ライフサイエンスコーパス: CD4 lymphocyte

1 duce the viral set point and preserve memory CD4 lymphocytes.

2 a median of 225 CD4 lymphocytes/mm3 and 17% CD4 lymphocytes.

3 erferon-gamma production by T helper 1 (Th1) CD4 lymphocytes.

4 CD8 lymphocyte activation, in the absence of CD4 lymphocytes.

5 f GPS platelets, neutrophils, monocytes, and CD4 lymphocytes.

6 tant, induced the death of activated primary CD4 lymphocytes.

7 Pin1 in GM-CSF expression by human PBMC and CD4+ lymphocytes.

8 ntimal lesion progression in the presence of CD4+ lymphocytes.

9 and absolutely contingent on the presence of CD4+ lymphocytes.

10 expression levels and replication in resting CD4+ lymphocytes.

11 1) nutrient responsiveness in lamina propria CD4+ lymphocytes.

12 ptured and delivered to target cell, such as CD4+ lymphocytes.

13 eceptors retained their enhanced function in CD4(+) lymphocytes.

14 ssociated genetic program in differentiating CD4(+) lymphocytes.

15 blood mononuclear cells (PBMCs) rather than CD4(+) lymphocytes.

16 f CD8(+) effector response and the number of CD4(+) lymphocytes.

17 h the CXCR4 receptor and induce apoptosis in CD4(+) lymphocytes.

18 ls, promote Th1/Th2 differentiation of naive CD4(+) lymphocytes.

19 for the production of infectious virions by CD4(+) lymphocytes.

20 Gal-I deficiency giving a marked decrease on CD4(+) lymphocytes.

21 nd were capable of immortalizing transfected CD4(+) lymphocytes.

22 and elevated CD25 expression on circulating CD4(+) lymphocytes.

23 cytometry to study the surface phenotype of CD4(+) lymphocytes.

24 ferential depletion of coreceptor-expressing CD4(+) lymphocytes.

25 , including innate lymphoid cells (ILCs) and CD4(+) lymphocytes.

26 tion of Treg effector lymphocytes from naive CD4(+) lymphocytes.

27 -free and cell-mediated infection in primary CD4(+) lymphocytes.

28 d CD8(+)-enriched TILs with a median of 0.3% CD4(+) lymphocytes.

29 ds on interferon gamma (IFN-gamma)-producing CD4(+) lymphocytes.

30 expansion and tissue infiltration of Tax(+), CD4(+) lymphocytes.

31 responses in lung tissue and in lung-derived CD4(+) lymphocytes.

32 T cells were involved, because depletion of CD4(+) lymphocytes 24 h before AG treatment prevented mo

33 action of patients with CTCL, the neoplastic CD4(+) lymphocytes acquire extracutaneous tropism, and w

34 MAPKs involved in facilitating diapedesis of CD4(+) lymphocytes across both types of MVECs, whereas E

35 es are capable of diminishing IL-18-mediated CD4 lymphocyte activation.

36 ultivariable regression analyses, CD8(+) and CD4(+) lymphocyte activation were associated significant

37 her willingness to adhere to treatment, and CD4 lymphocyte and HIV-1 RNA levels.

38 Propagation of R5 strains of HIV-1 on CD4 lymphocytes and macrophages requires expression of t

39 associated with blocking the recruitment of CD4 lymphocytes and monocytic MDSCs, respectively.

40 with normal kinetics contained both CD8 and CD4 lymphocytes and produced significant specific killin

41 a confirm that MCP-2 is a ligand for CCR5 on CD4(+) lymphocytes and can specifically block R5 HIV-1.

42 al memory (CD27(+)CD45RO(+)) CXCR3(+)CCR6(-) CD4(+) lymphocytes and corresponding cytokines, with red

43 transient increases in both the Th1 and Th2 CD4(+) lymphocytes and cytokine mRNAs compared to those

44 hallenge viruses, resulted in a reduction in CD4+ lymphocytes and an increase in CD8+ lymphocytes.

45 4, NK and gammadelta+ cells each outnumbered CD4+ lymphocytes and CD11b+ macrophages.

46 tion in reservoirs such as latently infected CD4+ lymphocytes and cells of the macrophage-monocyte li

47 with decreased expression of Fas on splenic CD4+ lymphocytes and granzyme B in hepatic CD8+ lymphocy

48 Enhancing ceramide levels in CD4+ lymphocytes and in monocyte-derived macrophages wit

49 ) with fewer than 0.2 x 10(9)/L (200/microL) CD4(+) lymphocytes, and 1.04-fold (95% CI, 1.03-1.06) pe

50 unselected young TILs with a median of 8.0% CD4(+) lymphocytes, and 35 patients received CD8(+)-enri

51 multiple Kv channels are expressed by naive CD4(+) lymphocytes, and that the current amplitude and k

52 ipts using RNA derived from peripheral blood CD4+ lymphocytes, and genome-wide genotype data for 516

53 c pulmonary inflammation, reduced numbers of CD4+ lymphocytes, and lower Th2 cytokines/chemokine prot

54 a HeLa-derived indicator cell line, TZM-bl, CD4+ lymphocytes, and monocytes.

55 firmed that CAV was absolutely contingent on CD4+ lymphocytes, and that CD8+ lymphocytes played an ad

56 on was primarily detected on a subset of CD3+CD4+ lymphocytes, and was undetectable on CD34+CD133+CD4

57 CD4(+) lymphocytes anergized through partial stimulation

58 erived source of MIG/CXCL9, and 3) recipient CD4 lymphocytes are necessary for sustained MIG/CXCL9 pr

59 Currents expressed in naive CD4(+) lymphocytes are consistent with Kv1.1, Kv1.2, Kv1

60 Macrophages and CD4(+) lymphocytes are the principal target cells for hu

61 e whether CD8 lymphocytes, in the absence of CD4 lymphocytes, are capable of causing the intimal lesi

62 etion of splenic lymphocytes and circulating CD4(+) lymphocytes, as well as an inability to manifest

63 d a nearly complete depletion of circulating CD4(+) lymphocytes at day 7.

64 In this study, we analyzed Fas expression in CD4+ lymphocytes at the mRNA and protein levels in a lar

65 nt model of allergic pulmonary inflammation, CD4(+) lymphocytes bearing CCR3, CCR5, and CXCR4 traffic

66 data implicate antibody in conjunction with CD4+ lymphocytes bearing a Th1 phenotype as the critical

67 inhibitory role in the infection of purified CD4+ lymphocytes by the same isolate.

68 s were observed in infected mice depleted of CD4+ lymphocytes by using in vivo transfer of the IL-12

69 Unprimed CD8 lymphocytes in the absence of CD4 lymphocytes can cause intimal lesions of CAV.

70 trate that HIV-1 infection of primary, human CD4+ lymphocytes causes G2 arrest in a Vpr-dependent man

71 s with EPTB and HIV-infection, patients with CD4 lymphocyte cell count <100 were more likely to have

72 ART alone initiated at a CD4 lymphocyte cell count <200 cells/microL (80% coverag

73 We compared CD4 lymphocyte cell count levels at seroconversion, decl

74 Comparisons were adjusted for CD4(+) lymphocyte cell count.

75 r understanding of how HIV-1 manipulates the CD4(+)-lymphocyte cell cycle and apoptosis induction in

76 ajor fractions of circulating CCR4(+) memory CD4 lymphocytes coexpress the Th1-associated receptors C

77 re induced by the alveolar environment or if CD4(+) lymphocytes coexpressing this unusual combination

78 s of the response to Listeria, we found that CD4(+) lymphocytes coexpressing TNF-alpha and IFN-gamma

79 Thus, sepsis unmasks CD4(+) lymphocyte control of gut apoptosis that is not p

80 of CAV, sustained RANTES production requires CD4+ lymphocytes, correlates with mononuclear cell recru

81 vealed an inverse association between IE and CD4 lymphocyte count (odds ratio [OR] for 200-499 cells/

82 Shortened survival was associated with low CD4 lymphocyte count (P<.0001), no ART (P<.0001), and cr

83 relationship between level of infection and CD4 lymphocyte count (R = -0.73; P < 0.001).

84 Cheaper, simpler alternatives to CD4 lymphocyte count and HIV-1 RNA detection for assessi

85 Median CD4 lymphocyte count at diagnosis of a new ADI increased

86 other non-Hodgkin lymphoma (NHL), by age and CD4 lymphocyte count categories, were estimated using Po

87 During antiretroviral therapy, CD4 lymphocyte count increases are modest in some patien

88 optosis are associated with the magnitude of CD4 lymphocyte count recovery during antiretroviral ther

89 in the incidence of ADIs overall and within CD4 lymphocyte count strata, the relationship with treat

90 national Prognostic Index scores; the median CD4 lymphocyte count was 112/mm(3) (range, 19/mm(3) to 7

91 antiretroviral therapy (ART), and the median CD4 lymphocyte count was 131 cells/microL.

92 The median CD4 lymphocyte count was highest with pathogen-free diar

93 ADIs was seen after stratification by latest CD4 lymphocyte count within each year (< or = 50, 51-200

94 of control subjects (odds ratio adjusted for CD4 lymphocyte count, 3.8; 95% confidence interval, 2.2-

95 ciated with the magnitude of the increase in CD4 lymphocyte count, as were haplotypes in genes encodi

96 lure or relapse was associated with baseline CD4 lymphocyte count, being 12.3% (9/73; 95% confidence

97 Specific studies at baseline should include CD4 lymphocyte count, HIV-1 RNA level, and gynecologic e

98 cardiovascular risk factors, HIV viral load, CD4 lymphocyte count, statin use, antihypertensive use,

99 county, age group, sex, HIV/AIDS status, and CD4 lymphocyte count.

100 progression, comparable with that of cutoff CD4(+) lymphocyte count <350 lymphocytes/mm(3) and HIV-1

101 Cell-mediated immunodeficiency (CD4(+) lymphocyte count <500 cells/mm(3)) was significan

102 p24 antigen level correlated with both CD4(+) lymphocyte count (r=-0.34; P<.0001) and HIV-1 RNA

103 age HIV-1 infection and correlated with both CD4(+) lymphocyte count and HIV-1 RNA level.

104 CD4(+) lymphocyte count and human immunodeficiency virus

105 At baseline, patients had a median CD4(+) lymphocyte count of 0.015 x 10(9) cell/L, median

106 HIV-1 infection and low CD4(+) lymphocyte count were strongly associated with HP

107 f the 494 study participants (median initial CD4(+) lymphocyte count, 518 lymphocytes/mm(3)), 90 (18%

108 After controlling for age, baseline CD4(+) lymphocyte count, baseline HIV-1 RNA level, and d

109 nonpregnant women according to age, baseline CD4(+) lymphocyte count, receipt of HAART, and date of c

110 infection and inversely correlates with the CD4(+) lymphocyte count.

111 eatment-naive or interferon-experienced, had CD4+ lymphocyte count >/=200 cells/microL or >/=14%, and

112 Weibull proportional hazards model, baseline CD4+ lymphocyte count <200, black race, other nonwhite r

113 l, body mass index, and (for those with HIV) CD4+ lymphocyte count and HIV RNA levels.

114 te, these effects remained significant after CD4+ lymphocyte count and plasma HIV-1 RNA load at basel

115 t HIV-1 disease progression independently of CD4+ lymphocyte count and plasma HIV-1 RNA load, suggest

116 increased with early infection, low maternal CD4+ lymphocyte count at recruitment, and frequent morbi

117 odeficiency virus-infected patients when the CD4+ lymphocyte count is < or =200 cells/mm3.

118 Initiating HAART with a CD4+ lymphocyte count of <200 cells/mm3 was associated w

119 The pre-ART viral load and CD4+ lymphocyte count trajectories were also comparable

120 om 1988 through 1998, the viral load and the CD4+ lymphocyte count were measured approximately every

121 points: plasma HIV-1 RNA level (viral load), CD4+ lymphocyte count, initiation of antiretroviral ther

122 are based on the viral load, rather than the CD4+ lymphocyte count, will lead to differences in eligi

123 interval, 0.0-4.5%) among those with higher CD4 lymphocyte counts (p < 0.01).

124 ence of both conditions increases with lower CD4 lymphocyte counts and higher HIV-1 RNA levels.

125 he same CD4 count, whereas women have higher CD4 lymphocyte counts at the time of AIDS diagnosis.

126 , a higher weight, and HIV viremia and lower CD4 lymphocyte counts at the time of HAV vaccination wer

127 se at 6 months of HAV vaccination and higher CD4 lymphocyte counts at vaccination were inversely asso

128 Despite higher plasma HIV levels and CD4 lymphocyte counts in infancy, HAART can result in ti

129 t indicated the need to change the threshold CD4 lymphocyte counts or HIV-RNA levels for initiation o

130 The decline in CD4 lymphocyte counts was strongly associated with initi

131 ed clinical, demographic, and exposure data, CD4 lymphocyte counts, and stool samples for detection o

132 rifamycin resistance among patients with low CD4 lymphocyte counts.

133 al reasons may account for BL deficit at low CD4 lymphocyte counts.

134 NHL incidence rose steadily with decreasing CD4 lymphocyte counts; in contrast, BL incidence was low

135 increased among HIV-seropositive women with CD4(+) lymphocyte counts <500 cells/mm(3) and among wome

136 sults were similar in patients with baseline CD4(+) lymphocyte counts less than 0.010 x 10(9) cells/L

137 aths, particularly in those individuals with CD4(+) lymphocyte counts less than 50/mm(3).

138 and cord-maternal ratios were independent of CD4(+) lymphocyte counts or HIV-1 viral load.

139 Despite dramatic increases in CD4(+) lymphocyte counts, IL-2 did not enhance immunizat

140 gly associated with HIV RNA levels than with CD4(+) lymphocyte counts.

141 correlated with lower viral loads and higher CD4(+) lymphocyte counts.

142 th past or current HGV infection have higher CD4+ lymphocyte counts and better AIDS-free survival rat

143 ficiency virus type 1 (HIV-1) RNA levels and CD4+ lymphocyte counts in HIV-infected patients improved

144 HAART should be initiated at CD4+ lymphocyte counts of >200 cells/mm3.

145 d progressed faster than those with baseline CD4+ lymphocyte counts of >350 cells/mm3 (P=.01).

146 durable virologic suppression with baseline CD4+ lymphocyte counts of >350 cells/mm3 (P=.40).

147 ollers (VCs) (<5,000 HIV-1 RNA copies/ml and CD4+ lymphocyte counts of >400 cells/mul) capable of sol

148 e virologic suppression, those with baseline CD4+ lymphocyte counts of <200 cells/mm3 tended to progr

149 to progress faster than those with baseline CD4+ lymphocyte counts of 201-350 cells/mm3 (P=.09) and

150 ease progression between those with baseline CD4+ lymphocyte counts of 201-350 cells/mm3 and those wi

151 esented with advanced extranodal disease and CD4+ lymphocyte counts of less than 200/mm3.

152 Mean (SD) baseline and nadir CD4+ lymphocyte counts were 553(217) and 177(117) cells/

153 Throughout the 100 weeks, CD4+ lymphocyte counts were higher in the OZ1 group.

154 rends toward progressive modest increases in CD4+ lymphocyte counts with GM-CSF treatment at 16 weeks

155 ith ongoing HIV replication but may increase CD4+ lymphocyte counts.

156 Follicular helper T cells (Tfh), CD4 lymphocytes critical for efficient antibody response

157 cyte numbers and rates of proliferation, and CD4(+)-lymphocyte cytokine production levels were compar

158 e measured innate and adaptive cell numbers, CD4+ lymphocyte cytokine profile, chemokine expression,

159 > or = 30 days of therapy, and had baseline CD4 lymphocyte data available were included in the study

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

161 Polyfunctional CD4 lymphocytes, defined as producing intracellular inte

162 Compared with undepleted animals, CD4+ lymphocyte-depleted RMs showed a similar peak of vi

163 control was insensitive to either CD8(+) or CD4(+) lymphocyte depletion and, at necropsy, cell-assoc

164 r, these new findings strongly indicate that CD4(+) lymphocyte depletion seen in AIDS is primarily a

165 HIV-related CD4(+) lymphocyte depletion was strongly associated with

166 e and apoptosis induction in the progressive CD4(+)-lymphocyte depletion characteristic of HIV-1 path

167 ycle disruption, cell death, and ultimately, CD4+ lymphocyte depletion.

168 ts in CD8-/- knockout recipients (containing CD4+ lymphocytes) developed CAV, but significantly less

169 d the expression of CCR4, CXCR3, and CCR5 on CD4(+) lymphocytes directly isolated from a wide variety

170 High CD4(+) lymphocyte discordance was defined as higher CD4%

171 e expression profile in circulating CD8+ and CD4+ lymphocytes distinguishes between individuals with

172 This study compared patients with stable CD4(+) lymphocytes during viral relapse while receiving

173 defined according to age, sex, percentage of CD4+ lymphocytes, educational level of the parent or gua

174 iated Vpr can contribute to the depletion of CD4(+) lymphocytes either directly or by enhancing Fas-m

175 CD4(+) lymphocytes emigrated more efficiently than CD8(+

176 -0.86 log(10)) and increase in the number of CD4(+) lymphocytes, especially naive cells, were observe

177 ocultures by a reduction in the frequency of CD4(+) lymphocytes exiting the first division of the cel

178 In addition, the proportion of CD4(+) lymphocytes expressing CD69, an early activation

179 here were greater percentages of memory CD3+/CD4+ lymphocytes expressing CCR4, CCR5, and CXCR3 than n

180 ry and sufficient to trigger adoption of the CD4 lymphocyte fate.

181 ntified through a genome-wide eQTL survey of CD4(+) lymphocytes for association with asthma.

182 major requires the development of IFN-gamma+CD4+ lymphocytes for the induction of microbicidal activ

183 ndividuals; P < 0.01) and approached that of CD4 lymphocytes from the same individuals (median, 3,660

184 nd to protect immortalized and primary human CD4(+) lymphocytes from in vitro infection by both T-tro

185 In marked contrast to CD4(+) lymphocytes from PB (9% +/- 5% expressing CD45RA

186 on of gamma interferon were decreased in the CD4(+) lymphocytes from the alcohol-consuming mice.

187 Moreover, the CD4(+) lymphocytes from these mice showed no evidence of

188 RNA transcriptome and epigenome sequences of CD4(+) lymphocytes from three MS-discordant, monozygotic

189 vo consequences of Vpr function, we isolated CD4+ lymphocytes from HIV-1-infected individuals and int

190 Analysis of HIV proviruses in CD4+ lymphocytes from individuals after prolonged cART r

191 We used CD4(+) lymphocyte genome-wide mRNA expression profiling

192 Subjects with < 17% CD4 lymphocytes had earlier disease progression, compare

193 rejection only in strain combinations where CD4(+) lymphocyte help is absolutely required.

194 increased the number of IFN-gamma-producing CD4 lymphocytes in ELISPOT, 3) neutralization of MIG/CXC

195 inhibits the macrophage-mediated deletion of CD4 lymphocytes in HIV-infected persons.

196 s express the HIV coreceptor, CXCR4, whereas CD4 lymphocytes in many other sites do not, it prompted

197 udies, exogenous CXCR3 ligands were added to CD4 lymphocytes in MLRs, and the proliferative responses

198 expressing lymphocytes generated from naive CD4 lymphocytes in vitro is a novel mechanism of T regul

199 demonstrated that FADS2 mRNA is increased in CD4(+) lymphocytes in asthmatic patients and that the as

200 inor population of CD69(bright) CD25(bright) CD4(+) lymphocytes in BAL (10% +/- 6%) that were consist

201 5RA and CD29), the majority (55% +/- 16%) of CD4(+) lymphocytes in BAL (ALs) simultaneously expressed

202 leukocytes following TBI, total depletion of CD4(+) lymphocytes in LTs such as the spleen is not achi

203 l DNA at 24 weeks and the absolute number of CD4(+) lymphocytes in the alveolar space.

204 Thus, CD4(+) lymphocytes in the lung paradoxically coexpress s

205 n was characterized by a progressive loss of CD4(+) lymphocytes in the peripheral blood and lymph nod

206 d accumulation of gamma interferon-producing CD4(+) lymphocytes in the site.

207 ctor responses correlated with the number of CD4(+) lymphocytes in women ( rho =-0.68; P=.005) but no

208 y virus type 1 (HIV-1)-mediated depletion of CD4+ lymphocytes in an infected individual is the hallma

209 y of alveolar macrophages and recruitment of CD4+ lymphocytes in B2-deficient lungs.

210 essing CCR4, CCR5, and CXCR3 than naive CD3+/CD4+ lymphocytes in RA PB and RA SF, and greater percent

211 rces of RANTES and (2) determine the role of CD4+ lymphocytes in RANTES production during CAV develop

212 ric analysis demonstrated an accumulation of CD4+ lymphocytes in the lung with elevated expression of

213 freshly isolated circulating CCR4(+) memory CD4 lymphocytes (including both CLA(+) and CLA(-) fracti

214 od nonintestinal (alpha(4)beta(7)(-)) memory CD4 lymphocytes, including almost all skin memory CD4(+)

215 CD4 lymphocytes increased by 31 +/- 84 cells/mm(3) with

216 ted interference of Murr1 in primary resting CD4+ lymphocytes increased HIV-1 replication.

217 patients with AIDS who experience sustained CD4 lymphocyte increases while receiving HAART.

218 To ascertain whether CD4(+) lymphocyte increases induced by interleukin (IL)-

219 irochetal antigen-specific and Th1-polarized CD4+ lymphocytes infiltrate the CSF during monophasic CN

220 splanted into Tg recipients showed decreased CD4(+) lymphocyte infiltration and diminished immune act

221 rkedly reduced levels of airway eosinophils, CD4(+) lymphocyte infiltration, and mucus production, as

222 Multiple lines of evidence suggest that CD4+ lymphocytes initiate autoimmune responses against m

223 nt study, donor CCR5 density (CCR5 receptors/CD4 lymphocytes) inversely correlated with VCV antiviral

224 KIR3DL2 expression on NK cells and CD4 lymphocytes is increased in SpA and ERA.

225 Expression of CCR4 by circulating memory CD4(+) lymphocytes is associated with cutaneous and othe

226 The event leading to ATR activation in CD4+ lymphocytes is the accumulation of replication prot

227 d differences in gene expression profiles of CD4(+) lymphocytes isolated from the peripheral blood of

228 athology of DED involves the infiltration of CD4(+) lymphocytes, leading to tear film instability and

229 e level was 650 cells/uL, and median nadir T-CD4 lymphocyte level was 176 cells/uL.

230 In PLHIV, the median T-CD4 lymphocyte level was 650 cells/uL, and median nadir

231 times for CD8 (LLN >/=0.2x10(9) cells/l) and CD4 lymphocytes (LLN >/=0.4x10(9) cells/l) were 20 month

232 al lesions, suggesting that fully functional CD4 lymphocytes may be required for the genesis of gastr

233 se, and strategies expanding STAT3-activated CD4(+) lymphocytes may be considered as future therapeut

234 Passenger CD4 lymphocytes might therefore contribute to chronic re

235 At baseline, subjects had a median of 225 CD4 lymphocytes/mm3 and 17% CD4 lymphocytes.

236 1) and of those subjects with > 350 absolute CD4 lymphocytes/mm3 at baseline (P=.03).

237 )-infected patients with > or = 200 absolute CD4 lymphocytes/mm3 is unknown.

238 ed subjects who initiated therapy with > 350 CD4 lymphocytes/mm3.

239 D4 lymphocytes/muL versus those with >/= 250 CD4 lymphocytes/muL (incidence rate ratio 0.3 [95% confi

240 ncidence was lowest among people with </= 50 CD4 lymphocytes/muL versus those with >/= 250 CD4 lympho

241 mbers of myofibroblasts, and accumulation of CD4(+) lymphocytes, NK T cells, macrophages, and type 2

242 associated with depletion of gut-associated CD4(+) lymphocytes, none of the animals maintained a vir

243 cytes in AIDS patients and with a decline in CD4 lymphocyte numbers.

244 cells that showed a significant increase in CD4+ lymphocyte numbers.

245 regulation of mRNA in both the monocytes and CD4 lymphocytes of scleroderma patients, together with t

246 for the beta2-adrenergic receptor (ADRB2) in CD4(+) lymphocytes of subjects with asthma, and it affec

247 philia, particularly with HBV infection, low CD4(+) lymphocytes, or older age.

248 ce the effect in these studies was mainly on CD4 lymphocytes, our goal was to evaluate the ability of

249 CD4 lymphocyte percentage < 17% was the strongest predic

250 CD4 lymphocyte percentage could add prognostic informati

251 In this cohort, CD4 lymphocyte percentage predicted disease progression

252 Naive CD4(+) lymphocyte phenotype and TREC levels were not sig

253 a potential mechanism by which deficiency of CD4 lymphocytes predisposes to bacterial pneumonia.

254 ted lymph node or splenic lymphocytes, naive CD4(+) lymphocytes preferentially migrated toward media

255 ents had significantly (p <= 0.05) increased CD4+ lymphocyte programmed death-1 and monocyte programm

256 We confirmed that the CD4+ lymphocytes proliferate and produce IFN-gamma in re

257 rated that 1) exogenous MIG/CXCL9 stimulated CD4 lymphocyte proliferation in a MHC class II-mismatche

258 Both proteins inhibited CD3(+)/CD4(+) lymphocyte proliferation induced by PMA and ionom

259 y T cells preferentially expanded within the CD4(+) lymphocytes, reaching their peak expansion at mon

260 osoma larvae has on the development of early CD4+ lymphocyte reactivity is unclear, yet it is importa

261 eral blood could be used to identify CD8+ or CD4+ lymphocytes recognizing neoantigens identified by w

262 rated by increased numbers of lamina propria CD4(+)lymphocytes, redistribution of CD11c+cells, increa

263 Moreover, memory CCR9(+)CD4(+) lymphocytes respond to CD2 stimulation with proli

264 ly active antiretroviral therapy (HAART) and CD4 lymphocyte response was assessed in a cohort of 249

265 ibody inhibition, whereas adding NK cells to CD4(+) lymphocytes restored inhibition.

266 sis is associated with discordant peripheral CD4(+) lymphocyte results, especially in the setting of

267 suggest that the emergence of IL-4-producing CD4(+) lymphocytes results from a suppression in DC func

268 iation of naive T cells into T-helper type 1 CD4+ lymphocytes secreting interferon-gamma.

269 in blood T cells is associated with CCR4(+) CD4 lymphocytes, significant numbers of freshly isolated

270 Frequencies of CD4(+) lymphocytes spontaneously producing IL-4, IL-10,

271 In the mouse model, activated CD4(+) lymphocytes started to emerge in the liver on day

272 laque expansion of an aggressive and unusual CD4(+) lymphocyte subpopulation lacking the CD28 recepto

273 vealed loss of virtually all IL-22-producing CD4(+) lymphocytes, suggesting that STAT3 activation was

274 Myoung and Ganem provide evidence that CD4(+) lymphocytes suppress KSHV replication, promoting

275 analyzed we identified circulating CD8+ and CD4+ lymphocytes targeting 6 and 4 neoantigens, respecti

276 d chemokine and the numbers of peribronchial CD4(+) lymphocytes that drive the ongoing Th2 immune res

277 kine, as well as the number of peribronchial CD4(+) lymphocytes that express Th2 cytokines that promo

278 (HIV-1) infects quiescent and proliferating CD4+ lymphocytes, the virus replicates poorly in resting

279 7F, IL-21, IL-22, and IFN-gamma secretion in CD4(+) lymphocytes through the induction of suppressor o

280 ese mice, but also in greater confinement of CD4(+) lymphocytes to CNS perivascular spaces.

281 Naive CD4 lymphocytes undergo a polarization process in the pe

282 The eye-infiltrating host CD4 lymphocytes underwent additional changes, acquiring

283 copies/10(6) cells; n = 9) than that of CD8+ CD4- lymphocytes (undetectable in seven of nine individu

284 viral load and depleted contaminating CD3(+)CD4(+) lymphocytes using magnetic beads.

285 d macrophages induced the migration of human CD4+ lymphocytes via the CXCL10 receptor (CXCR3).

286 ve immunotherapy with autologous "SIV naive" CD4(+) lymphocytes was sufficient to rescue cell-mediate

287 The median percentage of CD4+ lymphocytes was 19%; a total of 56% of the children

288 The presence of CD4+ lymphocytes was required for sustained RANTES produ

289 cient hosts, yet the survival of transferred CD4+ lymphocytes was the same in recipients with or with

290 tic accumulation of donor CD8, but not donor CD4, lymphocytes was significantly reduced in GvHD induc

291 Hepatic CD4(+) lymphocytes were chief producers of IL-17A in pat

292 owth inhibition was abolished when CD8(+) or CD4(+) lymphocytes were depleted.

293 Fewer CD4(+) lymphocytes were recruited to inflamed G2A(-/-) c

294 etion by lymphocytes, whereas IL-4-secreting CD4+ lymphocytes were sufficient for adoptively transfer

295 and A3R5 assays, cell-free virus or infected CD4+ lymphocytes were used as targets for neutralization

296 evels of IL-16, a key chemotactic factor for CD4(+) lymphocytes, were reduced and migration to injure

297 equired for maximal IL-2 production by naive CD4(+) lymphocytes, whereas none appears to play a role

298 The percentage of CD4 lymphocytes, which expressed the intracellular trans

299 (DCimm) capture, process, and present Ags to CD4(+) lymphocytes, which reciprocally activate DCimm th

300 lly demonstrate by single cell analysis that CD4+ lymphocytes with a classical Th2 phenotype (IL-4+,