ライフサイエンスコーパス: moDC

1 moDCs also represented the most potent DC subset in the

2 moDCs infected with a virus lacking G protein expression

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

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

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

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

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

8 A moDC library of 4,666 proteins was generated and protein

9 Accordingly, moDC depletion limits Treg generation and improves the t

10 Alloinduced moDC accumulation was significantly reduced when splenoc

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

12 during vaccination and paves the way for an moDC-targeting vaccine strategy to enhance immune respon

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

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

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

16 ntly reduced in patient peripheral blood and moDCs, respectively.

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

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

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

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

21 rentiation of monocytes into macrophages and moDCs.

22 Using MCs and moDCs, we confirmed that IgE/FceRI activation induces sF

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

24 NK-EVs also have an effect on monocyte and moDCs (monocyte-derived dendritic cells) function, drivi

25 e TNF mediates the induction of lung Bcl6(+) moDCs.

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

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

28 ediator in regulation of primary NK cells by moDC.

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

30 and sustain NK-cell proliferation induced by moDCs.

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

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

33 en and Toll-like receptor ligand to CD169(+) moDCs and Axl(+) CD169(+) DCs led to cytokine production

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

35 al9 axis on monocyte-derived dendritic cell (moDC) maturation and T-cell proliferation were determine

36 1-dependent monocyte-derived dendritic cell (moDC) population that functioned as an early sentinel ni

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

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

39 confronted monocyte-derived dendritic cells (moDC) and NK cells resulted in the same NK activation ph

40 vated macrophages (MPh) and dendritic cells (moDC) from 12 adult dairy cows.

41 ocytes and monocyte-derived dendritic cells (moDCs) also contain significant reserves of endo-lysosom

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

43 d on human monocyte-derived dendritic cells (moDCs) and PBMCs.

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

45 howed that monocyte-derived dendritic cells (moDCs) are responsible for lung IgA induction.

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

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

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

49 rations in monocyte-derived dendritic cells (moDCs) in response to stimulation with lipopolysaccharid

50 n of human monocyte-derived dendritic cells (moDCs) inhibits dendritic cell (DC) maturation, resultin

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

52 jection of monocyte derived dendritic cells (moDCs) that presented Candida albicans.

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

54 of these, monocyte-derived dendritic cells (moDCs) were determined to be the most efficient.

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

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

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

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

59 so), human monocyte-derived dendritic cells (moDCs), and murine bone marrow-derived mast cells (MC) w

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

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

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

63 igen-laden monocyte-derived dendritic cells (moDCs), promoting long-lasting humoral immunity against

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

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

66 ulation of monocyte-derived dendritic cells (moDCs).

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

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

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

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

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

72 CXCL4-moDCs strongly potentiated proliferation of autologous C

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

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

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

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

77 re able to induce human monocyte-derived DC (moDC) maturation in a concentration-dependent manner.

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

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

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

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

82 by in vitro-generated monocyte-derived DCs (moDCs) and macrophages and by ex vivo-isolated splenic m

83 Among these are monocyte-derived DCs (moDCs) and monocyte-derived macrophages (moMacs), which

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

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

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

87 demonstrate that human monocyte derived DCs (moDCs) support productive viral replication following in

88 iting method for human monocyte-derived DCs (moDCs) that mediates knockouts with a median efficiency

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

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

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

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

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

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

95 /6 mice and found that monocyte-derived DCs (moDCs), including CD11b(hi)Ly-6C(lo) tissue-resident and

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

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

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

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

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

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

102 52, as well as the recovery of donor-derived moDCs in a less inflammatory environment later after tra

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

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

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

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

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

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

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

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

111 Finally, moDCs are phenotypically heterogeneous and therefore nec

112 s unknown how other DC subsets distinct from moDCs respond to EBOV infection.

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

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

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

116 Human moDCs or PBMCs were incubated with proteins and evaluate

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

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

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

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

121 In moDC, mTOR inhibition increased expression of pro-inflam

122 d that they were both strongly implicated in moDC maturation induced by IFX aggregates.

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

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

125 o the global proteomic changes that occur in moDCs during antigen processing and presentation and fur

126 g this method, we perform genetic screens in moDCs, identifying mechanisms by which DCs tune response

127 26 can reliably distinguish FLT3-independent moDCs from FLT3-dependent cDCs in C57BL/6 mice.

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

129 Infected moDC were unable to efficiently stimulate FMDV-specific

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

131 Bilthoven infected moDCs less efficiently than Edmonston-Zagreb.

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

133 Functionally, WNV-infected moDCs dampened allogenic CD4 and CD8 T cell activation a

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

135 lture with mixed lymphocytes, mTOR-inhibited moDC exhibited a cytokine profile favoring a Th1 respons

136 the physiological requirements that initiate moDC differentiation in vivo.

137 lood, and monocytes were differentiated into moDCs.

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

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

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

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

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

143 l adjuvant cyclic di-GMP differentiated lung moDCs into Bcl6(+) mature moDCs promoting lung memory T(

144 reveals the functional heterogeneity of lung moDCs during vaccination and paves the way for an moDC-t

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

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

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

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

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

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

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

152 ifferentiated lung moDCs into Bcl6(+) mature moDCs promoting lung memory T(H) cells, but they are dis

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

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

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

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

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

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

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

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

161 gulate myeloid differentiation and monocytic-moDC lineage commitment, respectively.

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

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

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

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

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

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

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

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

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

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

172 Perturbations of moDC endo-lysosomal pH result in accumulation of HLA-B*3

173 wing RT is necessary for the accumulation of moDCs.

174 ivity as well as the tolerogenic capacity of moDCs.

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

176 ts unravel the immunosuppressive function of moDCs and identify GM-CSF as an immunotherapeutic target

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

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

179 T-cell activation without the involvement of moDCs.

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

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

182 th this model, when the endo-lysosomal pH of moDCs is disrupted, HLA-B allotypes display varying prop

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

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

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

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

187 Niche function depended on moDC delivery of ligand GPNMB to the basal ESC receptor

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

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

190 ated NETs alone had no discernable effect on moDC.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 ce and adoptive cell transfer, we found that moDCs are essential for lung mucosal responses but are d

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

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

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

209 These moDCs are characterized by the expression of CD301b and

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

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

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

213 ion and cytokine production when compared to moDC.

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

215 In contrast to moDCs, mouse cDC2s and cDC1s were poorly infected with E

216 d during the differentiation of monocytes to moDCs.

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

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

219 3 production compared with native Ab-treated moDCs.

220 Aggregate-treated moDCs enhanced allogeneic T cell proliferation and IL-5,

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

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

223 on of immunostimulation by normal uninfected moDCs.

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

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

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

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

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

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

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