ライフサイエンスコーパス: CD4

1 CD4 responses in NOD mice are dominated by insulin epito

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

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

4 CD4(+) Th cells are responsible for orchestrating divers

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

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

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

8 CD4+ T helper 17 (Th17) cells, characterized by IL-17 pr

9 CD4+Langerin+ cells were also more superficially located

10 CD4-based decoy approaches against HIV-1 are attractive

11 CD4:CD8 ratio inflation is a feature of HTLV-1 infection

12 PT class B or C at SVR (10.71 [1.32-87.01]), CD4 cell counts <200/uL at SVR time-point (4.42 [1.49-13

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

14 ture of the two immunodominant human VP11/12 CD4(+) T(EM) cell epitopes, but not with cryptic epitope

15 Median age was 40 years (IQR 35-48), CD4 cell count was 683 cells per muL (447-935), and body

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

17 PLWH with a CD4+ count <300 cells/mm3 underwent standardized neurolo

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

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

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

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

22 y different immune cells including activated CD4(+)Foxp3(+) regulatory T cells (Tregs) and CD4(+)Foxp

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

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

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

26 nfected antiretroviral therapy-naive adults (CD4+ >=50 cells/mm3).

27 ple Ags, we coencapsulated the high-affinity CD4(+) mimotope (BDC2.5(mim)) of islet autoantigen chrom

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

29 immune system, namely effector choice among CD4+ T helper (Th) cells.

30 itic cells (3.1% versus 2.1%; P = 0.023) and CD4 TN (4.4% versus 1.9%; P = 0.018) among those with SL

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

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

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

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

35 identifies highly polyfunctional CD8(+) and CD4(+)T(M) subsets; long-term CD8(+)T(M) maintenance is

36 Perforin contributed to both CD8+ and CD4+ CAR T cell cytotoxicity but was not required for in

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

38 f chemokine receptor 5 (CCR5) in T cells and CD4 in both T cells and macrophages.

39 d by CD40-CD40L interactions between DC1 and CD4(+) T lymphocytes.

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

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

42 centages of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive t

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

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

45 n disease between PIV-vaccinated Tbet KO and CD4 KO mice.

46 arly, double-strand breaks in the LPCAT3 and CD4 genes induced an LPCAT3-CD4 inversion rearrangement

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

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

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

50 ruses showed reduced sensitivity to sCD4 and CD4-Ig but remained sensitive to neutralization by CD4-V

51 al designs, including soluble CD4 (sCD4) and CD4-Ig, were ineffective.

52 ing, purely adaptive CD8(+) alphabeta T, and CD4(+) alphabeta T(H)1(*) cells unable to compensate for

53 D4(+)Foxp3(+) regulatory T cells (Tregs) and CD4(+)Foxp3(-) conventional T cells.

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

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

56 e of variation in daily B-cell levels or any CD4+ functional subset, it accounted for more than 25% o

57 alphabeta lineage T cells, most of which are CD4(+) or CD8(+) and recognize MHC I- or MHC II-presente

58 studies investigated the association of ART, CD4+ count, or HIV PVL on histology-confirmed CIN2+ dete

59 rom the standard of care (ART eligibility at CD4 counts of <350 cells/mm3 until September 2016 and <5

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

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

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

63 In multivariable analysis, baseline CD4 count <350 cells/mm3, female sex, and lower baseline

64 -randomised cohort died; the median baseline CD4 count for participants who died was 11 cells per muL

65 ently lower among participants with baseline CD4 count >=500 cells/uL (3.3%) compared to those with C

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

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

68 Norovirus-specific T cells comprised both CD4+ and CD8+ T cells that expressed markers for central

69 e of antigen processing and priming for both CD4(+) and CD8(+) T cells and of the direct orchestratio

70 tion of Galectin-9 (Gal-9) and VISTA on both CD4(+) and CD8(+) T cells in HIV-infected human patients

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

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

73 The effect was modified by CD4 cell count with protection conferred if CD4 count wa

74 but remained sensitive to neutralization by CD4-VLPs in vitro.

75 eiotropic cytokine produced predominantly by CD4+ T cells.

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

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

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

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

80 The lymphoid cells were positive for CD3, CD4, CD5, CD7 and negative for CD20, CD8, CD56, CD103, P

81 ges of activated CD8 (CD8+CD38+DR+) and CD4 (CD4+CD38+DR+) T cells in 586 women who were naive to hig

82 er cells and a newly identified CD3(-)CD68(+)CD4(+)GrB(+) subset.

83 IHC cell marker for CD45(+), CD3(+), CD8(+), CD4(+), and CD20(+) cells (all p < 0.001).

84 tios of CXCR5IFN-gammaCD8 T cell to combined CD4 Th1/Th2 cell subsets (IFN-gammaCD4 and IL-4CD4 cells

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

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

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

88 fection, group of exposure, nadir CD4 count, CD4:CD8 ratio, and last CD4 level, calendar period of di

89 Current CD4 count of <=200 cells/muL was the strongest predictor

90 CD4 count >=200 (56%), patients with current CD4 351-500 vs >500 cells/muL had an aIRR of 1.22 (95% C

91 Cytotoxic CD4 T cells are linked to cardiovascular morbidities and

92 l HIV Gag-specific poly-functional/cytotoxic CD4(+) and CD8(+) T cells were detected with the IL-4R a

93 cells have also been investigated in detail; CD4(+) cytotoxic T lymphocytes (suspected of promoting d

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

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

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

97 h interferon type I and III responses, early CD4(+) and CD8(+) T cell activation, and counterregulati

98 n HIV-1-infected humanized mice but elicited CD4-binding site mutations that reduced viral fitness.

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

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

101 in the lungs, with a depleted and exhausted CD4 and CD8 T-cell population that resides within a heav

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

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

104 CI, .41-.63]) vs 0.93 [95% CI, .76-1.13] for CD4 count >350 cells/uL).

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

106 t IRF4 expression by cDC is not required for CD4(+) regulatory T cell-mediated control of colitis.

107 mined that females had a 40% higher risk for CD4 + decline than males.

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

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

110 FOXP3+CD4+ regulatory T cells (Tregs) are critical for immune

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

112 ential for immune responses and develop from CD4(+)CD8(+) thymocytes.

113 developing thymocytes to differentiate from CD4(-)CD8(-) double-negative (DN) cell to CD4(+)CD8(+) d

114 rs), thus confirming their independence from CD4 counts and pVL.

115 usly, we discovered that influenza-generated CD4 effectors must recognize cognate Ag at a defined eff

116 l loads (VLs) >100,000 copies/mL and 47% had CD4 cell counts <200/mm 3.

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

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

119 ation antiretroviral therapy (cART), at high CD4 cell counts.

120 of immune activity, had significantly higher CD4+CD151+ T-cell frequencies than healthy controls, rai

121 al trial enrolled 850 participants with HIV (CD4 < 50 cells/uL) at ART initiation to receive either e

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

123 d that in vitro transduction of normal human CD4+ T lymphocytes with NPM-ALK results in their immorta

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

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

126 Beyond these known subsets, we identify CD4(-)CD8(-)TCRalphabeta(+), double-negative (DN) T cell

127 CD4 cell count with protection conferred if CD4 count was <=350 cells/muL (aHR, 0.51 [95% CI, .41-.6

128 e accumulation of pathogenic IL5(+) IL17A(+) CD4(+) effector T-cells.

129 of altitude therapy, CRTH2-expressing ILC2, CD4(+) and CD8(+) T cells and Treg cells showed attenuat

130 14 years, on ART >6 months, not acutely ill, CD4 count not <200 cells/mm3) and willingness to partici

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

132 omain to ibalizumab, a non-immunosuppressive CD4 antibody(12,13), and named it CD4 TGF-beta Trap (4T-

133 ic contexts for causal variants, implicating CD4 + effector memory T cells, as well as monocytes, B c

134 t of T cells, and PRRSV-induced apoptosis in CD4(pos)CD8(pos) thymocytes modulates cellular immunity

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

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

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

138 Thus, after adjustment for differences in CD4 counts and age, hrHPV prevalences were more similar

139 Mean increases in CD4 counts from baseline at week 96 were 205 cells per m

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

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

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

143 AT3-CD4 inversion rearrangement resulting in CD4 expression.

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

145 However, the best model included CD4 nadir (ie, the lowest CD4) from approximately 8.5 ye

146 otential confounders and mediators including CD4 count, a substantially higher mortality rate was pre

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

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

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

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

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

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

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

154 Salmonella-infected, CD4-depleted 129X1/SvJ mice remained chronically coloniz

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

156 rates that all antileishmanial drugs inhibit CD4 and CD8 T cell proliferation at the doses that are n

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

158 00 PYs difference), those who had an initial CD4 count < 100 cells/mul (+9.2 deaths/100 PYs differenc

159 eased coinfected patients had higher initial CD4 count (417 +/- 219 cells) than monoinfected ones wit

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

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

162 Isolated CD4(+)CD25(-) T cells were activated by using anti-CD3/a

163 uppressive CD4 antibody(12,13), and named it CD4 TGF-beta Trap (4T-Trap).

164 re, nadir CD4 count, CD4:CD8 ratio, and last CD4 level, calendar period of diagnosis was not associat

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

166 t stimulated effector generation, long-lived CD4 memory generation, and robust generation of Ab-produ

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

168 ith detectable HIV RNA, and those with lower CD4 cell counts (all P < .05).

169 est model included CD4 nadir (ie, the lowest CD4) from approximately 8.5 years to 6 months in the pas

170 n the LPCAT3 and CD4 genes induced an LPCAT3-CD4 inversion rearrangement resulting in CD4 expression.

171 filtrate (CTII) using the following markers (CD4, CD5, CD8, CD14, CD19, Elastase, and Syndecan).

172 Among PHIVs, the mean CD4 % was 34%, 93% had a viral load <=20 copies/mL, and

173 in meters squared) was 25.8, and the median CD4 cell count 620/uL.

174 Memory CD4 and cytotoxic CD8 T cells appeared early in islets,

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

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

177 igher frequency of antiviral effector memory CD4(+) T(EM) cells specific to two immunodominant epitop

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

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

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

181 eatic tumors and increases numbers of memory CD4+ and CD8+ T cells, eradicating all detectable tumor.

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

183 t is associated with the prevalence of MR1 + CD4/CD8 cells in the thymus.

184 , the cytotoxic marker expression by mucosal CD4(+) and CD8(+) T cells differed according to the muco

185 virus coinfection, group of exposure, nadir CD4 count, CD4:CD8 ratio, and last CD4 level, calendar p

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

187 timulated DCs induced proliferation of naive CD4(+) and CD8(+) T cells to a larger extent than B. bur

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

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

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

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

192 al subset, it accounted for more than 25% of CD4+ regulatory T-cell variation and over 50% of CD8+ ce

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

194 2c-producing plasma cells, and activation of CD4 and CD8 T cells.

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

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

197 The analysis of CD4(+) cells showed an increased percentage of intracell

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

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

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

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

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

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

204 ancestor (UCA) antibodies, while exposure of CD4-induced (CD4i) non-bNAb epitopes was inhibited.

205 significantly correlates with expression of CD4 and has the potential to alter clinical outcome in h

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

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

208 Intraperitoneal injections of CD4-CCR5-VLP produced only subneutralizing plasma concen

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

210 ts and refine the kinetic selection model of CD4(+) and CD8(+) T cell lineage commitment.

211 bsence of BD(L), the absolute cell number of CD4(+)Foxp3(+) T regulatory cells (Treg), essential for

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

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

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

215 RT)-treated individuals with a wide range of CD4 counts (137-1835 cells/mm(3)) indicated that neither

216 deficiency syndrome, given its slow rate of CD4 decline, low to undetectable viremia, and high neutr

217 er TL1A nor DR3 levels reflected recovery of CD4 counts with cART.

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

219 viously diagnosed partners with no report of CD4 count or viral load in the preceding 12 months were

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

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

222 r transcription factor of the Th17 subset of CD4(+) Th cells, is a promising target for treating a ho

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

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

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

226 nduced by administration of DSS, transfer of CD4(+)CD45RB(hi) T cells, or infection with Citrobacter

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

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

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

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

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

232 lock in differentiation from double-positive CD4(+)CD8(+) cells.

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

234 Among patients with lowest presuppression CD4 count >=200 (56%), patients with current CD4 351-500

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

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

237 2C elements drive gene expression in primary CD4+ T cells.

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

239 Both FTY720 and BAF312 caused a profound CD4+ and CD8+ T cell depletion in blood and lungs but on

240 stem was shown to elicit broadly protective CD4(+) and CD8(+) T cell responses.

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

242 ort-term Ag exposure to identify Ag-reactive CD4 cells.

243 To study the clonality of flagellin-reactive CD4 cells in Crohn patients, we used a common CD154-base

244 lls, binding of the virus to host receptors, CD4 and CCR5/CXCR4, triggers serial conformational chang

245 -2C, best known to induce CD25(+) regulatory CD4 T cell expansion, surprisingly causes robust inducti

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

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

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

249 ion of IFNgamma and TNFalpha by restimulated CD4+ cells but not CD8+ confirmed the specific ability o

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

251 -1 persists in a latent reservoir in resting CD4(+) T cells, and rebound viremia occurs following tre

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

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

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

255 ed for demographic factors, baseline HIV RNA/CD4 cell counts, AIDS defining events and the type of In

256 0, TNF-alpha, and other cytokines and severe CD4(+) and CD8(+) T-cell lymphopenia and coagulopathy.

257 ells; P = .004), while survivors had similar CD4 cell count at baseline, regardless of HTLV status.

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

259 trol, but initial designs, including soluble CD4 (sCD4) and CD4-Ig, were ineffective.

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

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

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

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

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

265 tive noninterventional study, BKPyV-specific CD4 and CD8 T cells were measured in 32 of 36 viremic pe

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

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

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

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

270 De novo neoantigen-specific CD4(+) and CD8(+) T cell responses were observed post-va

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

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

273 on is effectively mediated by virus-specific CD4+ and CD8+ T cells.

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

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

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

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

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

279 controls, whereas the extracellular survivin CD4(+) percentage was unaffected.

280 in 11 major cell subsets (i.e., B, CD3 + T, CD4 + T, CD8 + T, NK, TCR-gammadelta, Mucosal associated

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

282 tigen receptor (CAR) T cells, expressing the CD4 ectodomain to confer specificity for the HIV envelop

283 adjusted model, CT, HPV16, HPV53, HPV70, the CD4+/CD8+ ratio, and the interaction between CT and HPV1

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

285 led thymic and peripheral homeostasis in the CD4+ Th cell life cycle and invariant NK (iNK) T cell de

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

287 erval [CI], 3.5-51.0) and proportion of time CD4 <200 cells/uL from approximately 8.5 to 4.5 years in

288 In other words, Env binds to CD4 on key immune cells and transduces signals that can

289 om CD4(-)CD8(-) double-negative (DN) cell to CD4(+)CD8(+) double-positive (DP) cell.

290 e Env mutants renders the Env insensitive to CD4 binding.

291 Total CD4(+) and CD8(+) T cell frequencies were markedly lower

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

293 eins consisting of gp120 Core and one or two CD4-induced (CD4i) mAbs for masking nND epitopes, referr

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

295 eta and low TRIM32 ratio was associated with CD4+ cells in AD human skin compared with those in healt

296 sponses that were negatively associated with CD4+CD25+FOXP3+ T-cells and accompanied by increased fre

297 among either cohort, and no correlation with CD4 count or HAND status for the HIV-infected cohort.

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

299 >=500 cells/uL (3.3%) compared to those with CD4 count 200-499 cells/uL (9.2%) between months 18 and

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