ライフサイエンスコーパス: MDDC

1 MDDC from rs7282490 GG risk-carriers had reduced ICOSL e

2 MDDC-mediated HIV-1 transmission to CD4(+) T cells invol

3 MDDCs clustered most closely to CD14(+) DDCs; furthermor

4 ability of CT, LT, and Forskolin to activate MDDC.

5 h2 cells than immature or TNF/IL-1-activated MDDCs when cultured with naive CD4+ T cells.

6 Furthermore, PNAg-activated MDDCs induced 2- to 3-fold more IL-4- and IL-13-secretin

7 In this regard, PMT activates MDDC to mature in a dose-dependent manner through the ac

8 Both Mphi and MDDC synthesized PAF; however, MDDC accumulated signific

9 he IgG2 Ab response is dependent on PAF, and MDDC selectively induce IgG2 production, we predicted th

10 sion was observed in both CD4(+) T-cells and MDDCs in the presence of Vpr.

11 plication-competent HIV-1 infected PBMCs and MDDCs revealed similar levels of reverse transcription p

12 ngle-cycle HIV-1 infection of both PBMCs and MDDCs was significantly enhanced in the presence of Vpr

13 emonstrate that gp120 binding to DC-SIGN and MDDCs is largely if not wholly carbohydrate dependent.

14 Analysis of conjugates between MDDCs and T cells revealed that, in the absence of antig

15 markedly stimulated CCR5 expression on both MDDCs and LCs.

16 Uptake of HMPV by MDDC was found to be primarily by macropinocytosis.

17 y labeled blebs and BPI were internalized by MDDC under these conditions.

18 ce the ability of HMPV to be internalized by MDDC, resulting in a reduced ability of the HMPV-stimula

19 nd tumor necrosis factor alpha production by MDDC in the presence of saturating concentrations of lip

20 s fimbriae in the uptake of P. gingivalis by MDDCs and in induction of immunostimulatory Th1 response

21 ulate human monocyte-derived dendritic cell (MDDC) differentiation.

22 We used monocyte-derived dendritic cells (MDDC) and CD4 T cells and measured [(3)H]thymidine incor

23 (Mphi) and monocyte-derived dendritic cells (MDDC) come from a common precursor, they are distinct ce

24 d in human monocyte-derived dendritic cells (MDDC) from rs7282490 ICOSLG GG risk carriers.

25 (MDM) and monocyte-derived dendritic cells (MDDC) in virus-like particles, dramatically enhancing th

26 mary human monocyte-derived dendritic cells (MDDC) in vitro and on subsequent MDDC maturation and act

27 T on human monocyte-derived dendritic cells (MDDC) in vitro and show a novel activity for PMT.

28 V-8 enters monocyte-derived dendritic cells (MDDC) through DC-SIGN, resulting in nonproductive infect

29 f immature monocyte-derived dendritic cells (MDDC) were observed.

30 a than did monocyte-derived dendritic cells (MDDC), despite similar NOD1 expression, similar cytokine

31 ophages or monocyte-derived dendritic cells (MDDC).

32 n immature monocyte-derived dendritic cells (MDDCs) and peripheral blood myeloid DCs.

33 ates human monocyte-derived dendritic cells (MDDCs) and triggers a specific genetic program that up-r

34 activated monocyte-derived dendritic cells (MDDCs) as measured by MHC/costimulatory molecule up-regu

35 Monocyte-derived dendritic cells (MDDCs) can efficiently bind and transfer HIV infectivity

36 Human monocyte-derived dendritic cells (MDDCs) infected with Toxoplasma gondii induce T-lymphocy

37 onkey (Rh) monocyte-derived dendritic cells (MDDCs) modified by gene transfer to over-express active

38 f HIV from monocyte-derived dendritic cells (MDDCs) to permissive T cells.

39 ecifically monocyte-derived dendritic cells (MDDCs) understudied.

40 d by human monocyte-derived dendritic cells (MDDCs) was performed with quantitative polymerase chain

41 lecules in monocyte-derived dendritic cells (MDDCs), enabling effective Ag presentation to T cells.

42 Human monocyte-derived dendritic cells (MDDCs), myeloid dendritic cells, and plasmacytoid dendri

43 fection of monocyte-derived dendritic cells (MDDCs), one of the first cell types to encounter virus i

44 to that of monocyte-derived dendritic cells (MDDCs), which are less susceptible to HIV-1 infection.

45 ture human monocyte-derived dendritic cells (MDDCs).

46 ture human monocyte-derived dendritic cells (MDDCs).

47 ocesses of monocyte-derived dendritic cells (MDDCs).

48 s, monocyte-derived/myeloid dendritic cells (MDDCs/mDCs), and by plasmacytoid dendritic cells (pDCs)

49 hanced gene transfer to monocyte derived DC (MDDC) by retargeting adenoviral (Ad) vectors to a marker

50 the maturation of human monocyte-derived DC (MDDC) in vitro.

51 ly impair primary human monocyte-derived DC (MDDC) responses upon stimulation induced through the RIG

52 ith HIV-1 and HSV-2 on monocyte-derived DCs (MDDC).

53 so compared these with monocyte-derived DCs (MDDCs) and MUTZ3 Langerhans cells (LCs) to investigate t

54 how that HIV fusion to monocyte-derived DCs (MDDCs) both decreases and kinetically slows when DCs are

55 ess this, we generated monocyte-derived DCs (MDDCs) in vitro which phenotypically and functionally re

56 f HIV-1 replication in monocyte-derived DCs (MDDCs) is associated with an increased expression of p21

57 al maturation in human monocyte-derived DCs (MDDCs) similar to but distinct from the activity of the

58 uration state in human monocyte-derived DCs (MDDCs) similar to that induced by lipopolysaccharide (LP

59 vered to primary human monocyte-derived DCs (MDDCs) using a lentivirus-based expression system.

60 THP-1 cells and monocyte-derived DCs (MDDCs) were investigated as a model for testing the func

61 MDCs and inflammatory monocyte-derived DCs (MDDCs) with TLR ligands, resulting in maturation.

62 uctive infection using monocyte-derived DCs (MDDCs), blood myeloid DCs, and B-cell lines expressing D

63 C-SIGN is expressed in monocyte-derived DCs (MDDCs), macrophage subsets, activated B lymphocytes, and

64 erogenous DC subsets, (monocyte-derived DCs [MDDCs], CD34(+) hematopoietic stem cell [HSC])-derived L

65 use as model skin DCs, the in vitro-derived MDDC and MUTZ3 LC populations grouped within the skin DC

66 ranslated TNF mRNA more efficiently than did MDDC.

67 nfections of dividing PBMCs and non-dividing MDDCs were carried out with single-cycle and replication

68 -SIGN on iDDC, as we previously reported for MDDC.

69 HIV-1 was more efficiently transmitted from MDDC to T cells.

70 also showed that transmission of HIV-1 from MDDCs to autologous T cells was significantly reduced in

71 tworks involved in phenotypic and functional MDDC differentiation.

72 On the other hand, MDDCs acquiring nonviable T. gondii antigens directly, o

73 However, MDDC stimulated with DeltaSHG induced increased prolifer

74 Both Mphi and MDDC synthesized PAF; however, MDDC accumulated significantly more of this lipid.

75 To test this hypothesis, human MDDC were prepared by treating adherent monocytes with I

76 activating effects of cholera toxin on human MDDC and mouse bone marrow-derived dendritic cells, we f

77 Human MDDCs rapidly internalized Ag in a calcium- and glycan-d

78 In THP-1 cells and human MDDCs, BG60-DC-SIGN interaction led to the activation of

79 Immature human MDDCs exposed to galectin-1 up-regulated cell surface ma

80 -translational modifications (PTMs) in human MDDCs due to chronic alcohol exposure.

81 n-1 is a novel endogenous activator of human MDDCs that up-regulates a significant subset of genes di

82 er in vitro acute alcohol treatment of human MDDCs.

83 compared with LPS, galectin-1-treated human MDDCs exhibited significantly better chemotactic migrati

84 Within 4 days the prevalence of the immature MDDC was approximately twofold higher in LJP cultures th

85 slowly than 81A in both mature and immature MDDCs.

86 ([(125)I]AB-MECA) to membranes from immature MDDCs yielded B(max) of 298 fmol/mg of protein and K(D)

87 lly identical to that obtained from immature MDDCs.

88 ignaling and unequivocally identify immature MDDCs as native expressers of the human A3 receptor.

89 aboratory-adapted 81A over NL4-3 in immature MDDCs and in ex vivo Langerhans cells, indicating that t

90 was elevated more than 100-fold in immature MDDCs compared with monocyte precursors.

91 Binding of E2 to immature MDDCs was dependent on DC-SIGN interactions, while bindi

92 th CXCR4 tropism mediated fusion to immature MDDCs with efficiencies similar to those of primary CCR5

93 s was delayed in mature compared to immature MDDCs, and NL4-3 fused more slowly than 81A in both matu

94 ermore, MNK controlled TNF mRNA abundance in MDDC and MDM upon NOD1 triggering.

95 red the possibility that PAF accumulation in MDDC might result from reduced turnover due to lower lev

96 aling by the blebs as measured by changes in MDDC morphology, surface expression of CD80, CD83, CD86,

97 s produced Vpx and replicated efficiently in MDDC and MDM.

98 lower levels of expression of the enzyme in MDDC and allowed these cells to produce PGE(2) in respon

99 predicted that PAF levels would be higher in MDDC than in Mphi.

100 g cooperative involvement of these miRNAs in MDDC differentiation.

101 The reduced levels of PAFAH in MDDC could be attributed to lower levels of expression o

102 duced a potent type I interferon response in MDDC.

103 in MDDCs alone and in cell-to-cell spread in MDDC-CD4(+) T cell cocultures.

104 tion, as measured by HIV-1-DNA and p24 Ag in MDDCs.

105 powerful in reducing HIV-1 infection both in MDDCs and T cells.

106 IV was recruited to sites of cell contact in MDDCs.

107 virus-induced production of the cytokine in MDDCs.

108 The reduction in the pool of dNTPs in MDDCs appears rather mostly due to a p21-mediated suppre

109 ce tumor necrosis factor-alpha expression in MDDCs via, in part, Raf-1 signaling pathways.

110 onal and DNA-binding activities increased in MDDCs upon exposure to the MEK1/2 inhibitor U0126.

111 ced replication-competent HIV-1 infection in MDDCs, while it modestly promoted viral infection in act

112 Induction of p21 in MDDCs decreases the pool of dNTPs and increases the anti

113 ively suppressed dengue virus replication in MDDCs and macrophages.

114 egration restriction of HIV-1 replication in MDDCs and show that the interaction of Vpr with the DCAF

115 at are able to restrict HIV-1 replication in MDDCs by inducing hypermutations in the viral genome.

116 This restriction of HIV-1 replication in MDDCs was observed in a single round of virus replicatio

117 y proteins and restrict HIV-1 replication in MDDCs while keeping an immature nonmigratory phenotype,

118 are able to restrict HIV-1BaL replication in MDDCs without significant induction of A3G, A3A, or A3F.

119 pression and restricted viral replication in MDDCs.

120 pr-deficient virus replication and spread in MDDCs alone and in cell-to-cell spread in MDDC-CD4(+) T

121 e downstream effectors of galectin-1-induced MDDC activation and migration.

122 ired for the histamine effect on LPS-induced MDDC responses.

123 sferable with supernatants from RSV-infected MDDC and was not due to transfer of live virus or RSV F

124 Supernatants from RSV-infected MDDC, but not MDDC exposed to UV-killed RSV or mock cond

125 ort processes in single-cycle HIV-1 infected MDDCs, but not in CD4(+) T-cells.

126 nt of proviral integration in HIV-1-infected MDDCs was unaffected by the absence of Vpr, the transcri

127 Furthermore, in HIV-1-infected MDDCs, significant downregulation of CD4 by Nef expressi

128 ions in the env genes from HIV-1BaL-infected MDDCs treated with low quantities of IFN-alpha2b.

129 us-stripped supernatants from HSV-2-infected MDDCs were shown to enhance HIV-1 infection, as measured

130 e supernatant and also within HSV-2-infected MDDCs.

131 , we now demonstrate that T. gondii-infected MDDCs are poor at activating T lymphocytes and are unabl

132 T lymphocytes exposed to infected MDDCs are significantly impaired in upregulation of CD69

133 Interestingly, MDDCs but not MDCs were protected against IAV infection

134 ects have a propensity to differentiate into MDDC and that this differentiation may be related to the

135 nsity of LJP monocytes to differentiate into MDDC may have important implications for both the host r

136 ropensity of monocytes to differentiate into MDDC.

137 of 81A, was low in both immature and mature MDDCs.

138 defect in HIV replication observed in mature MDDCs stems at least in part from a decline in viral fus

139 results suggest that nonhuman primate mature MDDCs can be genetically engineered to function as alloa

140 sed with markedly lower efficiency to mature MDDCs than immature DCs.

141 C-SIGN interactions, while binding to mature MDDCs was partly independent of DC-SIGN, suggesting that

142 d endocytic capacity, similar to LPS-matured MDDCs.

143 of MDDCs was also induced; moreover, matured MDDCs induced proliferation of autologous CD4(+) T cells

144 Dendritic cells derived from monocytes (MDDCs) in the presence of IL-10 render the MDDCs less re

145 Moreover, MDDCs pulsed with 381 also stimulated a higher autologou

146 Supernatants from RSV-infected MDDC, but not MDDC exposed to UV-killed RSV or mock conditions, contai

147 on with TLR7/8 ligand protected MDCs but not MDDCs from IAV infection.

148 sion of 20 miRNAs during days 1, 3, and 5 of MDDC differentiation.

149 onse by regulating the accessory activity of MDDC.

150 Like LJP monocytes, cultures of MDDC generated with interleukin-4 and granulocyte-macrop

151 )-induced upregulation of surface markers of MDDC maturation and did not prevent LPS-triggered alloge

152 r both CT and LT to induce the maturation of MDDC and that this activation is strictly cyclic AMP (cA

153 5'-AMP and Forskolin mimic the maturation of MDDC induced by CT and LT.

154 these toxins failed to induce maturation of MDDC, whereas dibutyryl-cyclic-3',5'-AMP and Forskolin m

155 This activation of MDDCs is often accompanied by upregulation of apolipopro

156 t time, in vitro chronic alcohol exposure of MDDCs modulates H3 and H4 and induces a significant incr

157 found to be sufficient for the induction of MDDCs that prime Th2-skewed T cell responses.

158 The HTLV-1 infection of MDDCs also was achieved in blood myeloid DCs following t

159 was shown to play a role in the infection of MDDCs as well as model B-cell lines.

160 d not affect single-cycle viral infection of MDDCs, suggesting that newly synthesized Vpr plays a sig

161 Interestingly, infections of MDDCs with viruses that encode Vpr mutants unable to int

162 P. gingivalis (10 micro g/ml), maturation of MDDCs was also induced; moreover, matured MDDCs induced

163 ntially affects the ET-induced maturation of MDDCs while not inhibiting ET-induced migration.

164 creased, by lipopolysaccharide maturation of MDDCs.

165 d Ara h 1 induced Erk 1/2 phosphorylation of MDDCs, consistent with previous reports on the effect of

166 to the maintenance of the immature state of MDDCs and myeloid DCs is partly dependent on the activit

167 lammatory responses following stimulation of MDDCs with activators of RIG-I-like receptor (RLR) signa

168 oinflammatory responses after stimulation of MDDCs with RIG-I activators.

169 creased infectivity but had little effect on MDDC maturation.

170 ans and was substantially more infectious on MDDC and MDM than the wild-type virus.

171 esults show that the effects of CT and LT on MDDC are mediated by cAMP.

172 lectin-1 binding to surface CD43 and CD45 on MDDCs induced an unusual unipolar co-clustering of these

173 lated Syk to the CD43 and CD45 co-cluster on MDDCs.

174 ulatory molecule ICOS and the ICOS ligand on MDDCs amplified nucleotide-binding oligomerization domai

175 nsmission was observed when CD4 molecules on MDDCs and DC-SIGN-CD4-expressing cell lines were blocked

176 Ab to TNF-alpha and its receptor, TNF-R1, on MDDCs markedly inhibited the CCR5-stimulating effect of

177 ere, we identify the galectin-1 receptors on MDDCs and immediate downstream effectors of galectin-1-i

178 and JAG1 expression was important for proper MDDC differentiation.

179 Rh MDDC transduction with Ad vectors using conventional met

180 immune responses induced by control AdGFP Rh MDDC in an antigen-specific manner.

181 Notably, AdTGF-beta1 Rh MDDC abrogated alloimmune responses induced by control A

182 overexpress active TGF-beta1 (AdTGF-beta1 Rh MDDC) significantly suppressed alloimmune responses in [

183 sduction of Rh MDDCs by retargeting Ad to Rh MDDC CD40.

184 Rh MDDCs were modified by recombinant adenovirus (Ad) trans

185 method that allogeneic mature AdTGF-beta1 Rh MDDCs inhibited proliferation of CD4 and CD8 responder T

186 Mature Rh MDDCs that were transduced to overexpress active TGF-bet

187 permitted high-efficiency transduction of Rh MDDCs by retargeting Ad to Rh MDDC CD40.

188 nhibition of both miR-21 and miR-34a stalled MDDC differentiation, as quantified by DC-SIGN/CD14 expr

189 nously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting that miRNA-mediated inh

190 in a reduced ability of the HMPV-stimulated MDDC to activate CD4(+) T cells.

191 ependent on contact between virus-stimulated MDDC and CD4(+) T cells.

192 n memory CD4(+) T cells and virus-stimulated MDDC.

193 itic cells (MDDC) in vitro and on subsequent MDDC maturation and activation of autologous T cells.

194 Histamine suppressed MDDC chemokine and proinflammatory cytokine secretion, n

195 to modulate the immunological status of the MDDC.

196 ions, consistent with differentiation to the MDDC phenotype.

197 (MDDCs) in the presence of IL-10 render the MDDCs less responsive to maturation stimuli, such as lip

198 ll were recruited to the interface while the MDDCs concentrated HIV to the same region.

199 BPI-enhanced delivery of the blebs to MDDC did not increase cell activation but permitted CD14

200 -fold) in delivery of (14)C-labeled blebs to MDDC, but not to monocyte-derived macrophages in the pre

201 DC-SIGN expressing cell lines, as well as to MDDCs.

202 levels of inflammatory cytokines compared to MDDCs.

203 gingivalis DPG3, efficiently gains entry to MDDCs in a manner dependent on active cell metabolism an

204 , unlike LPS-matured DCs, galectin-1-treated MDDCs did not produce the Th1-polarizing cytokine IL-12.

205 ocytes differentiated into either cell type, MDDC contained significantly less PAFAH than did Mphi an

206 When MDDCs were pulsed with recombinant fimbrillin of P. ging

207 d not increase association of the blebs with MDDC.