ライフサイエンスコーパス: lymphocyte proliferation

1 an inflammatory ocular disease by inhibiting lymphocyte proliferation.

2 yte apoptosis, is paradoxically required for lymphocyte proliferation.

3 gulatory T cell recruitment and control of T lymphocyte proliferation.

4 to neurotransmission, vasoconstriction, and lymphocyte proliferation.

5 a potential mechanism by which HTLV-1 alters lymphocyte proliferation.

6 n kinase A as potential targets for altering lymphocyte proliferation.

7 ine the mechanism by which CO can modulate T lymphocyte proliferation.

8 (Z-VAD-FMK pan-caspase inhibitor) blocked T lymphocyte proliferation.

9 , IL-2, IL-4, IL-5, and IL-10 production and lymphocyte proliferation.

10 mulatory molecules required for AChR-induced lymphocyte proliferation.

11 L-2 receptors and thus is a key regulator of lymphocyte proliferation.

12 the coccidioidal Ag preparation T27K induced lymphocyte proliferation.

13 t activate NF-kappaB and did not stimulate B lymphocyte proliferation.

14 ive oxygen intermediates, which can suppress lymphocyte proliferation.

15 mino acids that are known to be required for lymphocyte proliferation.

16 coimmobilized with anti-CD3 mAb, activated T lymphocyte proliferation.

17 lity of 11 L-tryptophan analogues to support lymphocyte proliferation.

18 e [DP]) cells, and antigen-specific mature T-lymphocyte proliferation.

19 ocess the appropriate Ags for stimulation of lymphocyte proliferation.

20 ction of PBMC responses to peptides than did lymphocyte proliferation.

21 negatively, respectively, with inhibition of lymphocyte proliferation.

22 roduction alone is not sufficient to inhibit lymphocyte proliferation.

23 ability to inhibit lymphokine production and lymphocyte proliferation.

24 osis factor (TNF) family that costimulates B lymphocyte proliferation.

25 circulating carotenoid concentrations and T lymphocyte proliferation.

26 f the immune system, leading to increases in lymphocyte proliferation.

27 ly cytokine production, HLA expression, or T lymphocyte proliferation.

28 volve inhibition of T cell activation and/or lymphocyte proliferation.

29 of IL-2, IFN-gamma, and TNF-alpha, and on T lymphocyte proliferation.

30 However, Fas engagement also can costimulate lymphocyte proliferation.

31 ssessed by delayed type hypersensitivity and lymphocyte proliferation.

32 ation promotes continued TCR signaling and T-lymphocyte proliferation.

33 mplex with apalbumin1 capable of stimulating lymphocyte proliferation.

34 4 replicated this differential modulation of lymphocyte proliferation.

35 + cells functionally suppressed autologous T-lymphocyte proliferation.

36 on of FoxO in the nucleus and attenuation of lymphocyte proliferation.

37 ed that surfactant protein A (SP-A) inhibits lymphocyte proliferation.

38 er was combined with anti-caCD3 to stimulate lymphocyte proliferation.

39 nditional deletion of FADD leads to impaired lymphocyte proliferation.

40 nflagration associated with infection-driven lymphocyte proliferation.

41 nt to participate in cytokine production and lymphocyte proliferation.

42 blockade also reduced alloantigen-specific T lymphocyte proliferation.

43 neutralization of MIG/CXCL9 in MLR reduced T lymphocyte proliferation, 4) IFN-gamma-inducible protein

44 moattractant/CXCL11 had similar effects on T lymphocyte proliferation, 5) MIG/CXCL9 stimulated T lymp

45 blood cells were associated with impaired T lymphocyte proliferation, abnormal mononuclear cell cyto

46 Body temperature, leukocyte number, lymphocyte proliferation activity, and cell-associated v

47 onses, lowered leukocyte counts, and reduced lymphocyte proliferation activity.

48 by reductions in white blood cell counts and lymphocyte proliferation activity.

49 imals with each protein and assaying splenic lymphocyte proliferation against a series of overlapping

50 Antibodies and antigen-specific lymphocyte proliferation against Listeria increased in a

51 elated with inhibition of mitogen-stimulated lymphocyte proliferation, although urease inhibited IL-2

52 membrane is an indispensable step in normal lymphocyte proliferation and activation.

53 MPA inhibits both lymphocyte proliferation and activation.

54 IL)-4 and -13 are acknowledged regulators of lymphocyte proliferation and activation.

55 nal biologic effects including inhibition of lymphocyte proliferation and cell growth.

56 Two inhibitors of protein kinase A reduce lymphocyte proliferation and CREB-1 phosphorylation.

57 Parameters of immunity included lymphocyte proliferation and cytokine production in vitr

58 Lymphocyte proliferation and cytokine production were an

59 Positive lymphocyte proliferation and cytokine responses to PPD-M

60 Importantly, the fine specificity of lymphocyte proliferation and cytokine secretion in cord

61 o the inhibition of T cell receptor-mediated lymphocyte proliferation and cytokine secretion.

62 ell production but does increase CD4 and CD8 lymphocyte proliferation and death by inducing entry int

63 The lymphocyte proliferation and death rates in both CD4(+)

64 tical model to determine fractional rates of lymphocyte proliferation and death.

65 een Myc and Mad levels may normally modulate lymphocyte proliferation and development in part by cont

66 T lymphocyte proliferation and differentiation are control

67 multiple fundamental processes that drive T lymphocyte proliferation and differentiation.

68 tudies showed that D-4F reduced allogeneic T-lymphocyte proliferation and effector cytokine productio

69 udy demonstrates that MIG/CXCL9 stimulates T lymphocyte proliferation and effector cytokine productio

70 asal route showed increased antigen specific lymphocyte proliferation and enhanced the frequency of T

71 and NFATs (NFATc and NFATp), and c) inhibits lymphocyte proliferation and expression of proinflammato

72 In vitro immunologic markers of lymphocyte proliferation and gamma interferon (IFN-gamma

73 and bacterioferritin as measured by splenic lymphocyte proliferation and gamma interferon production

74 Lymphocyte proliferation and gamma interferon production

75 unoglobulin G2 (IgG2) and stimulate memory T-lymphocyte proliferation and gamma interferon secretion.

76 These MDSCs suppressed both T lymphocyte proliferation and IFN-gamma production and ha

77 ngly, PPTSP44 triggered the highest level of lymphocyte proliferation and IFN-gamma production.

78 In mice, ex vivo lymphocyte proliferation and IL-2 production were increa

79 stimulation assays revealed no difference in lymphocyte proliferation and IL-2 secretion between EGFP

80 ivity in the context of enhanced Ag-specific lymphocyte proliferation and IL-4 production.

81 ion of lymph nodes, H(4)R antagonism reduced lymphocyte proliferation and IL-4, IL-5, and IL-17 level

82 ession, IL-2- enhanced IFN-gamma production, lymphocyte proliferation and immune cell phenotype analy

83 eloid lineage and to selectively stimulate B-lymphocyte proliferation and immunoglobulin production.

84 B/WcKO mice, B/DcKO mice showed defective B-lymphocyte proliferation and impaired antibody responses

85 ia coli and all three parasites stimulated B-lymphocyte proliferation and increased macrophage produc

86 endrobatidis cells and supernatants impaired lymphocyte proliferation and induced apoptosis; however,

87 ultures, allogeneic CDCs elicited negligible lymphocyte proliferation and inflammatory cytokine secre

88 were induced after treatment, as measured by lymphocyte proliferation and interferon gamma enzyme-lin

89 We studied in vitro lymphocyte proliferation and interleukin 2 (IL-2) secret

90 t encodes a toxin that specifically inhibits lymphocyte proliferation and interleukin-2 (IL-2), IL-4,

91 ins play a significant role in EBV-induced B-lymphocyte proliferation and invasion.

92 Mycophenolic acid (MPA) is an inhibitor of lymphocyte proliferation and is well established as an i

93 Lymphocyte proliferation and MHC I expression in the set

94 ROCKs also play a role in lymphocyte proliferation and migration.

95 In vitro assays showed correction of the lymphocyte proliferation and neutrophil adhesion defects

96 between healthy eating patterns and greater lymphocyte proliferation and no evidence for an associat

97 of folate-deficient cells rapidly restored T lymphocyte proliferation and normal cell cycle, reduced

98 TAK-779 (a) decreased alloantigen-specific T-lymphocyte proliferation and number of IFN-gamma produci

99 the importance of metabolism in controlling lymphocyte proliferation and offer a novel explanation f

100 ith T lymphocytes and macrophages to cause T lymphocyte proliferation and overwhelming cytokine produ

101 -2) is a pleiotropic cytokine that regulates lymphocyte proliferation and peripheral tolerance.

102 Lymphocyte proliferation and production of gamma interfe

103 synthesized and evaluated for inhibition of lymphocyte proliferation and production of pro-inflammat

104 of transforming growth factor type beta1 on lymphocyte proliferation and production of tumor necrosi

105 ic E. coli (lifA) mediates the inhibition of lymphocyte proliferation and proinflammatory cytokine sy

106 ermined that iPSC-MSCs significantly inhibit lymphocyte proliferation and promote Treg response in PB

107 1 has an essential role in mediating B and T lymphocyte proliferation and requires its CARD to engage

108 Lymphocyte proliferation and skin-test responses were co

109 The inhibition of uveitogenic lymphocyte proliferation and suppression of EAU by p28/p

110 Regulators of lymphocyte proliferation and survival have also been ide

111 itantly, they up-regulated genes involved in lymphocyte proliferation and survival, most notably inte

112 ositide 3-kinase activation is important for lymphocyte proliferation and survival.

113 25+ T regulatory cells and increasing both T-lymphocyte proliferation and T memory cells.

114 ne being able to functionally promote both T lymphocyte proliferation and T(H)1 cytokine production.

115 H/HeJ mice were less potent stimulators of T lymphocyte proliferation and TH1/TH17 polarization compa

116 cellular responses, as measured by in vitro lymphocyte proliferation and Th2 cytokine production (i.

117 ization of CXCR3 reduced MIG/CXCL9-induced T lymphocyte proliferation and the number of IFN-gamma-pos

118 Inhibition of lymphocyte proliferation and the reduction of proinflamm

119 dy was to determine whether CO can inhibit T lymphocyte proliferation and then to determine the mecha

120 r that functions as a central regulator of T lymphocyte proliferation and trafficking.

121 that colon tumors expressing LIGHT stimulate lymphocyte proliferation and tumor cell-specific antitum

122 TT-specific lymphocyte proliferation and type 1/type 2 cytokine prod

123 Lymphocyte proliferation and viability were lost in vitr

124 oid and natural killer cell numbers, reduced lymphocyte proliferation, and abrogated phagocyte activi

125 sate (TSL), induce DC maturation, autologous lymphocyte proliferation, and antigen-specific lymphocyt

126 sociation of the capacity to induce uveitis, lymphocyte proliferation, and chemoattraction.

127 ponses (delayed-type hypersensitivity [DTH], lymphocyte proliferation, and cytokine production) were

128 n peripheral blood leukocyte subpopulations, lymphocyte proliferation, and cytokine responses were me

129 on with either tacrolimus or cyclosporine on lymphocyte proliferation, and expression of interleulin-

130 -1-specific immunoglobulin G (IgG) titers, T-lymphocyte proliferation, and gamma interferon productio

131 serologic responses to Salmonella Typhi LPS, lymphocyte proliferation, and interferon (IFN)- gamma pr

132 vitreous infiltrates, fewer granulomas, less lymphocyte proliferation, and lower serum IRBP antibody

133 rmation and proinflammatory cytokine levels, lymphocyte proliferation, and neutrophil recruitment.

134 resulted in lactate accumulation, inhibited lymphocyte proliferation, and prevented immunoglobulin p

135 erity, including chest radiograph, beryllium lymphocyte proliferation, and spirometry.

136 f clonal selection requires a rapid burst in lymphocyte proliferation, and this involves a metabolic

137 immunosuppression by its ability to inhibit lymphocyte proliferation, and with neurotoxicity through

138 sing inhibition of BLV-dependent spontaneous lymphocyte proliferation as a measure of antiviral activ

139 This study using lymphocyte proliferation as a model suggests that the re

140 7 treatment resulted in potent inhibition of lymphocyte proliferation as measured by in vitro mitogen

141 nt Ags 85A, 85B, and 85C induced significant lymphocyte proliferation as well as the production of ga

142 The 35-kDa protein also induced significant lymphocyte proliferation as well as the production of IF

143 dex showed modest effects of Myc to increase lymphocyte proliferation, as normal lymphocytes already

144 The early response was characterized by T-lymphocyte proliferation, as reflected by S-phase DNA, w

145 ed baseline interferon gamma (IFN-gamma) and lymphocyte proliferation assay (LPA) responses to antige

146 PBMC using the dexamethasone suppression of lymphocyte proliferation assay and repeated after the ad

147 ied by enzyme-linked immunosorbent assay and lymphocyte proliferation assay, showing that TprK is the

148 increased bioactivity in a peripheral blood lymphocyte proliferation assay.

149 reas cellular immunity was determined by the lymphocyte proliferation assay.

150 ed with heat-killed bacteria as antigen in a lymphocyte proliferation assay.

151 Tritiated thymidine based lymphocyte proliferation assays and interferon gamma (IF

152 ion of donor-specific reactivity by means of lymphocyte proliferation assays has also been used; howe

153 development was followed by flow cytometry, lymphocyte proliferation assays, and T-cell receptor Vbe

154 In vitro lymphocyte proliferation assays, chromium-release assays

155 tion were examined by chemotactic assays and lymphocyte proliferation assays, respectively.

156 ll responses that inhibit the EBV-mediated B lymphocyte proliferation associated with PTLD.

157 ich several compounds showed inhibition of T-lymphocyte proliferation at levels equal or superior to

158 munodeficiency virus type 1 (HIV-1)-specific lymphocyte proliferation before and after treatment with

159 creased neutrophils, accompanied by hampered lymphocyte proliferation but increased monocyte phagocyt

160 phorylation and impaired IL-4-induced CD4+ T lymphocyte proliferation but left unperturbed Stat6 acti

161 ) and spermine (SPM), also inhibit amphibian lymphocyte proliferation, but a third polyamine, cadaver

162 has been widely applied to investigate human lymphocyte proliferation, but solid tissue samples may a

163 nal transduction pathways regulating B and T lymphocyte proliferation, but the functional role of Ca(

164 ctivity were evaluated by flow cytometry and lymphocyte proliferation by (3)H-thymidine incorporation

165 Its most prominent mechanism is to inhibit lymphocyte proliferation by inhibition of inosine monoph

166 cted children and suggest that inhibition of lymphocyte proliferation by MV may play a role in the su

167 This study demonstrates that inhibition of lymphocyte proliferation by nonpolymorphic MHC class II

168 onducted to measure chemokine production and lymphocyte proliferation by peripheral blood mononuclear

169 trate that hydroquinone and catechol inhibit lymphocyte proliferation by quenching the essential tyro

170 We show here that STAT3 inhibits T-lymphocyte proliferation by up-regulating the expression

171 Spontaneous lymphocyte proliferation could be measured with splenocy

172 ne exchange factors plays a critical role in lymphocyte proliferation, cytoskeletal reorganization, a

173 tion of toleragenic cytokines, inhibition of lymphocyte proliferation, delivery of reparative and pro

174 BFT did not directly induce lymphocyte proliferation, dendritic cell stimulation, or

175 l-mediated inhibition of anti-CD3-stimulated lymphocyte proliferation did not require cell contact.

176 immune signals and metabolic cues to direct lymphocyte proliferation, differentiation and survival.

177 g the effect of adipocytes and adipokines on lymphocyte proliferation, differentiation, and activatio

178 e involved in signaling cascades mediating T-lymphocyte proliferation, differentiation, and migration

179 to maintain tolerance via the regulation of lymphocyte proliferation, differentiation, and survival.

180 ored, IFN-inducible protein that regulates T lymphocytes proliferation, differentiation, and developm

181 here is a paucity of data demonstrating that lymphocyte proliferation does occur in humans treated wi

182 3-kinase (PI3K) activation is essential for lymphocyte proliferation driven by receptors for antigen

183 s effect could account for the inhibition of lymphocyte proliferation during hypoxia.

184 d CS1 may play a role in the regulation of B lymphocyte proliferation during immune responses.

185 calcineurin (eg, cyclosporine, tacrolimus), lymphocyte proliferation (eg, azathioprine, mycophenolat

186 In addition, lymphocyte proliferation ex vivo was reduced under hyper

187 d on inflammation and coagulation markers, T lymphocyte proliferation/ex-vivo cytokine secretion, pla

188 feration following partial hepatectomy and T lymphocyte proliferation following anti-CD3 stimulation

189 h1 immune response characterized by in vitro lymphocyte proliferation, gamma interferon production, a

190 Increased antigen-specific lymphocyte proliferation, gamma interferon, and interleu

191 demonstrate the importance of this factor in lymphocyte proliferation, gene expression, and Th cell d

192 However, both methods necessitate in vitro lymphocyte proliferation, generating highly differentiat

193 The lymphocyte proliferation, histopathology, and systemic f

194 Lymphocyte proliferation, IFN-gamma production, STAT5 ph

195 lymphocyte functionality (CD4(+) and CD8(+) lymphocyte proliferations, IFN-gamma production, STAT5 p

196 or cyclosporine significantly inhibited the lymphocyte proliferation, IL-2 expression, and induced T

197 Furthermore, inhibition of splenic lymphocyte proliferation, IL-2, and IFN-gamma production

198 arried out a prospective kinetic analysis of lymphocyte proliferation in 13 rhesus macaques inoculate

199 DC stimulated Hc-specific lymphocyte proliferation in a concentration-dependent ma

200 Finally, DC stimulated Candida-specific lymphocyte proliferation in a concentration-dependent ma

201 d that 1) exogenous MIG/CXCL9 stimulated CD4 lymphocyte proliferation in a MHC class II-mismatched ML

202 ished the capacity of these moDC to induce T lymphocyte proliferation in both autologous and allogene

203 immune-induced wasting and enhanced ex vivo lymphocyte proliferation in broilers and decreased tumor

204 ls as detected by intracellular staining and lymphocyte proliferation in culture after BeSO(4) exposu

205 yte proliferation, 5) MIG/CXCL9 stimulated T lymphocyte proliferation in MHC class I- and total MHC-m

206 levels and showed suppression of IL-32 and T-lymphocyte proliferation in MLCs.

207 osome-depleted, nonpromoter sites to drive B-lymphocyte proliferation in primary human infection.

208 al loads in the presence of both antibodies, lymphocyte proliferation in response to blood monocytes

209 T lymphocyte proliferation in response to both HIV-1 antig

210 cellular immunity, characterized by reduced lymphocyte proliferation in response to both parasite an

211 Protection was associated with reduced lymphocyte proliferation in the draining cervical lymph

212 us studies showed that SP-A and SP-D inhibit lymphocyte proliferation in the presence of accessory ce

213 bserve gene expression changes indicative of lymphocyte proliferation in the spleen, which is associa

214 PX3.102 markedly suppressed antigen-specific lymphocyte proliferation in vitro at a concentration 10

215 molecules, and failed to support allogeneic lymphocyte proliferation in vitro.

216 he TSLP pathway, as were T lymphopoiesis and lymphocyte proliferation in vitro.

217 e wells) derived from Tri r 2 to stimulate T lymphocyte proliferation in vitro.

218 In this study, CsA inhibition of lymphocyte proliferation in whole-blood cultures ex vivo

219 tudinal analyses of neutralizing antibodies, lymphocyte proliferation, in vivo-activated and memory c

220 Both proteins inhibited CD3(+)/CD4(+) lymphocyte proliferation induced by PMA and ionomycin in

221 ns, specifically suppressed peripheral blood lymphocyte proliferation, induced expression of a wide p

222 IL-12p35 suppresses lymphocyte proliferation, induces expansion of IL-10-exp

223 elayed-type hypersensitivity, enhancement of lymphocyte proliferation, induction of an innate IL-12 r

224 CII-specific lymphocyte proliferation, interferon-gamma production, a

225 Lymphocyte proliferation is key to the regulation of the

226 Although PI3K activation is required for B-lymphocyte proliferation, it is not known whether PI3K-d

227 therapeutic potency, their ability to cause lymphocyte proliferation limits their application.

228 CMV lymphocyte proliferation (LP), responder-cell frequency

229 Palladium (Na(2) [PdCl(4)])-induced lymphocyte proliferation (LPT), Th1 and Th2 cytokine pro

230 Suppression of lymphocyte proliferation <60% was considered to indicate

231 les produced by the fungus that inhibit frog lymphocyte proliferation, methylthioadenosine (MTA) and

232 This peptide was more bioactive against lymphocyte proliferation, nearly equivalent to the comme

233 Similarly, significant reduction of lymphocyte proliferation occurred at much lower exposure

234 Mitogen-dependent lymphocyte proliferation of swine peripheral blood monon

235 cells, and they show an inhibitory effect on lymphocyte proliferation of two LST1 proteins although t

236 No differences in lymphocyte proliferation or expression of activation mar

237 ct on cytokine production and no effect on T lymphocyte proliferation or HLA expression.

238 beta-glucan, unlike CpG, had no effect on B lymphocyte proliferation or IgM production.

239 F-alpha; however, we measured no change in T lymphocyte proliferation or in the percentage of alveola

240 were failure to demonstrate either impaired lymphocyte proliferation or maternal T-cell engraftment.

241 significantly affect antigen-specific recall lymphocyte proliferation or type 1 cytokine production i

242 sociated with higher antibody (P = .006) and lymphocyte proliferation (P = .041), and lower CD4+ T ly

243 an autoantigen for IPF CD4 T cells, inducing lymphocyte proliferation (P = 0.004) and IL-4 production

244 tion of cytokine responses in the absence of lymphocyte proliferation, particularly during the early

245 pport emerging evidence that HTLV-1 promotes lymphocyte proliferation preceding early viral spread in

246 , there is a significant discrepancy between lymphocyte proliferation rates estimated in different st

247 IgG subclass deficiency, impaired Ag-induced lymphocyte proliferation, reduced cytokine production by

248 There was a secondary lymphocyte proliferation response to third party (AO str

249 expression, which governs much of the early lymphocyte proliferation responses.

250 BLV viremia was assessed by spontaneous lymphocyte proliferation (SLP) in cultures of blood mono

251 ive animals invariably displayed spontaneous lymphocyte proliferation (SLP) in vitro.

252 ic immune abnormalities, such as spontaneous lymphocyte proliferation (SP), increased STAT5 phosphory

253 ound that incubator oxygen levels influenced lymphocyte proliferation stimulated by two commonly used

254 and inflammatory responses and contribute to lymphocyte proliferation, survival, and oncogenesis.

255 ne interleukin-7 (IL-7) functions to enhance lymphocyte proliferation, survival, and recruitment of i

256 Cs and bone marrow-derived MSCs (BM-MSCs) on lymphocyte proliferation, T-cell phenotypes and cytokine

257 We evaluated the beryllium lymphocyte proliferation test (BeLPT), bronchoalveolar l

258 We established a flow cytometric lymphocyte proliferation test (LPT) for the detection of

259 The beryllium lymphocyte proliferation test is the cornerstone of both

260 The blood beryllium lymphocyte proliferation test is used in medical surveil

261 A confirmed abnormal beryllium lymphocyte proliferation test without evidence of lung d

262 and diminished microfilarial antigen-driven lymphocyte proliferation than cells from children of uni

263 ess IFN-gamma and TNF-alpha production and T lymphocyte proliferation than in cultures with platelets

264 pleens of acceptors more potently suppressed lymphocyte proliferation than Treg from rejectors in the

265 a potent and selective inhibitor of B and T lymphocyte proliferation that has proven effective in re

266 ment, it was found that the PRRSV-specific T lymphocyte proliferation, the percentages of CD4(+), CD8

267 emonstrate that c-FLIP(L) is essential for T lymphocyte proliferation through an NF-kappaB-independen

268 ABCG1 as an important negative regulator of lymphocyte proliferation through the maintenance of cell

269 gamma-induced intracellular enzyme, inhibits lymphocyte proliferation through tryptophan degradation.

270 ersistent, maximal cytokine production and T lymphocyte proliferation, thus contributing to the devel

271 nhibition of calcineurin, and inhibit mature lymphocyte proliferation to antigen.

272 permitted its profound inhibitory effect on lymphocyte proliferation to be observed.

273 his study supports the concept that in vitro lymphocyte proliferation to HIV-1 antigens, augmented af

274 had CD4(+) T-cell lymphopenia and decreased lymphocyte proliferation to mitogens.

275 ponses to presentation 1 and presentation 2; lymphocyte proliferation to Salmonella Typhi flagellin o

276 Lymphocyte proliferation to the immunizing antigen (gp12

277 ction of virus capsid-specific antibodies or lymphocyte proliferation to the virus antigen (class II

278 n A-stimulated whole blood assays to measure lymphocyte proliferation (tritium labeled thymidine inco

279 a cell cycle inhibitory checkpoint, allowing lymphocyte proliferation, tumor targeting, and regressio

280 udies provide clear evidence that control of lymphocyte proliferation via c-Rel is linked to a cyclin

281 T lymphocyte proliferation was assessed by (3)H-thymidine

282 hasone to inhibit phytohemagglutinin-induced lymphocyte proliferation was assessed by (3)H-thymidine

283 Increased CD8(+) T-lymphocyte proliferation was associated with cell expans

284 Lymphocyte proliferation was blocked by anti-HLA antibod

285 d only 10 to 20% by MV coinfection; however, lymphocyte proliferation was decreased by 60 to 90% and

286 and plasma of infected subjects to suppress lymphocyte proliferation was demonstrated by (3)H thymid

287 We found that CD4+CD45RO+ and CD8+CD45RO+ T lymphocyte proliferation was elevated in HTLV-1-infected

288 cultures of PBMCs with iPSC-MSCs or BM-MSCs, lymphocyte proliferation was evaluated using 3H-thymidin

289 al CD8+ T lymphocyte numbers were higher and lymphocyte proliferation was increased in tumor-bearing

290 Lymphocyte proliferation was inhibited after 2 h of nora

291 Lymphocyte proliferation was measured in one-way MLC wit

292 Lymphocyte proliferation was tested by H(3)-thymidine in

293 of 250 parts per million CO, CD3-activated T lymphocyte proliferation was, remarkably, inhibited by 8

294 when hepatocytes were co-cultured with liver lymphocytes, proliferation was inhibited by IFN-gamma/ST

295 To establish the role of c-FLIP(L) in T lymphocyte proliferation, we have generated a conditiona

296 on of glutamate and in the immune system for lymphocyte proliferation, we tested the effect of the gl

297 itreous infiltrates, retinal granulomas, and lymphocyte proliferation were assessed in OPN-null and W

298 ular IL-10 production, and allergen-specific lymphocyte proliferation were performed.

299 n of CD4 lymphocytes significantly decreased lymphocyte proliferation whereas CD8 cell depletion did

300 ctivated dendritic cells induced increased T lymphocyte proliferation within the aorta 72 h after ado