ライフサイエンスコーパス: CD4 lymphocyte

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

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

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

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

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

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

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

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

9 expression levels and replication in resting CD4+ lymphocytes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 4, NK and gammadelta+ cells each outnumbered CD4+ lymphocytes and CD11b+ macrophages.

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

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

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

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

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

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

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

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

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

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

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

53 CD4(+) lymphocytes anergized through partial stimulation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 irologic outcome (P < 0.001) and increase in CD4 lymphocyte count (P = 0.006).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 Disease progression was defined as CD4(+) lymphocyte count <200/microl or the presence of a

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

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

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

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

102 CD4(+) lymphocyte count and human immunodeficiency virus

103 The median CD4(+) lymphocyte count at lymphoma diagnosis has decrea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 rifamycin resistance among patients with low CD4 lymphocyte counts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 Polyfunctional CD4 lymphocytes, defined as producing intracellular inte

158 through CD40 can replace the requirement of CD4(+) lymphocytes, demonstrated by the development of c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 -0.86 log(10)) and increase in the number of CD4(+) lymphocytes, especially naive cells, were observe

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

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

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

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

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

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

180 Culture of autologous CD4 lymphocytes from peripheral blood mononuclear cells

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

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

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

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

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

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

187 ve demonstrated that retroviral infection of CD4+ lymphocytes from either autoantigen-stimulated TCR

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

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

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

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

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

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

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

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

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

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

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

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

200 5RA and CD29), the majority (55% +/- 16%) of CD4(+) lymphocytes in BAL (ALs) simultaneously expressed

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 The number of peripheral blood CD3(+) and CD4(+) lymphocytes is reduced 6- and 10-fold, respective

226 ctin (sFN) and that HIV infection of primary CD4+ lymphocytes is enhanced by >1 order of magnitude in

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

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

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

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

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

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

233 against Mycobacterium tuberculosis requires CD4+ lymphocyte-mediated immune responses and IFN-gamma

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

271 flow cytometric techniques we found that the CD4 lymphocyte subset was preferentially recruited to th

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

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

274 dye DiI, myelin basic protein (MBP)-specific CD4 lymphocytes that expressed low or high levels of ver

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

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

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

278 7F, IL-21, IL-22, and IFN-gamma secretion in CD4(+) lymphocytes through the induction of suppressor o

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

280 Naive CD4 lymphocytes undergo a polarization process in the pe

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

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

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

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

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

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

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

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

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

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

291 Substantial proliferative responses by CD4(+) lymphocytes were demonstrated to both antigens in

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+,