .05), CD4+IFNgamma+ cells (P < .01), CD4+IL17A+ cells (P < .01), and CD4+CXCR5+interleukin 21

7 s of IgM+CD21-/low memory B cells (P < .05), CD4+IFNgamma+ cells (P < .01), CD4+IL17A+ cells (P < .01

8 VRC01 is an HIV-1 CD4 binding site broadly neutralizing antibody (bnAb) th

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

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

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

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

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

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

15 ine regimen containing Env cross-linked to a CD4-mimetic miniprotein (gp140-M64U1) in rhesus macaques

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

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

18 ocytes and with an accumulation of activated CD4(+) Foxp3(-) (forkhead box P3) IFN-gamma(+) T cells i

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

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

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

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

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

24 ch exhibit variable E-selectin binding among CD4(+) and CD8(+) T cells but no binding by B cells.

25 s (P < .01), CD4+IL17A+ cells (P < .01), and CD4+CXCR5+interleukin 21+ follicular T-helper (Tfh) cell

26 also reduced Nef interactions with AP-2 and CD4 and restored CD4 expression to the surface of HIV-in

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

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

29 region of a number of genes and for CD8 and CD4 cells.

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

31 +) double-positive thymocytes and CD8(+) and CD4(+) single-positive thymocytes.

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

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

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

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

36 T cells (iTregs: CD4(+)CD25(-)Fopx3(+)) and CD4(+) and CD8(+) T cells were significantly decreased a

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

38 rimer base, minimize both CD4 reactivity and CD4-induced non-nAb epitope exposure, and increase therm

39 ing the immunological imbalance of Tregs and CD4(+) IFN-gamma(+) cells in the lacrimal gland.

40 Foxp3-deficient mice using nondepleting anti-CD4 Abs.

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

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

43 ification of three lymphocyte cell types (B, CD4+ T, and CD8+ T cells) with high sensitivity and spec

44 ks on treatment, adjusting for age, baseline CD4+, and WHO stage.

45 Fifty-one of 1452 participants with baseline CD4 count <350 cells/muL developed IRIS.

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

47 trong correlation between CCR5 CRPA and both CD4 counts and CD4 T cell apoptosis.

48 g cytokines in total splenocytes and in both CD4 and CD8 T cells following immunization with LdCen(-/

49 n the V3-loop and trimer base, minimize both CD4 reactivity and CD4-induced non-nAb epitope exposure,

50 he closely related virus SIVmac316 uses both CD4 orthologs equally well.

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

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

53 ere randomly assigned (1:1) to point-of-care CD4 cell counts (366 compounds with 417 participants) or

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

55 2, the percentages of CD4+CD28-, CD8+CD28-, CD4+CD38+HLA-DR+, and CD8+CD38+HLA-DR+ T cells, dehydroe

56 was also detected in Dau c 1-reactive CD3(+) CD4(+) CFSE(low) cells.

57 1, LAG-3) and immune cell (IC) subsets (CD3, CD4, CD8, CD68).

58 counts and % of CD4+ T cells and Treg cells (CD4 + CD25 + FOXP3 + CD127dim/-) were evaluated using fl

59 d to isolate keratinocytes, dendritic cells, CD4+ T effector cells, and CD8+ T effector cells from he

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

61 ral envelope glycoprotein (Env) and cellular CD4 receptors and coreceptors.

62 tunistic infections increases as circulating CD4+ lymphocytes decrease to less than 200 cells/muL; ho

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

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

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

66 lls/muL; however, the numbers of circulating CD4+ cells in the HIV-negative (HIV-) brain-dead donor (

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

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

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

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

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

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

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

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

75 onducted using a CD19 CAR product of defined CD4/CD8 composition, uniform CAR expression, and limited

76 tantial increase in peripheral blood-derived CD4(+) CD127(+) CD25(high) cells that display a Th1/Th17

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

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

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

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

81 ts subsequent disease progression and drives CD4 decline independently of the viral load.

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

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

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

85 report that formation of the pre-fusion Env-CD4-coreceptor complexes triggers non-apoptotic cell sur

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

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

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

89 on ART adherence be enhanced and account for CD4 levels at ART initiation.

90 83, 95% CI 0.70-0.99; I(2)=51%, adjusted for CD4 cell count and ART duration), and there was some evi

91 ges was associated with a lower affinity for CD4.

92 c cell (DC) subsets with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically d

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

94 igen tubes to elicit an immune response from CD4(+) and CD8(+) T lymphocytes.

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

96 annels Kv1.4 and Nav1.6 and the glycoprotein CD4.

97 0 and act as competitive inhibitors of gp120-CD4 engagement.

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

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

100 ere bacterial infections in people with high CD4 cell counts have not been well described.

101 es of isolated viral envelope antigens, host CD4 receptors, and cognate antibodies.

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

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

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

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

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

107 lizes rhesus CD4 less efficiently than human CD4.

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

109 model virus, more efficiently utilizes human CD4 than the CD4 of rhesus macaques, whereas the closely

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

111 FOXP3 orthologue as a marker, we identified CD4-enriched, mature T lymphocytes with properties of T

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

113 The positive selection of immature CD4(+)CD8(+) double-positive thymocytes and their commit

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

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

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

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

118 uL (range -472 to 266) with little change in CD4 cell percentage (-2.1%, range -8.4 to 5.9).

119 , IL-13, IL-9, IL-17, and IL-22 cytokines in CD4(+) and CD8(+) T cells.

120 onality could be linked to a major defect in CD4 binding induced by the replacement of H375 by a seri

121 virological failure, and mean differences in CD4 cell count.

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

123 ell-specific protein with high expression in CD4(+)CD8(+) thymocytes, has a crucial role in positive

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

125 Establishment of latent HIV-1 infection in CD4(+) T could be inhibited by viral-specific CD8(+) T c

126 w study reports that RORgammat inhibition in CD4(+)CD8(+) thymocytes resulted in skewed T cell repert

127 vement in thermostability and a reduction in CD4 affinity.

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

129 ioning in vivo, we concomitantly inactivated CD4 and CD8 genes in mice with intact MHC class I and cl

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

131 ghting an important role for vaccine-induced CD4(+) cells in cross-protective vaccine efficacy.

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

133 ranscriptionally silent in latently infected CD4+ T cells.

134 In vitro, M2 macrophages inhibit CD4(+) and CD8(+) T cells.

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

136 s and polarized a subset of these cells into CD4+CD25+FoxP3+ regulatory T cells (Tregs).

137 ncies of induced regulatory T cells (iTregs: CD4(+)CD25(-)Fopx3(+)) and CD4(+) and CD8(+) T cells wer

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

139 induces the expansion of an ICOS(+) Th1-like CD4 effector population in addition to engaging specific

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

141 e with advanced HIV infection and with a low CD4 cell count or re-present with persistent low CD4 cel

142 cell count or re-present with persistent low CD4 cell counts because of poor adherence, resistance to

143 itted infections were also observed at lower CD4 cell counts after adjusting for age.

144 bacterial infections, and mortality at lower CD4 cell counts, as expected.

145 harboring NRTI-DRMs had significantly lower CD4 cells than those with NRTI-DRMs on ART (p = 0.042).

146 re predominantly composed of T cells, mainly CD4(+) for H. pylori and CD8(+) for H. felis.

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

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

149 atopoietic precursor to the CD45RA(+) mature CD4(+) and CD8(+) single-positive (SP) T cells.

150 Sixty patients were included (median CD4 count 53 cells/microL (interquartile range [IQR], 22

151 Of the remaining 1177 patients (median CD4 count 165 cells per muL [IQR 75-271]), 163 (14%) had

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

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

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

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

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

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

158 Small-molecule CD4-mimetic compounds (CD4mc) bind gp120 and act as comp

159 ) on a stable regimen for at least 6 months, CD4 count of more than 100 cells per muL, and no history

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

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

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

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

164 n of inducible Treg (iTreg) cells from naive CD4(+) human T cells.

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

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

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

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

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

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

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

172 in the gp120 Phe 43 cavity, where Phe 43 of CD4 contacts gp120, results in the spontaneous sampling

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

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

175 Due to their unique combination of CD4 and CD8 T cell effector functions, these CD4(-) CD8a

176 ulation of adaptive immunity by depletion of CD4 Th cells most likely contributes to loss of immune c

177 Depletion of CD4(+) cells after an established humoral response in im

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

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

180 cement of TM2 by the transmembrane domain of CD4, the asialoglycoprotein receptor, or the transferrin

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

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

183 iabetes on the presence and functionality of CD4(+)Foxp3(+) T cells.

184 s often persistent, leading to generation of CD4 effector and effector memory T cells that contribute

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

186 ion were associated with increased hazard of CD4 decline and death.

187 ted, reciprocal depletion or inactivation of CD4(+) T lymphocytes decreased vessel normalization, ind

188 d this outcome appeared to be independent of CD4+ count or WHO stage.

189 on of resident microglia and infiltration of CD4(+) and CD8(+) T lymphocytes was observed.

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

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

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

193 CXCL12 interactions during the maturation of CD4(+)CD8(+) thymocytes, including downstream stages of

194 efore DAA therapy, had a lower percentage of CD4+CD25hiFoxP3+ regulatory T cells (P < .01), but highe

195 tly greater immune senescence (percentage of CD4+CD28- or CD8+CD28- T cells) and immune activation (p

196 sis factor alpha 1 and 2, the percentages of CD4+CD28-, CD8+CD28-, CD4+CD38+HLA-DR+, and CD8+CD38+HLA

197 cells) and immune activation (percentages of CD4+CD38+HLA-DR+ and CD8+CD38+HLA-DR+ T cells).

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

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

200 patients with ALF had a higher proportion of CD4(+) CTLA4(+) T cells than controls; patients with inf

201 CR resulted in more efficient redirection of CD4(+) and CD8(+) T cells against a panel of established

202 emtricitabine, and efavirenz) regardless of CD4 cell count (intervention) or according to national g

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

204 A distinct subpopulation of CD4(+) effector memory T (TEM) cells that secrete IL-17A

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

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

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

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

209 , the transfer of mycobacteria-specific (P25 CD4(+) TCR transgenic) wild-type spleen cells into sanro

210 f-care (318 compounds with 353 participants) CD4 cell counts done at one of three referral laboratori

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

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

213 d naive CD4 T cells occurred, and peripheral CD4 and CD8 T cells had reduced chemoattractant response

214 The frequency of Pf-specific polyfunctional CD4 memory T cells was associated with protection.

215 cumented transfers, and in cohorts with poor CD4 count documentation, whereas higher patient load was

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

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

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

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

220 e show increased numbers of GM-CSF-producing CD4 and CD8 lymphocytes in the blood and joints of patie

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

222 mbers of IL-17A(+)GM-CSF(+) double-producing CD4, CD8, gammadelta and NK cells.

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

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

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

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

227 incubated with CMV antigens, induce a recall CD4(+) TH1 proliferation response only in CMV-seropositi

228 five factors, including the HIV co-receptors CD4 and CCR5, that are required for HIV infection yet ar

229 suppresses NF-kappaB activation and reduces CD4 cell surface expression.

230 ne the role of IL-27 and IL-37 in regulating CD4(+) and CD8(+) T cell responses in S. stercoralis inf

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

232 interactions with AP-2 and CD4 and restored CD4 expression to the surface of HIV-infected cells.

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

234 It has been shown that HIV-1 utilizes rhesus CD4 less efficiently than human CD4.

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

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

237 rable accumulation of high-affinity signaled CD4(+)CD8(+) double-positive thymocytes and CD8(+) and C

238 e present novel evidence that Treg-DC skewed CD4(+) naive T cell polarization toward a regulatory phe

239 uced Env epitopes in the presence of soluble CD4 (sCD4).

240 Our findings reveal that Ag-specific CD4 TRM cells play a critical role in adaptive immunity

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

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

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

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

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

246 ntended to engage and render gluten-specific CD4-positive T cells unresponsive to further antigenic s

247 immunodominant epitopes for gluten-specific CD4-positive T cells.

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

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

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

251 exacerbated disease mediated by MPO-specific CD4(+) cells in Rag1(-/-) mice.

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

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

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

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

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

257 -4, LAG-3, PD-1, and Tim-3 on virus-specific CD4 and CD8 T cells in relation to their functional T ce

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

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

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

261 ll compartment, inhibiting all cell subsets (CD4, CD8, WC-1, and gammadelta T cell receptor [gammadel

262 2C) to non-neutralizing antibodies targeting CD4-induced Env epitopes in the presence of soluble CD4

263 on of alloreactive donor T effectors (Teffs; CD4(+)CD25(-)FOXP3(-)) and the direct antiproliferative

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

265 61/sec strain generated large numbers of Th1 CD4(+) ESAT-6(+) splenic T cells compared to those of mi

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

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

268 These data show that CD4(+) T(Pam3) cells are capable of Th1 differentiation

269 These findings suggest that CD4(+)CD161(+) T cells with rapid efflux capacity contri

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

271 more efficiently utilizes human CD4 than the CD4 of rhesus macaques, whereas the closely related viru

272 itive thymocytes and their commitment to the CD4(+)CD8(-) single-positive stage are impaired in Themi

273 ampling of an Env conformation closer to the CD4-bound state.

274 ned to immediate ART or deferral until their CD4 cell counts were lower than 350 cells per muL.

275 CD4 and CD8 T cell effector functions, these CD4(-) CD8alphaalpha T cells are likely able to serve as

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

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

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

279 mine risk of subsequent NMSCs in relation to CD4 count and VL.

280 This resistance to CD4-induced conformational changes was associated with a

281 ntibody response with the need to respond to CD4 binding.

282 his hypothesis by applying RNA sequencing to CD4(+), CD8(+), and CD19(+) lymphocyte populations isola

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

284 sing on the generation of suppressive Tregs (CD4(+)CD25(+)FOXP3(+)) through the in vivo conversion of

285 ts: a second WB set (n = 448, acute) and two CD4 sets (n = 300, chronic; n = 77, acute).

286 bstantially alter the proportions of the two CD4-bound conformations.

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

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

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

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

291 type B B41 SOSIP Env trimers in complex with CD4 and antibody 17b, or with antibody b12, at resolutio

292 ine and transcription factor expression with CD4(+) Th2 cells, but functional diversity of the ILC2 l

293 that the interaction of the Lck kinase with CD4 or CD8 coreceptors is critical for generation of MHC

294 strongly with PD-L1 (0.90), moderately with CD4 and CD8A, and weakly with PD1.

295 rial in ART-naive HIV-positive patients with CD4 cell count of more than 500 cells per muL assigned t

296 o ADCs and NADCs were highest for PWHIV with CD4 counts <100 cells/mm3.

297 s on suppressive antiretroviral therapy with CD4+ counts >350 cells/muL and detectable plasma HIV-1 R

298 were reconstituted by adoptive transfer with CD4+ or CD8+ T-cells subsets were reconstituted in T-cel

299 To determine the role of ROCK2 acting within CD4(+) cells in allergic airways responses.

300 of MPO431-439-specific CD8(+) cells without CD4(+) cells mediated glomerular injury when MPO was pla