ライフサイエンスコーパス: phytohemagglutinin

1 ulation with alloantigen but not to mitogen (phytohemagglutinin).

2 mumps, bovine serum albumin), and a mitogen (phytohemagglutinin).

3 onses to certain stimulants and responses to phytohemagglutinin.

4 s of lymphoproliferative responses to Gag or phytohemagglutinin.

5 ity outbreak, showed suppressed responses to phytohemagglutinin.

6 r induction by Tat was distinct from that by phytohemagglutinin.

7 epeat (LTR) by the T cell receptor activator phytohemagglutinin.

8 s and in human T lymphocytes stimulated with phytohemagglutinin.

9 ocytes or on their proliferative response to phytohemagglutinin.

10 ibly greater response at the highest dose of phytohemagglutinin.

11 py and FACS analysis with the plant lectin l-phytohemagglutinin.

12 orbol-myristate acetate and ionomycin, or by phytohemagglutinin.

13 stimulated with either lipopolysaccharide or phytohemagglutinin.

14 proved avidity for wheat germ agglutinin and phytohemagglutinin.

15 ns, alloantigen (donor and third-party), and phytohemagglutinin.

16 d some proliferative response to the mitogen phytohemagglutinin.

17 less than 20-fold proliferative responses to phytohemagglutinin.

18 ression of DOR transcripts when activated by phytohemagglutinin.

19 ated adhesion of Jurkat cells in response to phytohemagglutinin.

20 was induced following T cell activation with phytohemagglutinin.

21 d the T lymphocyte proliferative response to phytohemagglutinin.

22 n the T lymphocyte proliferative response to phytohemagglutinin.

23 lood mononuclear cells (PBMC) activated with phytohemagglutinin 1 day after virus inoculation (restin

24 ls were cultured and stimulated ex vivo with phytohemagglutinin (10 microg/ml), and culture supernate

25 sed to the drug for 96 hrs, with addition of phytohemagglutinin (2.5 microg/ mL) for the last 48 hrs,

26 stimulation of their purified lymphocytes by phytohemagglutinin A (PHA), and (3) degree of inhibition

27 cells induced by influenza A virus (Flu) or phytohemagglutinin A (PHA), but had no effect on CD8(+)

28 ion upon stimulation with concanavalin A and phytohemagglutinin A was only 40-50% of that in iron-suf

29 he response to the polyclonal T-cell mitogen phytohemagglutinin A.

30 /Sezary syndrome (SS) stimulated with either phytohemagglutinin, a conventional mitogen, or a combina

31 ment with hBD1 and hBD2, in both resting and phytohemagglutinin-activated cells.

32 or the enhanced transcription of dor gene in phytohemagglutinin-activated EL-4 cells, a mouse T cell

33 hymocyte preparation Thymoglobulin (rATG) on phytohemagglutinin-activated human lymphocyte models des

34 it can be inhibited by A3G/A3F, we infected phytohemagglutinin-activated human PBMCs and A3G/A3F-pos

35 we performed a yeast two-hybrid screen of a phytohemagglutinin-activated human T-cell cDNA library w

36 We have identified a cDNA from a human phytohemagglutinin-activated lymphoblast library encodin

37 high- and low-affinity binding sites seen on phytohemagglutinin-activated lymphoblasts.

38 er 24 hr of treatment with supernatants from phytohemagglutinin-activated peripheral blood mononuclea

39 Phytohemagglutinin-activated peripheral blood mononuclea

40 ed for their ability to mediate infection of phytohemagglutinin-activated peripheral blood mononuclea

41 of adhesion molecules on plasma-derived and phytohemagglutinin-activated peripheral blood mononuclea

42 the stimulated transcription of DOR gene in phytohemagglutinin-activated T cells.

43 he dor promoter activity in both resting and phytohemagglutinin-activated T cells.

44 Phytohemagglutinin activation of these CD25- cells resul

45 Lymphocyte responses to phytohemagglutinin after 2 to 10 courses (median, 3.5) w

46 T-cell proliferation in response to phytohemagglutinin and concanavalin A remained stable or

47 On assessment using phytohemagglutinin and herpesvirus antigen-stimulated pr

48 rly developed higher lymphocyte responses to phytohemagglutinin and higher numbers of CD3(+) and CD45

49 eplication advantage in PBMC stimulated with phytohemagglutinin and interleukin-2 after infection, bu

50 erapy cycle, and cell cycle parameters after phytohemagglutinin and interleukin-2 stimulation were as

51 d rapidly at the beginning of maturation, as phytohemagglutinin and phaseolin mRNAs were induced.

52 After 6-9 months, responses to phytohemagglutinin and recall antigens improved.

53 iferative reactions were seen in response to phytohemagglutinin and Staph-A mitogens, as well as to c

54 heral blood lymphoproliferative responses to phytohemagglutinin and Staph-A mitogens, as well as to c

55 0 production stimulated by a T-cell mitogen, phytohemagglutinin, and by bacterial lipopolysaccharide.

56 d mononuclear cells activated with anti-CD3, phytohemagglutinin, and concanavalin A.

57 -year mononuclear cells were stimulated with phytohemagglutinin, and cytokine-response profiles were

58 myristate 13-acetate (PMA) + anti-CD3, PMA + phytohemagglutinin, and PMA + ionomycin] is unaffected b

59 3/CD28 antibodies, phorbol myristate acetate/phytohemagglutinin, and prostratin, as much (if not more

60 ononuclear cell proliferation in response to phytohemagglutinin, and this inhibition was overcome by

61 mRNAs for both receptors were present in phytohemagglutinin- and interleukin-2-activated peripher

62 hocyte phenotypes and mitogenic responses to phytohemagglutinin; and serum C-reactive protein levels.

63 id not influence proliferation stimulated by phytohemagglutinin, another commonly used mitogen.

64 phocytes with several polyclonal activators (phytohemagglutinin, anti-CD3 antibody and interleukin-2)

65 fold) during a 4-wk culture with IL-2, IL-7, phytohemagglutinin, anti-CD3, and anti-CD28 mAbs.

66 followed by treatment with trypsin, and then phytohemagglutinin antigen (PHA)-stimulated at days 4, 7

67 C2 and EC3, were shown by leucoagglutinating phytohemagglutinin binding to express at least some beta

68 Bioactive IL-12 (p70) was measured by the phytohemagglutinin blast proliferation assay and confirm

69 y-stimulating factor, lipopolysaccharide, or phytohemagglutinin, but not with interferon-gamma.

70 DBMC proliferated in MLC and in response to phytohemagglutinin, but to a lower magnitude than donor

71 ctivates transcription from MAT promoters of phytohemagglutinin (DLEC2) and beta-phaseolin (PHS beta)

72 recovered an excellent in vitro response to phytohemagglutinin, donor and third-party alloantigen, a

73 Moreover, addition of IL-2 and phytohemagglutinin during the infection completely rescu

74 ition, stimulation of Jurkat cells or normal phytohemagglutinin-expanded T lymphoblasts through TCR-C

75 hatase SHP-1 in both Jurkat cells and normal phytohemagglutinin-expanded T lymphoblasts.

76 Monocyte-depleted PBMCs were treated with phytohemagglutinin for 72 hours and then cultured in the

77 ood mononuclear cells even in the absence of phytohemagglutinin/IL-2.

78 ses of peripheral-blood mononuclear cells to phytohemagglutinin in 83 patients with severe combined i

79 ssed in thymus and spleen, and is induced by phytohemagglutinin in human peripheral blood mononuclear

80 in transforming growth factor beta 1 and in phytohemagglutinin-induced atherogenic cytokine producti

81 d Toxoplasma-infected APC strongly inhibited phytohemagglutinin-induced cell proliferation, whereas f

82 The ability of dexamethasone to inhibit phytohemagglutinin-induced lymphocyte proliferation was

83 completed for the following: spontaneous and phytohemagglutinin-induced production of interleukin 1 a

84 y affect CD4+ T-cell recovery or recovery of phytohemagglutinin-induced T-cell proliferation.

85 tivation of peripheral blood leukocytes with phytohemagglutinin induces strong expression of cell sur

86 onist Wy14643, inhibited IL-2 production and phytohemagglutinin-inducible proliferation in human peri

87 han that in uninfected control subjects, and phytohemagglutinin induction of additional GITR expressi

88 T cells from normals, following culture with phytohemagglutinin, interferon-gamma, recombinant human

89 all but 1 patient underwent apoptosis after phytohemagglutinin/interleukin-2 activation.

90 omide prevents T cell progression induced by phytohemagglutinin into the S phase of the cell cycle.

91 timal T-cell receptor (TCR) stimulation with phytohemagglutinin L supports efficient viral replicatio

92 the MAT genes DLEC2 and PHS beta, coding for phytohemagglutinin L-subunit and beta-phaseolin, respect

93 cient detection and quantification of p24 in phytohemagglutinin-L (PHA)-stimulated CD4(+) T cells fro

94 l-Phytohemagglutinin lectin binding and swainsonine inhibi

95 h2 [CD4(+)IL4(+)] cells) to stimulation with phytohemagglutinin, leptin, and dust mite, and classical

96 beta1,6-branching [determined by leukocytic phytohemagglutinin (LPHA) lectin-histochemistry] in 119

97 and PD 144795 also inhibit the induction by phytohemagglutinin of the transcription mediated by an H

98 Both primary activation, with phytohemagglutinin or antibodies to CD3, and costimulati

99 Mononuclear cells were stimulated with phytohemagglutinin or by mixing cells from two different

100 onse to phorbol 12-myristate 13-acetate plus phytohemagglutinin or calcium ionophore but not to anti-

101 ineage cells and had the ability to suppress phytohemagglutinin or mixed lymphocyte reaction-induced

102 cellular Ca(2+) with T cell receptor agonist phytohemagglutinin P or with Ca(2+)-mobilizing agents io

103 uppressed baseline proliferative response to phytohemagglutinin (P < .03) that increased during thera

104 ls when PBMC were incubated with the mitogen phytohemagglutinin (P = 0.03).

105 erleukin 4 (IL-4)-dependent proliferation of phytohemagglutinin (PHA) activated T cells noncompetitiv

106 rus stocks at various times before and after phytohemagglutinin (PHA) activation.

107 mma) production, was measured in response to phytohemagglutinin (PHA) and an M. avium antigen prepara

108 ompared with that evoked by stimulation with phytohemagglutinin (PHA) and anti-CD3.

109 ed in the presence of tetanus toxoid (TT) or phytohemagglutinin (PHA) and either killed whole-cell S.

110 d tumor necrosis factor-alpha in response to phytohemagglutinin (PHA) and of IL-2 in response to Derm

111 autologous or heterologous in vitro-infected phytohemagglutinin (PHA) blasts.

112 and killing virus peptide loaded autologous phytohemagglutinin (PHA) blasts.

113 ed with allogeneic mature dendritic cells or phytohemagglutinin (PHA) but did not induce apoptosis.

114 ma and interleukin-12 (IL-12) in response to phytohemagglutinin (PHA) but normal amounts of IFN-gamma

115 siveness to recall antigen, alloantigen, and phytohemagglutinin (PHA) following the in vitro addition

116 of wild-type and mutant alleles of the bean phytohemagglutinin (PHA) gene has been examined in tobac

117 than either IL-2 alone or IL-2 combined with phytohemagglutinin (PHA) in CD8-depleted PBMCs.

118 tained from blood center, and activated with phytohemagglutinin (PHA) in the presence or absence of r

119 (PBLs) undergoing stimulation in vitro with phytohemagglutinin (PHA) or OKT3 monoclonal antibody.

120 eripheral blood T lymphocytes by the mitogen phytohemagglutinin (PHA) or the superantigen staphylococ

121 a synthetic sequence were introduced into a phytohemagglutinin (PHA) reporter gene.

122 lysaccharide (LPS), concanavalin A (ConA) or phytohemagglutinin (PHA) stimulated canine peripheral bl

123 of normal metaphase chromosomes derived from phytohemagglutinin (PHA) stimulated peripheral blood lym

124 ymphocytes (PBLs) were treated in vitro with phytohemagglutinin (PHA) to determine levels of prolacti

125 re, nonstructural NS3/4 and NS5) and control phytohemagglutinin (PHA) was monitored prospectively and

126 f blood lymphocytes in vitro to optimal dose phytohemagglutinin (PHA) was reduced on days 60 (P = 0.0

127 en stimulated ex vivo with a T-cell mitogen, phytohemagglutinin (PHA), and cytokine release was deter

128 ts of PBLs before and after stimulation with phytohemagglutinin (PHA), anti-CD3 antibody, or CD40L.

129 Proliferative responses to phytohemagglutinin (PHA), influenza virus (Flu), and HPV

130 Phytohemagglutinin (PHA), purified protein derivative (P

131 .e., phorbol12-myristate 13- acetate [PMA]), phytohemagglutinin (PHA), sodium butyrate, or combinatio

132 f T-cell proliferative responses in vitro to phytohemagglutinin (PHA), tetanus toxoid, and normal don

133 t in peripheral blood leukocytes, microglia, phytohemagglutinin (PHA)- or PHA/interleukin-2-stimulate

134 osine phosphorylated in response to IL-12 in phytohemagglutinin (PHA)-activated human T cells.

135 ith single channel resolution in resting and phytohemagglutinin (PHA)-activated human T cells.

136 d lower in phorbol myristate acetate (PMA) + phytohemagglutinin (PHA)-activated mononuclear cells (MN

137 Phytohemagglutinin (PHA)-activated T cells were cultured

138 Toll-like receptor 4 (TLR4), and suppressed phytohemagglutinin (PHA)-mediated proliferation of norma

139 t, Fas-Ligand (Fas-L) membrane expression of phytohemagglutinin (PHA)-stimulated blood lymphocytes wa

140 In phytohemagglutinin (PHA)-stimulated CD8-depleted periphe

141 viability was normal, or cellular anergy, as phytohemagglutinin (PHA)-stimulated mPEG-PBMC demonstrat

142 tro, replication of MV-Edm was restricted in phytohemagglutinin (PHA)-stimulated peripheral blood lym

143 tion of interleukin-2 (IL-2) production from phytohemagglutinin (PHA)-stimulated peripheral blood mon

144 nd that PMNLs incubated with supernatants of phytohemagglutinin (PHA)-stimulated peripheral blood mon

145 MMG eliminated phytohemagglutinin (PHA)-stimulated proliferation of PBM

146 t the capacity to proliferate in response to phytohemagglutinin (PHA).

147 us laevis by injection of killed bacteria or phytohemagglutinin (PHA).

148 d in HPBL following mitogenic stimulation by phytohemagglutinin (PHA).

149 d with purified protein derivative (PPD) and phytohemagglutinin (PHA).

150 mal ATP release to Concanavalin A (ConA) and phytohemagglutinin (PHA; 190+/-86 ng/mL, 328+/-163 ng/mL

151 Phytohemagglutinin (Phaseolus vulgaris agglutinin; PHA;

152 ct inhibitory effect of IL-4 on anti-CD3- or phytohemagglutinin/phorbol 12-myristate 13-acetate-stimu

153 treatment with phorbol myristate acetate and phytohemagglutinin (PMA/PHA).

154 a significantly smaller [Ca2+]i signal after phytohemagglutinin protein stimulation of SF T cells (pe

155 s inversely associated with Th1/Th2 ratio to phytohemagglutinin (r = -0.43; P = 0.01) and directly wi

156 he association between treatment outcome and phytohemagglutinin response suggests more global and ant

157 ary data suggested little immunosuppression (phytohemagglutinin responses).

158 ll stimulation by phorbol myristate acetate, phytohemagglutinin, soluble or cross-linked antibodies t

159 proviral DNA levels were similar to infected phytohemagglutinin-stimulated adult PBMCs.

160 D3sFv, with an IC50 of 1 to 2 nmol/L against phytohemagglutinin-stimulated and alloantigen-stimulated

161 o = 0.61; P < 0.005) and was present in both phytohemagglutinin-stimulated and unstimulated periphera

162 The 3-IAABU total growth inhibition of phytohemagglutinin-stimulated healthy human lymphocytes

163 Suppression of IL-5 production from Ag- or phytohemagglutinin-stimulated human PBMCs by the TLR7 an

164 e-activated peripheral blood lymphocytes and phytohemagglutinin-stimulated lymphoblasts.

165 C and swine leukocyte antigen (SLA)-matched, phytohemagglutinin-stimulated lymphocyte targets but not

166 ed SLAdd miniature swine lysed only PAEC and phytohemagglutinin-stimulated lymphocytes from SLAdd ori

167 A time-course study of phytohemagglutinin-stimulated lymphocytes revealed that

168 Cord blood mononuclear cell phytohemagglutinin-stimulated lymphoproliferative respon

169 ce 10- to 80-fold-lower production of IFN by phytohemagglutinin-stimulated peripheral blood lymphocyt

170 The host-cell system used was phytohemagglutinin-stimulated peripheral blood mononucle

171 d by an HIV-1 p24 antigen reduction assay in phytohemagglutinin-stimulated peripheral blood mononucle

172 y against some primary HIV-1 isolates, using phytohemagglutinin-stimulated peripheral blood mononucle

173 -sensitive HIV-1 isolates, A012 and A018, in phytohemagglutinin-stimulated peripheral blood mononucle

174 ned in three assays: the GHOST cell assay, a phytohemagglutinin-stimulated peripheral blood mononucle

175 However, in phytohemagglutinin-stimulated pig-tailed macaque periphe

176 so significantly increased anti-CD3/CD28 and phytohemagglutinin-stimulated T cell proliferation, and

177 -2 receptor alpha-chain (CD25) expression on phytohemagglutinin-stimulated T cells.

178 A phytohemagglutinin-stimulated whole-blood cytokine assay

179 effect on viability of control (uninfected) phytohemagglutinin-stimulated/peripheral blood mononucle

180 on peripheral blood mononuclear cells during phytohemagglutinin stimulation and interleukin 2 priming

181 Phorbol 12-myristate 13-acetate and phytohemagglutinin stimulation of Jurkat cells expressin

182 more activated T cell cytokine profile after phytohemagglutinin stimulation were more developmentally

183 ID50, 13.3 microM without and 11 microM with phytohemagglutinin stimulation) and failed to induce apo

184 -cell proliferation after CD3 cross-linking, phytohemagglutinin stimulation, or phorbol myristate ace

185 and produced tumor necrosis factor-alpha on phytohemagglutinin stimulation.

186 tion status, and in normal lymphocytes after phytohemagglutinin stimulation.

187 teer T cells, but could be induced following phytohemagglutinin stimulation.

188 proliferative responses of IELs to mitogen (phytohemagglutinin), superantigen (staphylococcal entero

189 ctional expression in Lec15 cells, employing phytohemagglutinin/swainsonine selection.

190 In primary human leukocytes stimulated with phytohemagglutinin, telomerase activity increased > 10-f

191 tive response of PBMCs to the T cell mitogen phytohemagglutinin that was not significantly different

192 when they were simulated with either IL-2 or phytohemagglutinin, therefore showing that Hsp70 could a

193 Infected cells were then stimulated with phytohemagglutinin to render them permissive for viral r

194 ed by culturing autologous virus isolates in phytohemagglutinin-treated peripheral blood mononuclear

195 interleukin 2, while T cell activation with phytohemagglutinin was ineffective.

196 envelope (Env) peptides, tetanus toxoid, and phytohemagglutinin was measured in peripheral blood mono

197 Nonspecific activation using phytohemagglutinin was robust in chimpanzee T cells, ind

198 ens influenza and tetanus, alloantigens, and phytohemagglutinin were determined prospectively.

199 redominant proteins of PBPI were vicilin and phytohemagglutinins whereas the predominant proteins of