ライフサイエンスコーパス: moDC

1 moDCs infected with a virus lacking G protein expression

2 moDCs, however, required 0.5-1 log greater numbers than

3 nflammatory cytokine gene expression on IL-4-moDCs through the deacetylation of the promoters of thes

4 Gene expression profiling of IL-4-moDCs was defined by using mouse genome microarrays.

5 IL-4-moDCs were tested for their capacity to induce house dus

6 ifferentiation (IL-4-conditioned moDCs [IL-4-moDCs]) were analyzed for T(H)1-polarizing/inflammatory

7 Alloinduced moDC accumulation was significantly reduced when splenoc

8 DC-stimulated T-cell proliferation, or alter moDC development in vitro.

9 w-derived mouse dendritic cells (BMDCs), and moDC/naive CD4(+) T-cell cocultures were analyzed by usi

10 eted the bioactive heterodimer IL-12p70, and moDCs phagocytosed significantly more dying tumor cells

11 In both gammadelta T-APCs and moDCs, internalized antigen was transported across insul

12 cations at the Ccr7 locus of murine cDCs and moDCs.

13 -dependent T-cell proliferation, B cells and moDCs were pulsed with IgE-NIP-tetanus toxoid complexes

14 ent on cell-cell contact between B cells and moDCs, which was explained by increased upregulation of

15 C binding was CD23-dependent in B cells, and moDCs and CD23 aggregation, as well as IgE-IC internaliz

16 rentiation of monocytes into macrophages and moDCs.

17 f expanding T cells from aAPCs to moDCs, and moDCs to aAPCs, reversed the phenotypes.

18 surmise that such division of labor between moDCs and cDCs has implications for their respective rol

19 nsferred Gr-1(+) monocytes give rise to both moDC and exMACs in influenza-infected lungs.

20 degranulation marker CD107a, were primed by moDC, LC, and idDC to HIV-1 Gag and reverse transcriptas

21 and sustain NK-cell proliferation induced by moDCs.

22 ue to the lack of IFN-alpha/beta released by moDCs, since this effect was reversed by addition of exo

23 the cell surface, enabling IgE-IC uptake by moDCs in cocultures.

24 SF-dependent FcgammaRIII(+)PD-L2(+)CD209a(+) moDCs but generated iNOS(+) macrophages more efficiently

25 ing human primary monocytic dendritic cells (moDC) and co-culture with autologous T cells.

26 ocytes and monocyte-derived dendritic cells (moDC) and lower moDC costimulatory maturation.

27 generated monocyte-derived dendritic cells (moDCs) and macrophages are used clinically, e.g., to ind

28 g in human monocyte-derived dendritic cells (moDCs) and T cells, our data show no effect on moDC matu

29 fection of monocyte-derived dendritic cells (moDCs) contribute to immune suppression.

30 Monocyte-derived dendritic cells (moDCs) dramatically increase in numbers upon infection a

31 Monocyte-derived dendritic cells (moDCs) expressed abundant CD52 as expected.

32 autologous monocyte-derived dendritic cells (moDCs) or HLA-A2-Ig-based artificial APCs (aAPCs).

33 expressing monocyte-derived dendritic cells (moDCs) that represent classical antigen-presenting cells

34 Neonatal monocyte-derived dendritic cells (moDCs) were exposed to various combinations of TLR agoni

35 HLA-typed monocyte-derived dendritic cells (moDCs) were incubated with cellular fragments or necroti

36 f DI RNAs, monocyte-derived dendritic cells (moDCs) were infected with the wild-type Bilthoven strain

37 on of host monocyte-derived dendritic cells (moDCs) without any increase in conventional DCs.

38 (moMphis), monocyte-derived dendritic cells (moDCs), and myeloid-derived suppressor cells (MDSCs).

39 n D) human monocyte-derived dendritic cells (moDCs), bone marrow-derived mouse dendritic cells (BMDCs

40 re, mature monocyte-derived dendritic cells (moDCs), or PBMCs.

41 ytes can differentiate into dendritic cells (moDCs), which are potent inducers of adaptive immune res

42 cells and monocyte-derived dendritic cells (moDCs).

43 ophages or monocyte-derived dendritic cells (moDCs).

44 ell types (monocyte-derived dendritic cells [moDCs], PBMCs [peripheral blood mononuclear cells] and e

45 d combinations of human leukocytes (T cells, moDCs, and eosinophils) with each virus.

46 ring their differentiation (IL-4-conditioned moDCs [IL-4-moDCs]) were analyzed for T(H)1-polarizing/i

47 In contrast, moDCs require exogenous rhuIL-15 to phosphorylate STAT5

48 CXCL4-moDCs strongly potentiated proliferation of autologous C

49 ed secretion of IL-12 and TNF-alpha by CXCL4-moDCs exclusively upon stimulation with polyinosinic-pol

50 ble to that of moDCs, Ag processing by CXCL4-moDCs was impaired.

51 or to TLR- or Ag-specific stimulation, CXCL4-moDCs displayed a more matured phenotype.

52 eloped a model based on monocyte-derived DC (moDC) and calibrated NETs isolated from fresh human PMN.

53 Bovine monocyte-derived DC (moDC) were exposed to integrin-binding and cell culture-

54 s of CCR2(+) monocytes, monocyte-derived DC (moDC), and exudate macrophages (exMACs).

55 wever, in comparison to monocyte-derived DC (moDC), they respond to pathogen encounter with only low

56 Human monocyte-derived DCs (moDCs) and circulating conventional DCs coexpress activa

57 e response, we studied monocyte-derived DCs (moDCs) and plasmacytoid DCs (pDCs) in two HPS2 siblings.

58 Monocyte-derived DCs (moDCs) conditioned by IL-4 during their differentiation

59 MNs from chronic patients to MN-derived DCs (moDCs) induced cross-presentation of the intracellular r

60 ure, immunogenic human monocyte-derived DCs (moDCs) up-regulate the immune-inhibitory enzyme, indolea

61 itioned human immature monocyte-derived DCs (moDCs) with RA (RA-DCs), before pulsing them with HIV an

62 mpared the capacity of monocyte-derived DCs (moDCs) with that of CD34+ hematopoietic progenitor cell

63 -induced activation of monocyte-derived DCs (moDCs), as downregulation of its expression by small int

64 rately generated blood monocyte-derived DCs (moDCs), as well as Langerhans cells (LCs) and dermal-int

65 revealed that CCR2(+) monocyte-derived DCs (moDCs), but not conventional DCs, were critical for in v

66 /6 mice and found that monocyte-derived DCs (moDCs), including CD11b(hi)Ly-6C(lo) tissue-resident and

67 lammatory cytokines in monocyte-derived DCs (moDCs), with the notable exception of alpha/beta interfe

68 gens in vitro than are monocyte-derived DCs (moDCs).

69 Cs compared with human monocyte-derived DCs (moDCs).

70 notype and function of monocyte-derived DCs (moDCs).

71 differentiate in situ into inflammatory DCs (moDCs) and F4/80(+) macrophages.

72 maRIII(+)PD-L2(+)CD209a(+), GM-CSF-dependent moDCs but was distal from the DC lineage, as shown by fa

73 52, as well as the recovery of donor-derived moDCs in a less inflammatory environment later after tra

74 However, monocyte-derived (moDCs) in the lung express very low levels of Ccr7 and c

75 of Abs against CD88 and CD26 to distinguish moDCs and cDCs in multiple organs and mouse strains will

76 ytokine milieu for T-cell activation than do moDCs, thus accounting for their superior stimulation of

77 Moreover, the presence of NETs during moDC maturation diminished the capacity of these moDC to

78 d tissue myeloid DC targeted by HIV-1, i.e., moDC, LC, and idDC, can prime multispecific, polyfunctio

79 ted significantly more IL-15 than did either moDCs or DDC-IDCs, which is especially important to the

80 Despite their prominence, how emergent moDCs and resident conventional DCs (cDCs) divide their

81 specific CD4(+) memory T cells, but exposing moDC to IC containing inactivated FMDV resulted in signi

82 Finally, moDCs are phenotypically heterogeneous and therefore nec

83 This newly generated moDC population and not the resident DCs (or macrophages

84 Mature HPS2 moDCs showed impaired expression of CD83 and DC-lysosome

85 Studies on human moDC revealed an activation of TLR2 and NOD2 receptors a

86 L lactis G121-treated murine BMDCs and human moDCs released TH1-polarizing cytokines and induced TH1

87 pha/beta production by DENV in primary human moDCs is a novel mechanism of immune evasion.

88 Unlike infection of immature moDCs, infection of mature moDCs is not lytic and result

89 ucing nTreg expansion compared with immature moDCs or PBMCs in an HLA-DR- and CD80/CD86-dependent way

90 ri W620 showed a lack of IL-12 production in moDC due to missing transcription of the IL-12p35 mRNA.

91 Although IgE-ICs were degraded in moDCs, B cells did not degrade the complexes but recycle

92 26 can reliably distinguish FLT3-independent moDCs from FLT3-dependent cDCs in C57BL/6 mice.

93 In contrast, they downregulated LPS-induced moDC maturation, as shown by decreased surface expressio

94 Infected moDC were unable to efficiently stimulate FMDV-specific

95 Interestingly, DENV-2-infected moDCs fail to prime T cells, most likely due to the lack

96 Bilthoven infected moDCs less efficiently than Edmonston-Zagreb.

97 or the transfer of supernatant from infected moDCs depleted of infectious virions, is nevertheless su

98 resident and CD11b(hi)Ly-6C(hi) inflammatory moDCs, express the complement 5a receptor 1/CD88, wherea

99 the physiological requirements that initiate moDC differentiation in vivo.

100 lood, and monocytes were differentiated into moDCs.

101 eukin-4 induce monocyte differentiation into moDCs in vitro, but little is known about the physiologi

102 Intriguingly, moDCs potently reduced the ability of cDCs to stimulate

103 IL-4 licensed moDCs for the induction of T(H)2 responses, causing hous

104 generated by stimulation with peptide-loaded moDCs and aAPCs, T cell function, assessed by expression

105 yte-derived dendritic cells (moDC) and lower moDC costimulatory maturation.

106 Mature moDC-expanded nTregs were highly demethylated at the Tre

107 Allogeneic mature moDC-expanded nTregs were at low ratios (<1:320), potent

108 The allogeneic mature moDC-expanded nTregs were fully characterized by analysi

109 without IL-2 could facilitate optimal mature moDC-induced nTreg expansion.

110 Allogeneic mature moDCs and skin-derived DCs were superior in inducing nTr

111 Human allogeneic mature moDCs are highly efficient stimulator cells, in the pres

112 Although mature moDCs can generate Tregs by this IDO-dependent mechanism

113 nditions without exogenous cytokines, mature moDCs expand regulatory T cells (Tregs) by an IDO-depend

114 ells with autologous, IDO-expressing, mature moDCs results in up to 10-fold expansion of CD4(+)CD25(b

115 may establish a nonlytic reservoir in mature moDCs that inhibits DC-mediated T-cell responses.

116 In contrast, we show that infected mature moDCs lose surface CD83 while maintaining intracellular

117 s in the supernatants of CMV-infected mature moDCs, and CD83 immunodepletion removes the inhibitory e

118 of a small percentage of CMV-infected mature moDCs, or the transfer of supernatant from infected moDC

119 ction of immature moDCs, infection of mature moDCs is not lytic and results in minimally decreased su

120 This would mitigate moDC phagocytosis and presentation of host-derived antig

121 h direct and indirect presentation by murine moDCs versus cDCs.

122 ced robust secretion of IL-12p70 by neonatal moDCs by unlocking transcriptional control on the p35 su

123 Coactivation of neonatal moDCs through Dectin-1 allows TLR-mediated IL-12p70 secr

124 The capacity of neonatal moDCs to differentiate naive CD4 TH cells was evaluated

125 cytes of HIV-1-negative adults and neonates (moDC) and by Langerhans cells (LC) and interstitial, der

126 delivering Mtb to lymph nodes, cDCs but not moDCs induce proliferation of Mtb-specific CD4 T cells.

127 Furthermore, cDCs, but not moDCs, stimulated naive T cell proliferation.

128 a more robust recruitment and activation of moDC that opposes rapid fungal expansion during the affe

129 Infection of moDC by the FMDV IC was productive and associated with h

130 Next-generation sequencing of mRNA of moDC-expanded nTregs revealed a strong induction of Treg

131 nd Th17-mediated disease is its endowment of moDCs to induce Th17 differentiation in vivo, although i

132 D32a and hence reduces the immunogenicity of moDCs even for a strong stimulus like alloantigen.

133 ts TLR4-dependent signaling, as infection of moDCs with recombinant hMPV lacking G protein inhibited

134 T-cell activation without the involvement of moDCs.

135 igand was mediated by CD1d, as maturation of moDCs was inhibited by anti-CD1d antibodies and Pru p 3-

136 ine stocks resulted in greater maturation of moDCs, inhibition of virus replication, and induction of

137 ared innate and adaptive immune responses of moDCs with those that were differentiated in the presenc

138 ernalization of Ag was comparable to that of moDCs, Ag processing by CXCL4-moDCs was impaired.

139 s than did wild-type virus, and treatment of moDCs with purified G protein resulted in a similar inhi

140 mphoid chemokine receptors CCR7 and CXCR4 on moDC were not altered when moDC matured in the presence

141 DCs) and T cells, our data show no effect on moDC maturation/activation, alloreactive T-cell prolifer

142 on in vivo, although it has little effect on moDC numbers.

143 ated NETs alone had no discernable effect on moDC.

144 imulatory molecules CD86 and MHC class II on moDCs induced by B cells.

145 Only moDCs secreted the bioactive heterodimer IL-12p70, and m

146 osis and endosomal acidification in BMDCs or moDCs impaired the release of TH1-polarizing cytokines,

147 pport the use of mRNA-electroporated LCs, or moDCs supplemented with exogenous rhuIL-15, as vaccines

148 vity for inflammatory iNOS(+) macrophages or moDCs.

149 When expanded from bone marrow precursors, moDCs were enriched at the Ccr7 locus for trimethylation

150 ly by T-cell depletion, but also by removing moDCs and their precursors.

151 Treg expansion requires moDC contact, CD80/CD86 ligation, and endogenous interle

152 We found that CXCL4 exposure can sensitize moDCs for TLR-ligand responsiveness, as illustrated by a

153 Similarly, moDCs prepared from the lung also displayed increased le

154 n adaptive immune responses, modulating some moDC functions and thereby participating in the control

155 C class II expression and in vitro survival, moDCs were 20-fold less efficient than cDCs at inducing

156 es a new role for IL-4 by demonstrating that moDCs are conditioned by IL-4 for the induction of T(H)2

157 ern blot, and microscopy, we determined that moDCs express the cell adhesion molecule mucosal vascula

158 unctional comparison in vitro indicated that moDCs are the most potent type of Th17-inducing DCs comp

159 nt circulating viral antigen and showed that moDCs from chronically infected patients stimulated expa

160 maturation diminished the capacity of these moDC to induce T lymphocyte proliferation in both autolo

161 A major component of this moDC accumulation appears to be recruitment.

162 Despite this, moDCs were more potent at inducing Th1 and Th17 differen

163 ed RSV-induced activation of T cells through moDCs, rhinovirus was not inhibited; UV inactivation did

164 ion and cytokine production when compared to moDC.

165 onditions of expanding T cells from aAPCs to moDCs, and moDCs to aAPCs, reversed the phenotypes.

166 d during the differentiation of monocytes to moDCs.

167 LCs nevertheless proved superior to moDCs and DDC-IDCs in stimulating CTL against a recall v

168 the precursor activities of monocytes toward moDCs or microbicidal macrophages.

169 ut also processed and presented by HLA-typed moDC, monocytes, and PBMCs.

170 HLA-typed moDC, monocytes, or PBMCs were incubated with HLA class

171 on of immunostimulation by normal uninfected moDCs.

172 CCR7 and CXCR4 on moDC were not altered when moDC matured in the presence of NETs.

173 CD8(+) T cells were multifunctional, whereas moDC-generated cells were mostly monofunctional.

174 d FoxP3 expression within CD4 cells, whereas moDCs drive T-cell proliferation.

175 bled in vivo inflammatory macrophages, while moDCs resembled in vivo inflammatory DCs.

176 lication in DC-T cell mixtures compared with moDCs.

177 per cell than CD8(+) T cells generated with moDCs.

178 Without moDCs, rhinovirus induced T-cell proliferation of both C