ライフサイエンスコーパス: CD4 T-cell

1 ore severe splenitis than infected mice with CD4 T cells.

2 n the frequency of persistent HIV in resting CD4 T cells.

3 terferon-stimulated gene (ISG) expression in CD4 T cells.

4 f lymphoma remained intact in the absence of CD4 T cells.

5 ch function to present peptides and activate CD4 T cells.

6 madelta T cells and IL-17 secretion by human CD4 T cells.

7 quenced HIV-1 outgrowth viruses from resting CD4+ T cells.

8 dominant targets for virus-specific CD8+ and CD4+ T cells.

9 2C elements drive gene expression in primary CD4+ T cells.

10 CR-mediated activation and proliferation, of CD4+ T cells.

11 re activated upon HIV-1 infection of primary CD4+ T cells.

12 ed replication-competent virus cultured from CD4+ T cells.

13 nascent transcripts in resting and activated CD4+ T cells.

14 eiotropic cytokine produced predominantly by CD4+ T cells.

15 nce of NOD-PerIg CD8(+) T cells but required CD4(+) T cells.

16 is, also regulates adhesion and migration in CD4(+) T cells.

17 he specific ability of filariae to stimulate CD4(+) T cells.

18 D8(+) T cells, VME1 was mainly recognized by CD4(+) T cells.

19 and metabolism-related genes within effector CD4(+) T cells.

20 ransforming growth factor-beta production by CD4(+) T cells.

21 rily on the elimination of latently infected CD4(+) T cells.

22 nd ORMDL3/GSDMB, IL6ST/ANKRD55, and JAZF1 in CD4(+) T cells.

23 ability to polarize naive OVA-TCR transgenic CD4(+) T cells.

24 ing to the VS and therefore the infection of CD4(+) T cells.

25 (p < 0.05) increased IFN-gamma production by CD4(+) T cells.

26 to worse renal function than transfer of WT CD4(+) T cells.

27 the boost for the expansion of self-reactive CD4(+) T cells.

28 ryl hydrocarbon receptor (AhR) expression by CD4(+) T cells.

29 triggered antiviral responses in myeloid and CD4(+) T cells.

30 onse that was dependent on ST2 expression by CD4(+) T-cells.

31 c effects of RMD were reduced proportions of CD4+ T cells 24 hours after infusions 2, 3, and 4 (media

32 9.8-fold; P < 0.001) for IFN-gamma-producing CD4+ T cells, 4.9-fold (CI, 1.3- to 40.0-fold; P < 0.001

33 a-telangiectasia-mutated (ATM) deficiency in CD4 T cells accelerates DNA damage, telomere erosion, an

34 nd and present pathogen-derived peptides for CD4 T cell activation.

35 erved profound differences in viral load and CD4(+) T cell activation from the earliest time points i

36 y effects at eight time points during memory CD4(+) T cell activation with high-depth RNA-seq in heal

37 men exhibited significantly higher levels of CD4(+) T cell activation, a difference that was lost ove

38 that suppression of Malat1 is a hallmark of CD4(+) T cell activation, but its complete deletion resu

39 in mouse dendritic cells and MHCII-dependent CD4(+) T cell activation.

40 Unexpectedly, early priming of CD4(+) T cells against tumour-derived antigens also requ

41 addition to helper and regulatory potential, CD4(+) T cells also acquire cytotoxic activity marked by

42 Nerve and islet-infiltrating CD4(+) T cells also differed by expression patterns of C

43 to 782 and from 193 to 1436 cells per 10(6) CD4(+) T-cells among influenza A/H3N2 and B-infected pat

44 omposition and function of both conventional CD4(+) T cell and regulatory T cell (T(reg)) compartment

45 gulate IL-10 at the mRNA or protein level in CD4(+) T cells and did not drive the transcription of th

46 In addition, CD4(+) T cells and HLA-DQ8 have a crucial role in the li

47 les of SCFAs in inducing IL-22 production in CD4(+) T cells and ILCs to maintain intestinal homeostas

48 d upon cognate interactions between effector CD4(+) T cells and mononuclear phagocytes (MPs).

49 Both CD4(+) T cells and myeloid cells produced pathogenic lev

50 tor (CAR) T cell to target both HIV-infected CD4(+) T cells and the FDC reservoir in vitro Although C

51 In addition, CD4+ T cells and CD8+ T cells may be vital for altering

52 68% African American), higher CD45RO+ memory CD4+ T cells and lower CD38+ CD4+ T cells were associate

53 ctivated subsets of Treg cells, conventional CD4 T cells, and cells expressing a Foxp3 reporter null

54 lts from enhanced function of tumor-specific CD4 T cells, and ultimately requires tumor-intrinsic IFN

55 atory profile of their proinsulin-responsive CD4(+) T cells, and improved regulation of CD4(+) T cell

56 -1 persists in a latent reservoir in resting CD4(+) T cells, and rebound viremia occurs following tre

57 for controlling viral replication, restoring CD4+ T cells, and preventing opportunistic infection, it

58 with HIV significantly increased weight and CD4+ T cells, and such interventions can be integrated i

59 ation status, increasing the pool of resting CD4(+) T cells; and impair CD8(+) T cell function, favor

60 ing telomere loss, premature cell aging, and CD4 T-cell apoptosis or depletion via dysregulation of t

61 Cytotoxic CD4 T cells are linked to cardiovascular morbidities and

62 In summary, the current study suggests that CD4(+) T cells are critical for controlling acute-stage

63 CD4(+) T cells are critical to fighting pathogens, but a

64 function during host defense, but whether MP CD4(+) T cells are functionally heterogeneous and, if so

65 This is particularly striking, as memory CD4(+) T cells are generally regarded as the main source

66 ) mice demonstrated that antigen-experienced CD4(+) T cells are sufficient to generate protection.

67 Long-lasting, latently infected resting CD4(+) T cells are the greatest obstacle to obtaining a

68 Although CD4+ T cells are implicated in MS pathogenesis and have

69 (S1PR1) expression and glucose metabolism in CD4(+) T cells as potential mechanisms for LXA(4) regula

70 olyfunctional IFN-gamma-producing CD107(ab+) CD4(+) T cells associated with protective immunity again

71 s an essential signal for differentiation of CD4(+) T cells at the epithelium, yet differentiated IEL

72 he relevant peptides that induced pathogenic CD4(+) T cells at the initiation of diabetes derived fro

73 total HIV DNA isolated from peripheral blood CD4(+) T-cells at weeks 16 and 18 after randomisation.

74 In this study, we show that in primary human CD4(+) T cells, both TNF-alpha(+) and IL-2(+) vesicles c

75 Using a mouse TCR transgenic CD4(+) T cell, BthetaOM, that is specific for B. thetaio

76 termined by functionally discrete subsets of CD4(+) T cells, but it has remained unclear to what exte

77 ng growth factor-beta receptor 2 (TGFBR2) in CD4(+) T cells, but not CD8(+) T cells, halts cancer pro

78 ia can be due to expanded clones of infected CD4+ T cells carrying replication-competent virus.

79 parsimonious explanation is that coordinated CD4(+) T cell, CD8(+) T cell, and antibody responses are

80 variety of immune cell populations including CD4(+) T cells, CD8(+) T cells, B cells, macrophages, an

81 the T-cell compartment (CD3CD19) revealed 2 CD4 T-cell clusters at higher frequency among those with

82 ases in H3K9ac+ and phosphorylated P-TEFb in CD4 + T cells compared to placebo (p<=0.02).

83 numbers of IL-17A-producing peripheral blood CD4(+) T cells compared to PBC patients and healthy cont

84 nal studies, we find that human blood sLeX(+)CD4(+)T cells comprise a subpopulation expressing high l

85 antigen presentation, neither HDACi-treated CD4(+) T cell condition induced clone degranulation.

86 test antigens, clones of antigen-responsive CD4+ T cells containing defective or intact latent provi

87 specific cytokines produced by autoreactive CD4 T cells contribute to the pathogenesis of MS.

88 Because MHC-II restricted CD4(+) T cells control and orchestrated most immune resp

89 Specific deletion of LAT1 in gammadelta and CD4 T cells controls the inflammatory response induced b

90 The frequency of naive CD4+ T cells correlated inversely with HTLV-1 pVL (rs =

91 The median CD4 T-cell count was 664 cells/muL.

92 ite with a median age at switch of 50 years, CD4+ T-cell count 512 cells/muL, and BMI 26.4 kg/m2.

93 Mean increases from baseline in CD4+ T-cell count through 48 weeks were 195.5 cells/mm3

94 nrandomized cohort; the mean increase in the CD4+ T-cell count was 139 cells per cubic millimeter and

95 as observed between microbiome diversity and CD4+ T-cell count, HIV viral load, or HIV-associated chr

96 lysis, after controlling for the most recent CD4+ T-cell count, pregnancy incidence rates in HIV-posi

97 Before ART initiation, PTCs had higher CD4 T cell counts, lower plasma viremia, and SIV-DNA con

98 therapy with suppressed HIV viremia and high CD4 T cell counts, the efficacy of conventional chemothe

99 nificantly reduced viral loads and increased CD4+ T cell counts in blood and bronchoalveolar lavage (

100 younger individuals, those with higher nadir CD4+ T-cell counts, and those who had received lopinavir

101 ion of metabolically activated and quiescent CD4 T cells (cultured with 2 ng/ml interleukin-7).

102 In contrast, single-cell analysis of CD4(+) T cells demonstrates several tumor-specific state

103 facilitating the establishment of an anti-BP CD4 T cell-dependent adaptive immune response leading to

104 CD4(+) T-cell depletion studies or the adoptive transfer

105 CD4+ T cells derived from individuals with latent Mtb in

106 on to characterize the mechanisms underlying CD4 T-cell destruction by analyzing the telomeric DNA da

107 The glycopeptide specific CD4(+) T cells display a prominent feature of Th2 and Th

108 IL-1beta production and its consequences in CD4(+) T cell-driven autoimmune pathology.

109 D45RB(lo) CD4(+) T cells prevented CD45RB(hi)CD4(+) T cell-driven colitis in both Cre(+) and Cre(-) r

110 CD4(+) T cell-mediated immunity and modulate CD4(+) T cell effector responses during infection was ma

111 The cytokine TNF produced by activated CD4(+) T cells engaged its receptor TNFR on MPs, leading

112 e with a mixture of these two immunodominant CD4(+) T cell epitopes induced a robust antiviral CD4(+)

113 However, the mechanisms of CD4(+) T cell exhaustion are still poorly understood.

114 To study CD4(+) T cell exhaustion, we used the TCR-transgenic B6

115 CD4(+) T cells exhibit much more profound stiffness depe

116 nally, recipient mice with Iqgap1(-/-) donor CD4(+) T cells exhibited significantly higher EAE scores

117 -2C, best known to induce CD25(+) regulatory CD4 T cell expansion, surprisingly causes robust inducti

118 The fractions of CD4(+) T cells expressing K(i) -67 increased up to 80% i

119 Frequencies of interferon-gamma +CD4+T cells expressing CD38, HLADR, and/or Ki67 were ass

120 dy (IgG, IgG3 binding, and neutralizing) and CD4+ T-cell (expressing interferon-gamma, interleukin-2,

121 ite their intact cGAS sensing pathway, human CD4(+) T cells failed to mount a reverse transcriptase (

122 CD4+ T cell failure is a hallmark of chronic hepatitis C

123 framing of the Th1/Th2 paradigm ignited the CD4(+) T cell field.

124 nderpinning the differentiation of cytotoxic CD4(+) T cells following immunotherapy.

125 med by in vitro MHC binding.RESULTSActivated CD4+ T cell frequencies in bronchoalveolar lavage correl

126 In this study, we show that stimulation of CD4 T cells from C57BL/6 mice not only decreases total a

127 ular transcriptomes of CD103(+) and CD103(-) CD4 T cells from the blood and rectum of HIV-negative (H

128 analysis of >100,000 viral antigen-reactive CD4(+) T cells from 40 COVID-19 patients.

129 In ex vivo CD4(+) T cells from ARV-suppressed individuals, both HDA

130 gative regulation within the Akt1 pathway in CD4(+) T cells from ASC and SCZ patients, in addition to

131 in (VP11/12) encoded by UL46 are targeted by CD4(+) T cells from HSV-seropositive asymptomatic indivi

132 The data suggest CD4(+) T cells from lactating cows have an altered metab

133 er rates of glycolytic function in activated CD4(+) T cells from late lactation and dry cows compared

134 Adoptive transfer of NGAL-deficient CD4(+) T cells from NGAL KO mice into CD4 KO or WT mice

135 Adoptive transfer of CD4(+) T cells from PIV-vaccinated WT mice to naive CD4-

136 Analysis of resting CD4(+) T cells from tissues after AZD5582 treatment reve

137 Interestingly, CD4(+) T cells from two Blau syndrome patients show elev

138 In vitro, CD4+ T cells from all donors respond to nickel but the i

139 inflammation, recovery of pathogen-specific CD4 T-cell function, and lung injury prior to and after

140 These HCV-specific CD4+ T cells had an effector-memory phenotype.

141 Proliferation of CD4+ T cells harboring HIV-1 proviruses is a major contr

142 tors in HIV-1 trans-infection between DC and CD4(+) T cells has the potential for the development of

143 CD4(+) T cells have also been investigated in detail; CD

144 ver, proinsulin epitopes recognized by human CD4(+) T cells have not been comprehensively characteriz

145 These results suggest that limiting CD4 T-cell help mteaserrlie the diminished or altered an

146 enerated during ehrlichial infection require CD4(+) T cell help and IL-21 signaling for their develop

147 rized by a severe impairment of HCV-specific CD4+ T cell help that is driven by chronic antigen stimu

148 dence that the profound loss of HCV-specific CD4+ T cell help that results in chronic infection is re

149 lper 17 (Th17) cells, an important subset of CD4(+) T cells, help to eliminate extracellular infectio

150 ytotoxic T-cell responses for the former and CD4(+) T-cell helper responses for the latter.

151 Upon activation of primary human CD4(+) T cells, hHS-8 and the TNF and LTA promoters disp

152 he molecular mechanisms of telomeric DDR and CD4 T-cell homeostasis during HIV infection.IMPORTANCE T

153 ated it, and it was not found in Notch1-null CD4 T cells, identifying the Notch pathway as a major me

154 they harbor high levels of HIV/SIV; reverse CD4(+) T cell immune activation status, increasing the p

155 ter pregnancy is associated with recovery of CD4+ T cell immunity.

156 significant impact on HPV-specific CD8+ and CD4+ T cell immunity.

157 during Staphylococcus aureus sepsis induces CD4+ T-cell impairment and increases susceptibility to s

158 Mycobacterium tuberculosis antigen-specific CD4 T cells in a cohort of HIV-infected persons starting

159 These results illuminate a role for CD4 T cells in brain development and a potential interco

160 ntity of VZV-specific plasma cells (PCs) and CD4 T cells in the bone marrow (BM) of healthy young adu

161 We have examined the priming of naive CD4 T cells in vitro at fever temperatures, and we repor

162 allografts, and suppressed proliferation of CD4 T cells in vitro.

163 To interrogate the function of autoreactive CD4(+) T cells in atherosclerosis, we used a novel tetra

164 e expression patterns of SARS-CoV-2-reactive CD4(+) T cells in distinct disease severities.

165 Spike-reactive CD4(+) T cells in healthy donors were primarily active a

166 and the combination promotes the decline in CD4(+) T cells in HIV-infected mice.

167 ed elevated production of IL-17A and -F from CD4(+) T cells in the absence of S100A8 and S100A9, as w

168 ice, we showed a partial role for Th1 subset CD4(+) T cells in vaccine protection.

169 d in vivo classical complement activation on CD4+ T cells in 14% of the whole cohort.CONCLUSIONOur da

170 ate and characterize tumor-specific CD8+ and CD4+ T cells in murine tumor models.

171 in the lungs, percentage of antigen-specific CD4-T-cells in the spleen, and enhanced overall cytokine

172 uppressive therapy, levels of BKPyV-specific CD4 T cells increased while plasma BKPyV-DNAemia decline

173 ases integrin expression in antigen-specific CD4(+) T cells, increases the number of granulocyte-like

174 itamin D and VDR inhibited LPS- or activated CD4(+) T cell-induced miR-27a/b reductions in HOKs.

175 remia, rca-RNA, and the frequency of resting CD4(+) T-cell infection (RCI) was measured at baseline a

176 telets or T cells displayed reduced cerebral CD4(+) T-cell infiltration and thrombotic activity follo

177 ted to the presence of a pathogen, activated CD4(+) T cells initiate distinct gene expression program

178 fic CD8+ T cells recruited to the CNS during CD4+ T cell-initiated EAE engaged in determinant spreadi

179 ejection, consistent with a role for cognate CD4(+) T cell interactions and CD40 signalling in cDC1 l

180 rks by reprogramming autoantigen-experienced CD4+ T cells into autoimmune disease-suppressing T regul

181 Fever sensing by CD4 T cells involved transient receptor potential vanill

182 d that in GA lesions IFN-gamma production by CD4(+) T cells is upregulated and is associated with inf

183 le following pregnancy, and this recovery of CD4+ T cells is associated with at least transient contr

184 Immunophenotyping and CD4 T-cell ISG expression analysis revealed marginal dif

185 Quiescence is a hallmark of CD4(+) T cells latently infected with human immunodefici

186 Depleting CD4 T cells led to increased myeloid cells in peripheral

187 on by contributing to both viral control and CD4(+) T cell loss, an effect that extends into the chro

188 kin phenotypes and decreased infiltration of CD4 T cells, macrophages, and neutrophils.

189 ne and cytokine expression by lamina propria CD4(+) T cells, many of which were BHLHE40 dependent, in

190 eature of HTLV-1 infection, whereas enhanced CD4+ T cell maturation and monocyte aggregation are feat

191 odies in ICL, some of which are specific for CD4+ T cells, may contribute to pathogenesis, and may re

192 ell infiltration contributes to autoreactive CD4 T cell-mediated skin autoinflammation.

193 and neutrophils is required for autoreactive CD4 T cell-mediated skin disease pathogenesis and that t

194 ound that the ability of B cells to suppress CD4(+) T cell-mediated immunity and modulate CD4(+) T ce

195 A heterogeneous magnitude of CD4(+) T cell-mediated memory responses was observed in

196 However, the underlying mechanisms of CD4(+) T cell-mediated pathogenesis are largely unknown.

197 -directed autoimmune myocarditis (TnI-AM), a CD4(+) T-cell-mediated disease, was induced in mice lack

198 e does not promote resurrection of exhausted CD4(+) T-cell memory in chronic infection.

199 s), and can be found in the peripheral blood CD4(+) T cells of patients at all stages of HIV-1 infect

200 Among nickel-specific CD4+ T cells of allergic and non allergic donors, TCRs e

201 Enrichment of PD-1(+)CD4(+) T cells only within a granulocyte CN positively c

202 d number of B cells (P = .016) and activated CD4 T cells (P = .016).

203 -responders (INR) fail to reconstitute their CD4 + T cell pool after initiation of antiretroviral the

204 Conventional CD4(+) T cell populations in thymus, blood, and spleen o

205 (TCR) deep sequencing, tetramer-guided naive CD4 T-cell precursor enumeration, and whole-body imaging

206 Cotransfer of CD25(+)CD45RB(lo) CD4(+) T cells prevented CD45RB(hi)CD4(+) T cell-driven

207 ss II molecules in cDC1 also prevented early CD4(+) T cell priming.

208 eity of antigen-presenting cells involved in CD4+ T cell priming.

209 ron availability in vitro severely inhibited CD4 T cell proliferation and cell cycle progression.

210 y described suppressive effects of CB-LDG on CD4(+) T cell proliferation are exclusively due to phago

211 zed mice exhibited much stronger Ag-specific CD4(+) T cell proliferation ex vivo.

212 However, upon viral control, CD4+ T cells quickly downregulated inhibitory receptors

213 and potentially enhance our understanding of CD4(+) T cell recognition.

214 cular inflammation to promote eosinophil and CD4+ T cell recruitment.

215 lity variants are over-represented in memory CD4(+) T cell regulatory elements(1-3).

216 HIV subjects occur in vitro in HIV-infected CD4 T cells remains unknown.

217 ncing, to dissect the human naive and memory CD4+ T cell repertoire against the influenza pandemic H1

218 easingly shaped the circulating HCV-specific CD4+ T cell repertoire, suggesting antigen-independent s

219 ncing revealed that in the absence of murine CD4 T cells, resident microglia remained suspended betwe

220 atency in proliferating and nonproliferating CD4(+) T cells, respectively.

221 antigens to polarize mainly naive CD8(+) or CD4(+) T cells, respectively.

222 matory IL-2C can deliver survival signals to CD4 T cells responding to influenza A virus that improve

223 ) T cell epitopes induced a robust antiviral CD4(+) T cell response in the cornea that was associated

224 Glycopeptide-induced CD4(+) T cell response prior to Env trimer immunization

225 ntify characteristics of the peanut-specific CD4(+) T-cell response in peanut-allergic patients that

226 CD4+ T-cell response rates were higher at month 18 than

227 significantly higher EBOV-specific CD8+ and CD4+ T-cell response.

228 healthy young adults that VZV-specific B and CD4 T cell responses are detectable in bone marrow (BM)

229 provides crucial co-stimulatory signals for CD4 T cell responses, however the precise cellular inter

230 on induced type 1 helper T-cell (Th1)-biased CD4 T-cell responses and low or undetectable Th2 or CD8

231 gh studied at the level of B-cell responses, CD4 T-cell responses have not yet been examined.

232 ion between them, polyfunctional gE-specific CD4 T-cell responses, safety, and confirmed HZ cases wer

233 and broad induction of FSP-specific CD8 and CD4 T-cell responses.

234 ncrease humoral responses, it blunted type 1 CD4(+) T cell responses against the SIV envelope protein

235 FNgamma(+)TNFalpha(+) and IFNgamma(+) IL2(+) CD4(+) T cell responses respectively, in comparison to 3

236 e CD4(+) T cells, and improved regulation of CD4(+) T cell responses to proinsulin at 9 months of age

237 protective range, multifunctional CD8(+) and CD4(+) T cell responses with S protein-specific killing

238 he envelope V2 loop and of envelope-specific CD4(+) T cell responses.

239 l as functional capacity of peptide-specific CD4(+) T-cell responses characterized after vaccination,

240 g of mothers with T1D had reduced cord blood CD4(+) T-cell responses to proinsulin and insulin, a red

241 ve highly defective ECTV-specific CD8(+) and CD4(+) T-cell responses to WT ECTV.

242 Untoward effector CD4+ T cell responses are kept in check by immune regula

243 Chen et al. revealed that initial CD4+ T cell responses are similar during early infection

244 IV-uninfected study participants in terms of CD4+ T-cell responses after anti-CD3 stimulation (P = .1

245 The Matrix-M1 adjuvant induced CD4+ T-cell responses that were biased toward a Th1 phen

246 ommon on ART, relate to greater ART-mediated CD4 T-cell restoration, and are associated with the pers

247 Depletion of CD4(+) T cells showed unique pathological bulbar vacuola

248 D40L) expression on cytokine-positive memory CD4(+) T cells significantly increased after the second

249 sma using macrophage-specific (CD14) but not CD4+ T cell-specific (CD3) antibodies, suggesting that M

250 The discovery of CD4(+) T cell subset-defining master transcription facto

251 signaling to exert divergent effects across CD4(+) T cell subsets and highlight specific roles for t

252 ic ability to trans-differentiate into other CD4(+) T cell subsets remains mostly uncharacterized.

253 sequences could also be detected in multiple CD4(+) T cell subsets, suggesting that infected cells ca

254 uences were also found in multiple different CD4(+) T cell subsets.

255 Analysis of CD4(+) T-cell subsets and TCR variable beta classes from

256 CD4(+) T-cell subsets from 86 patients without T-cell ly

257 pertoires of human naive and effector/memory CD4(+) T-cell subsets, irrespective of antigen specifici

258 gulatory and inflammation related cell (IRC) CD4+ T-cell subsets in 705 individuals across the IA-con

259 iposome administration, adoptive transfer of CD4(+) T cells suppressed the development of diabetes in

260 Coss et al. showed that HCV-specific CD4+ T cells temporarily recovered in some women followi

261 om DENV monovalent vaccinees induced CD8 and CD4 T cells that cross-reacted within the DENV serocompl

262 oir in vitro Although CAR-T cells eliminated CD4(+) T cells that express HIV, they did not respond to

263 F secretion in a rare population of CD11c(+) CD4(+) T cells that express the transcription factor Bhl

264 ] cells) or derived from mature conventional CD4(+) T cells that underwent TGF-beta-mediated conversi

265 In support, adoptive transfer of old CD4(+) T cells that were transfected with a lentiviral v

266 e the elimination of a reservoir of infected CD4+ T cells that persists despite HIV-specific cytotoxi

267 of Hodgkin lymphoma (HL) is the presence of CD4+ T cells that surround, protect, and promote surviva

268 oma 2 (BCL-2) as a distinguishing feature of CD4+ T cells that survived CTL killing.

269 ugh their receptors (IL-17RA and IL-17RC) on CD4+ T cells themselves, but not through their action on

270 ckade increased HIV-1 replication in primary CD4(+) T cells, thereby suggesting that Tim-3 expression

271 viral entry in human primary macrophages and CD4(+) T cells through the downregulation of C-C motif c

272 s Tim-3 from the surface of infected primary CD4(+) T cells, thus attenuating HIV-1-induced upregulat

273 Determining dynamic adhesion of CD4(+) T cells to MAdCAM-1 and the in vitro response to

274 The contribution of CD4(+) T cells to protective or pathogenic immune respon

275 or the adoptive transfer of WT OVA-specific CD4(+) T cells to WT or Pag1(-/-) recipients demonstrate

276 status and influences the susceptibility of CD4+ T cells to HIV-1 replication.

277 ells impairs the ability of antigen-specific CD4+ T cells to promote inflammation in vivo during anti

278 expressed on a subset of FOXP3(+) regulatory CD4 T cells (Tregs), and CD137(+) Tregs are the main sou

279 tion of both peripherally induced regulatory CD4(+) T cells (Tregs) and effector Th17 cells.

280 , a complex process in which quiescent naive CD4 T cells undergo transcriptional changes to effector

281 hermore, IL-36R-mediated IL-22 production by CD4(+) T cells was dependent upon NFkappaB-p65 and IL-6

282 Chemokine receptor expression on CD4+ T cells was determined using flow cytometry.

283 aluating the risk of progression using naive CD4+ T-cells was predictive of progression along the who

284 However, when naive CD4 T cells were primed via antigen and dendritic cells

285 We further showed that central memory CD4(+) T cells were enriched with DNA from human herpesv

286 The number of memory CD4(+) T cells were reduced, while CD8(+) T cells consis

287 he absolute number and proportion of splenic CD4(+) T cells were reduced, while the proportion of CD8

288 CD45RB(hi)CD4(+)T cells were transferred to Lacc1(-/-)Rag2(-/-) mi

289 CD45RO+ memory CD4+ T cells and lower CD38+ CD4+ T cells were associated with prevalent diabetes, an

290 Recipient CD4+ T cells were not required for immunoprophylaxis eff

291 CD4+ T cells were poorly restored specifically in the lu

292 HIV) reservoir is composed of resting memory CD4(+) T cells, which often express the immune checkpoin

293 r rare circumstances, particularly in memory CD4+ T cells, which represent the main barrier to HIV er

294 IL-6 overexpression promoted activation of CD4(+) T cells while suppressing CD5(+) B-1a cell develo

295 elevated Granzyme K expression was linked to CD4(+) T cells, whilst Granzyme B/TIA-1 to CD8(+) T cell

296 he validation of our observations in primary CD4 T cells with active or drug-suppressed HIV infection

297 data suggest the existence of apoB-specific CD4(+) T cells with an atheroprotective, regulatory T ce

298 his phenomenon in vitro, we infected primary CD4+ T cells with an HIV construct expressing GFP and, a

299 k of HIV infection is a gradual depletion of CD4 T cells, with a progressive decline of host immunity

300 tment in HCT116, Jurkat, and primary resting CD4 T cells, yet return to baseline levels after an 18-h