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1                                              pDC depletion ablated interferon production and increase
2                                              pDC-induced Foxp3 T cells suppressed proliferation of B6
3                                              pDCs and T-cell cultures were adoptively transferred bef
4                                              pDCs are not readily detectable in healthy human skin, b
5                                              pDCs express Fyn and Lyn and their activating residues a
6                                              pDCs from murine bone marrow, native kidneys, and sponta
7                                              pDCs were key mediators of the immunoinflammatory cascad
8 n human FLT3-differentiated mBMDCs and CAL-1 pDCs.
9                                       DBA/2J pDCs were more potent in inducing Foxp3 in B6 T cells th
10 mAb that binds blood DC antigen 2 (BDCA2), a pDC-specific receptor that inhibits the production of IF
11       Collectively, we present evidence of a pDC subset in the TME that favors antitumor immunity.
12                                      Using a pDC-targeted vaccine model to deliver antigens specifica
13 and may add to our understanding of aberrant pDC function in cancer and autoimmune disease.
14 well as treatment with SFK inhibitors ablate pDC (but not conventional DC) responses both in vitro an
15                In this study, we asked about pDC behavior in the setting of virus-free inflammation.
16                                 Accordingly, pDC depletion after allergen challenge or during rhinovi
17 ithin hours of infection through a bile acid-pDC-IFN signaling axis, which affects viremia, dissemina
18 ed the mechanism through which HIV-activated pDCs produce IFN as well as how both monoclonal HIV-spec
19 n increased frequency of partially activated pDCs in the blood before detection of HIV RNA.
20 f ENO1 with ENO1 inhibitor (ENO1i) activates pDCs, as well as increases pDC-induced MM-specific CD8(+
21 signs of impaired antiviral immune activity, pDCs from infected host have distinct transcriptional re
22 ors previously implicated in both B cell and pDC development to activate RAG1 and RAG2 gene transcrip
23 l and plasmacytoid dendritic cells (cDCs and pDCs, respectively) resident in the steady-state thymus
24 creases ENO1 expression in both MM cells and pDCs.
25 ian numbers and frequencies of total DCs and pDCs in both SS and SR asthmatics.
26                                    PBMCs and pDCs isolated from children with exacerbation-prone asth
27 rompt a re-evaluation of previously ascribed pDC involvement in skin disease.
28 ments pDC IFN-alpha responses and attenuates pDC FcepsilonRIalpha protein expression and provide evid
29  indicate that omalizumab treatment augments pDC IFN-alpha responses and attenuates pDC FcepsilonRIal
30 g our coculture models of patient autologous pDC-T-NK-MM cells, we examined whether targeting ENO1 ca
31                                    BCAP(-/-) pDC had decreased actin polymerization and Rac1 activati
32                Although interactions between pDC and fungal cells were not detected, pDCs regulated n
33 uggesting collaborative interactions between pDCs and other immune cells, particularly B cells.
34 e to HIV-1 and suggest that changes in blood pDC frequency and function can be used as an indicator o
35 to early HIV-1 replication, we studied blood pDCs in 29 HIV-infected participants who initiated antir
36 etabolic enzyme Alpha-Enolase (ENO1) in both pDCs and MM cells.
37 dicating that sensing of the viral genome by pDCs activates cDCs in trans to cross-present capsid ant
38                           Foxp3 induction by pDCs in vitro was dependent on pDC viability, immaturity
39 e resistive tuning on IFN-alpha induction by pDCs, thereby contributing to SLE pathogenesis.
40 atory role of 2-AG on IFN-alpha induction by pDCs.
41 in controlling the IFN-I amounts produced by pDCs in response to Toll-like receptor (TLR) activation.
42 osomes (pDCexos), that were also produced by pDCs under various conditions.
43 ajor initiating factor for IFN production by pDCs.
44 hibitory loop that impedes IFN production by pDCs.
45  of BCMA and reduced the release of sBCMA by pDCs.
46 ) pathway, marked by CD123 and BTLA, carried pDC, cDC1, and DC2 trajectories, while the common myeloi
47  that transient plasmacytoid dendritic cell (pDC) depletion during primary Pneumovirus infection alon
48  for B cell and plasmacytoid dendritic cell (pDC) development, but its molecular function(s) in early
49 rker, CD14; the plasmacytoid dendritic cell (pDC) marker, BDCA4, identifying neuropilin-1 (NRP1); and
50 y TLR9-mediated plasmacytoid dendritic cell (pDC)-hyperactivation and interferon-alpha production.
51                Plasmacytoid dendritic cells (pDC) are specialized in secretion of type I interferon i
52                Plasmacytoid dendritic cells (pDC) are type I interferon-producing cells with critical
53  quantities by plasmacytoid dendritic cells (pDC) in response to engagement of TLR7 and TLR9 with end
54 a) response of plasmacytoid dendritic cells (pDC) to MHV68 was reduced in Tlr9 (-/-) cells compared t
55 8 signaling in plasmacytoid dendritic cells (pDCs) and blunts systemic production of type I interfero
56  as well as in plasmacytoid dendritic cells (pDCs) and CD141(+) DCs from rhesus macaques, compared to
57 bly increasing plasmacytoid dendritic cells (pDCs) and interferon signaling.
58 e discovery of plasmacytoid dendritic cells (pDCs) and of their extraordinary ability to produce type
59                Plasmacytoid dendritic cells (pDCs) are a major source of type I interferon (IFN-I).
60                Plasmacytoid dendritic cells (pDCs) are a unique sentinel cell type that can detect pa
61                Plasmacytoid dendritic cells (pDCs) are important in antiviral immunity and in maintai
62                Plasmacytoid dendritic cells (pDCs) are potent producers of type I and type III IFNs a
63 HIV infection, plasmacytoid dendritic cells (pDCs) are rendered dysfunctional, as measured by their d
64                Plasmacytoid dendritic cells (pDCs) are robust producers of IFNalpha and one of the fi
65                Plasmacytoid dendritic cells (pDCs) are the major producers of IFN-alpha, an antiviral
66                Plasmacytoid dendritic cells (pDCs) express Toll like receptors (TLRs) that modulate t
67 FN-I-producing plasmacytoid dendritic cells (pDCs) facilitate the differentiation of DNA-reactive AFC
68 s investigated plasmacytoid dendritic cells (pDCs) from the blood of individuals living with HIV.
69 ls (mDCs), and plasmacytoid dendritic cells (pDCs) from three individuals with ZIKV infection.
70       Although plasmacytoid dendritic cells (pDCs) have been shown to play a critical role in generat
71 transcribed in plasmacytoid dendritic cells (pDCs) in both blood and lymphoid tissue.
72    Bone marrow plasmacytoid dendritic cells (pDCs) in patients with multiple myeloma (MM) promote tum
73                Plasmacytoid dendritic cells (pDCs) produce abundant type I IFNs (IFN-I) in response t
74                Plasmacytoid dendritic cells (pDCs) produce type I interferon (IFN-I) and are traditio
75                Plasmacytoid dendritic cells (pDCs) rapidly produce large amounts of type 1 interferon
76                Plasmacytoid dendritic cells (pDCs) require a particularly tight regulation of endosom
77                Plasmacytoid dendritic cells (pDCs) that secrete large amounts of IFN have recently be
78 nventional and plasmacytoid dendritic cells (pDCs) under low and high doses, respectively, through CD
79                Plasmacytoid dendritic cells (pDCs) were identified as the major source of IFN-Is.
80                Plasmacytoid dendritic cells (pDCs) were isolated from whole blood, stimulated with To
81  the influx of plasmacytoid dendritic cells (pDCs), an Interferon (IFN)-responsive macrophage populat
82 basophils, and plasmacytoid dendritic cells (pDCs), are regulated by IgE binding to FcepsilonRIalpha.
83 or function of plasmacytoid dendritic cells (pDCs), because these cells are potent inducers of Foxp3
84                Plasmacytoid dendritic cells (pDCs), prominent cells of antiviral immunity, exhibit pr
85 Using isolated plasmacytoid dendritic cells (pDCs), we demonstrated that TLR7 is an innate recognitio
86 monstrate that plasmacytoid dendritic cells (pDCs), which are prototypically antiviral cells, partici
87 a responses of plasmacytoid dendritic cells (pDCs), which can be deficient in patients with allergic
88 is receptor in plasmacytoid dendritic cells (pDCs), which preferentially express the SLAMF9 transcrip
89 ls, especially plasmacytoid dendritic cells (pDCs).
90 IFNs being the plasmacytoid dendritic cells (pDCs).
91 d by activated plasmacytoid dendritic cells (pDCs).
92 ouse and human plasmacytoid dendritic cells (pDCs).
93 ation of human plasmacytoid dendritic cells (pDCs).
94 r signaling crosstalk among the tumor cells, pDCs and immune cells will identify novel therapeutic ap
95 by stimulating plasmacytoid dendritic cells-(pDCs)-Type I interferon (IFN-I) and acts as autoantigen
96            During aspergillosis, circulating pDCs entered the lung in response to CXCR3-dependent sig
97 enge or rhinovirus infection and conditioned pDCs for proinflammatory function.
98                    Depending on the context, pDCs can promote or suppress antitumor immune responses.
99 ractory to physiological stimuli controlling pDC functions and development.
100                                  Conversely, pDC development and serum IFN-I responses to lymphocytic
101 etween interferon-producing plasmacytoid DC (pDC) and antigen-presenting classical DC (cDC) is contro
102  share surface markers with plasmacytoid DC (pDC) but have distinct functional properties that were p
103                            Plasmacytoid DCs (pDC) produce large amounts of type I IFN (IFN-I), cytoki
104 t on DC subsets, including plasmacytoid DCs (pDCs) and the classical DC lineages cDC1 and cDC2.
105                   Although plasmacytoid DCs (pDCs) are a primary source of IFN, the mechanisms that r
106 dendritic cells (cDCs) and plasmacytoid DCs (pDCs) are required for the crosspriming of capsid-specif
107                            Plasmacytoid DCs (pDCs) are typically thought to be key in antiviral defen
108 hat shares properties with plasmacytoid DCs (pDCs) but potently activates T cells, thus redefining pD
109                            Plasmacytoid DCs (pDCs) support antiviral immunity by linking innate and a
110 myeloid DCs (mDCs) but not plasmacytoid DCs (pDCs) was observed in the blood of SR as compared to SS
111                            Plasmacytoid DCs (pDCs), the major producers of type I interferon, are pri
112 gen 2 (BDCA-2) receptor on plasmacytoid DCs (pDCs).
113 g with increased PD-L1, on plasmacytoid DCs (pDCs).
114                   Additionally, RS decreased pDCs, interferon pathways, organ involvement, and mortal
115 ween pDC and fungal cells were not detected, pDCs regulated neutrophil NADPH oxidase activity and con
116 duced AAD exacerbations were used to dissect pDC function in vivo and unwind the potential mechanisms
117 f pDCs by STING agonist 2'3' cGAMP or dsDNA, pDC-s produced type I, and type III IFN.
118 cf4 was required for its upregulation during pDC differentiation, revealing a positive feedback loop.
119 e that Tim-3 is a biomarker of dysfunctional pDCs and may negatively regulate IFN-alpha, possibly thr
120       This study suggests that dysfunctional pDCs are a key initial mechanism associated with poor HI
121 ted from HIV-infected subjects also enhanced pDC production of IFN in response to HIV.
122 nction of Tim-3 was investigated on enriched pDC populations from donors not infected with HIV.
123 AD and rhinovirus-induced AAD exacerbations, pDCs were recruited to the lung during inflammation and
124                             Here we examined pDC spatiotemporal dynamics during viral infection to un
125 ain containing molecule-3 (Tim-3)-expressing pDCs in the blood of HIV-infected donors.
126            The frequency of Tim-3-expressing pDCs correlated inversely with CD4 T cell counts and pos
127                             Tim-3-expressing pDCs had reduced IRF7 levels.
128  antigen transfer to cDCs as a mechanism for pDCs to achieve cross-priming.
129 ara et al. (2020) reveal a critical role for pDCs in antifungal immunity.
130 imilar efficiency in acquiring antigens from pDCs, cDC1s but not cDC2s were required for cross-primin
131                           sBCMA derived from pDCs might determine local availability of its high-affi
132                        Antigen transfer from pDCs to cDCs was mediated by previously unreported pDC-d
133 us began to spread, an apparently functional pDC response emerged.
134                         What other functions pDCs exert in vivo during viral infections is controvers
135 which myeloid dendritic cells sense haptens, pDCs are primary sensors of imiquimod.
136 suppress antitumor immunity, whether and how pDCs cross-prime CD8 T cells in vivo remain controversia
137  novel immunomodulatory role of MYC in human pDC and may add to our understanding of aberrant pDC fun
138 d not induce IFN-alpha or TNF-alpha in human pDC.
139                 The interaction of the human pDC receptor immunoglobulin-like transcript 7 (ILT7) wit
140      During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce l
141  Src family kinases (SFK) in mouse and human pDCs.
142                            Circulating human pDCs contained BCMA protein without displaying it on the
143 ing of DNA in cytosolic compartment in human pDCs remains relatively unexplored.
144 scovered a regulatory role of ABHD6 in human pDCs through modulating the local abundance of its subst
145 o the TLR9-mediated DNA recognition in human pDCs with cross-talk between these two pathways.
146  and stimulator of IFN gene (STING) in human pDCs.
147  The display of BCMA on the surface of human pDCs was accompanied by release of soluble BCMA (sBCMA);
148 the innate virus-directed responses of human pDCs.
149 end the spectrum of BCMA expression to human pDCs.
150                       In contrast with human pDCs, murine pDCs did not express BCMA, not even after T
151 stine in terms of draining LNs, and identify pDC as active sentinels of colonic inflammation and/or m
152 nd Ifit1 expression in blood and an immature pDC phenotype associated with higher IFN production.
153 9(-/-) mice revealed an increase of immature pDCs in the bone marrow and enhanced accumulation of pDC
154 ompanied by a prominent increase of immature pDCs in the lymph node, with a reduced costimulatory pot
155 y in pDCs, and its deletion in mice impaired pDCs development and led to the expansion of non-canonic
156 on analysis showed that ENO1 is expressed in pDC and MM cells; and importantly, that pDC-MM coculture
157 FN-alpha increased the expression of IDO1 in pDC during AIA, and Ab-mediated depletion of pDC, either
158                                 Increases in pDC-specific markers were observed in peripheral blood o
159 buting to the IFN-alpha response to MHV68 in pDC are TLR7 and TLR9, but the contribution of TLR7 is m
160 romoting TLR-induced IFN-alpha production in pDC and in systemic lupus erythematosus pathogenesis.
161          TLR-induced IFN-alpha production in pDC requires DOCK2-mediated activation of Rac1 leading t
162             Omalizumab-induced reductions in pDC FcepsilonRIalpha levels were significantly associate
163 gesting that cDC1s played a critical role in pDC-mediated cross-priming independent of their function
164 esults suggest the crucial role of SLAMF9 in pDC differentiation, homeostasis, and function in the st
165 induced IFN-alpha production specifically in pDC.
166  this work, we examined the role of SphK2 in pDC development and activation and in the pristane-induc
167 , whether Hv1 is important for pH control in pDCs is presently unknown.
168  TLR9 signaling is specifically essential in pDCs but not in cDCs, indicating that sensing of the vir
169 er ATI, decreased expression of IFN genes in pDCs inversely correlated with the time to viral detecti
170 hematosus (SLE), LL37 also triggers IFN-I in pDCs and is target of pathogenic autoantibodies.
171      However, the IRF7 regulatory network in pDCs remains largely unknown.
172 c(+) cells had a cell-intrinsic reduction in pDCs and cDC2s, coupled with an increase in cDC1s.
173 ING induced expression of SOCS1 and SOCS3 in pDCs, indicating a possible autoinhibitory loop that imp
174 ng Tcf4 isoform is expressed specifically in pDCs, and its deletion in mice impaired pDCs development
175  specific inhibition or deletion of SphK1 in pDCs mitigates uptake of CpG oligonucleotide ligands by
176  regulated by IRAK4 and BTK by cell type: In pDCs, IRAK4 positively regulated NF-kappaB and MAPK sign
177 n progenitors and was further upregulated in pDCs, correlating with stage-specific activity of multip
178  HSV and HIV, thus functionally inactivating pDC.
179 equently, peripheral immune cells, including pDCs, macrophages, neutrophils, and B cells infiltrated
180 oreover, although absence of SphK2 increased pDC frequency in pristane-induced lupus, there were no m
181 (ENO1i) activates pDCs, as well as increases pDC-induced MM-specific CD8(+) CTL and NK cell activity
182  in vivo with omalizumab treatment increases pDC antiviral IFN-alpha responses in inner-city children
183    We propose a new model for how individual pDCs are endowed to exert different functions in vivo du
184 nfluenza-induced PBMC and rhinovirus-induced pDC IFN-alpha responses in the presence of IgE cross-lin
185 fine the role of SLAMF9 during inflammation, pDCs lacking SLAMF9 were followed during induced experim
186 ural monoamines and synthetic amines inhibit pDC activation by RNA viruses.
187 CR4) as a receptor used by amines to inhibit pDC.
188 essed low amounts of LIFR and developed into pDCs less efficiently after being exposed to LIF, consis
189                               Using isolated pDCs and mDCs for in vitro culture with allopeptide+self
190  as in Tlr7 (-/-) Tlr9 (-/-) double-knockout pDC, the IFN-alpha response to MHV68 was completely abol
191 ent study, we characterize in depth and link pDC activation states in animals infected by mouse cytom
192 o support ZIKV replication steps; meanwhile, pDCs exhibit a unique expression pattern of gene modules
193                               In adult mice, pDC depletion predisposed to severe bronchiolitis only a
194 both BDCA-2 and CD123, potentially mimicking pDCs.
195 mall molecules targeting SFKs could modulate pDC responses in human diseases.
196  of Hvcn1, which encodes Hv1, impaired mouse pDC activation by CpG oligonucleotides in vitro and in v
197            In this study, we show that mouse pDCs require Hv1 to achieve potent type I IFN responses
198            In this study, we find that mouse pDCs selectively express the receptor for LIF that signa
199          In contrast with human pDCs, murine pDCs did not express BCMA, not even after TLR9 activatio
200 ed in natural HIV infection modulated normal pDC sensing of HIV.
201 s study, we identified a naturally occurring pDC subset expressing high levels of OX40 (OX40+ pDC) en
202 regulatory T (T reg) cells in the absence of pDC-derived semaphorin 4a (Sema4a).
203      Thus, Tim-3 may serve as a biomarker of pDC dysfunction in HIV infection.
204 pe-specific positive and negative control of pDC function should pave the way for translational appli
205 pDC during AIA, and Ab-mediated depletion of pDC, either during mBSA sensitization or after triggerin
206  the transcription factor SpiB, elevation of pDC survival, and attenuated IFN-alpha and TNF-alpha pro
207 fies CXCR4 as a potential 'on-off' switch of pDC activity with therapeutic potential.
208 ective role for the microbiome, treatment of pDC-depleted neonates with the microbial-derived metabol
209 view summarizes our current understanding of pDC biology, including transcriptional regulation, heter
210 tected a transient decline in the ability of pDCs to produce IFNalpha in vitro, which correlated with
211 the bone marrow and enhanced accumulation of pDCs in the lymph nodes.
212                                Activation of pDCs alleviates AHR and airway inflammation by suppressi
213                   We show that activation of pDCs through Toll-like receptor 7/8 suppresses ILC2-medi
214                                  Analysis of pDCs in SLAMF9(-/-) mice revealed an increase of immatur
215 s of unique interferon-producing capacity of pDCs.
216 ally located in the cytosolic compartment of pDCs and time-dependently colocalized with non-CpG doubl
217 eactivity and reveal a major contribution of pDCs, endosomal Toll-like receptors (TLRs), and IFN-I to
218 lowed for the interaction and cooperation of pDCs and XCR1(+) DCs, thereby optimizing XCR1(+) DC matu
219                       Moreover, depletion of pDCs in the murine OX40+ pDC-rich tumor model accelerate
220 nd airway inflammation and that depletion of pDCs reverses this suppression.
221                         A lower frequency of pDCs expressing Tim-3 produced IFN-alpha or TNF-alpha in
222 wards a discrete but integrative function of pDCs in the human immune responses to ZIKV infection.
223 e I IFN production, the hallmark function of pDCs, commending Hv1 as an attractive target for modulat
224                                Generation of pDCs from bone marrow dendritic cell (DC) progenitors an
225 atory potential and enhanced infiltration of pDCs into the central nervous system.
226 in-1 to enable the long term interactions of pDCs with Treg cells, thereby enhancing suppression of T
227 further studied to determine the presence of pDCs and correlation with inflammation.
228         We sought to investigate the role of pDCs in allergic airway inflammation and acute asthma ex
229 ies uncover a previously unsuspected role of pDCs in asthma exacerbations with potential diagnostic a
230             We sought to address the role of pDCs in regulating ILC2 function and ILC2-mediated airwa
231                   Upon direct stimulation of pDCs by STING agonist 2'3' cGAMP or dsDNA, pDC-s produce
232                               Stimulation of pDCs with LIF inhibited IFN-I, TNF, and IL-6 responses t
233 CMA was detected also on the cell surface of pDCs.
234 ey also propose the therapeutic targeting of pDCs and IL-25 for the treatment of acute asthma.
235  induction by pDCs in vitro was dependent on pDC viability, immaturity, and class II MHC mismatch and
236                      The effects of IL-25 on pDCs in vitro were also assessed.
237  myeloma should consider possible effects on pDCs.
238 ministration led to BDCA2 internalization on pDCs, which correlated with circulating BIIB059 levels.
239 erum BIIB059 concentrations, BDCA2 levels on pDCs, and IFN-responsive biomarkers in whole blood and s
240 ssion of HLA-DR and ILT3 was also reduced on pDCs in all patients.
241 g advantage of an in vitro system where only pDCs had access to antigens, we further demonstrated tha
242 orms, both of which are required for optimal pDC development in vitro.
243 eover, depletion of pDCs in the murine OX40+ pDC-rich tumor model accelerated tumor growth.
244 subset expressing high levels of OX40 (OX40+ pDC) enriched in the tumor microenvironment (TME) of hea
245                                        OX40+ pDCs were distinguished by a distinct immunostimulatory
246          Consistently, in asthmatic patients pDC numbers were markedly increased during exacerbations
247                         Concurrent with peak pDC frequency, we detected a transient decline in the ab
248 ) cells and myeloid (mDCs) and plasmacytoid (pDCs) dendritic cells on control of virus replication an
249                                       Potent pDC-activating stimuli, such as CpG, imiquimod, and Send
250               Surprisingly, cross-presenting pDCs required conventional DCs (cDCs) to achieve cross-p
251 e further demonstrated that cross-presenting pDCs were unable to efficiently prime CD8 T cells by the
252 ystander cDCs, similarly to cross-presenting pDCs, thus identifying pDCexo-mediated antigen transfer
253                           IFN-beta-producing pDCs exhibit a distinct transcriptome profile, with high
254 yn and Lyn as important factors that promote pDC responses, describe the mechanisms involved and high
255 monocyte-derived DCs and neutrophils recruit pDCs, which promote neutrophil fungicidal activity.
256 cted murine Mo-DCs and neutrophils recruited pDCs to the lung by releasing the CXCR3 ligands, CXCL9 a
257  potently activates T cells, thus redefining pDCs; a new subdivision within the CD1C(+) subset of DCs
258 he presence of IgE cross-linking and reduced pDC surface FcepsilonRIalpha expression.
259 n pDCs decrease in circulation and remaining pDC produce lower amounts of IFN-alpha in response to vi
260 y induces SOCS3, Bcl3, and Id2, which render pDCs and late DC progenitors refractory to physiological
261 dary bile acid deoxycholic acid, can restore pDC- and MyD88-dependent type I IFN responses to restric
262 CD34(+) CD123(+) progenitors with restricted pDC, cDC, and monocyte potential, whereas Delta-like1 si
263     The expression of Tcf4 and the resulting pDC differentiation were selectively sensitive to the in
264 T cell activation were performed by the same pDC, but these occurred sequentially in time and in diff
265 letion markedly decreased the IFN signature, pDC activation, and glomerulonephritis.
266 ) in SSc blood, and that CXCL4-positive skin pDCs coexpress IFN-I-related genes.
267                                Specifically, pDCs upregulate neuropilin-1 to enable the long term int
268 ubset (mDCs) and the plasmacytoid DC subset (pDCs).
269 r results indicate that T. gondii suppresses pDC activation by mimicking IL-10's regulatory effects t
270                                 Via targeted pDC ablation, we found that pDCs were essential for host
271              The data suggest that targeting pDCs may be beneficial for patients with SLE, especially
272 ells from BAL had even greater function than pDC cells from blood (P = .008).
273 cifically to pDCs, we have demonstrated that pDC-targeted vaccination led to strong cross-priming and
274  Using oligonucleotide arrays, we found that pDC-MM interactions induce metabolic enzyme Alpha-Enolas
275 d in pDC and MM cells; and importantly, that pDC-MM coculture further increases ENO1 expression in bo
276                  Our data also indicate that pDC prestimulation of cGAS-STING dampened the TLR9-media
277                    In addition, we show that pDC commitment to IFN-I production was marked early on b
278                      These data suggest that pDC-induced regulatory T cells are dependent on downstre
279 the time to viral detection, suggesting that pDC IFN loss is part of an effective early immune respon
280 dermatitis with the distinctive feature that pDCs are the primary sensors, leading to an IL-23/TH17 d
281                                We found that pDCs accumulated at sites of CD8(+) T cell antigen-drive
282     Via targeted pDC ablation, we found that pDCs were essential for host defense in the presence of
283  with plasma IFNalpha2 levels, implying that pDCs were refractory to in vitro stimulation after IFNal
284                         We further show that pDCs suppress cytokine production and the proliferation
285            In summary, our data suggest that pDCs employ a unique mechanism of pDCexo-mediated antige
286 There is increasing evidence suggesting that pDCs and/or IFN-I can also have a detrimental role in a
287  pDC development, SphK1 is essential for the pDC activation and production of type I IFN and pro-infl
288                 Although dispensable for the pDC development, SphK1 is essential for the pDC activati
289 hosphate (S1P), plays a critical role in the pDC functions and interferon production.
290                               Notably, these pDCs were initially capable of producing high levels of
291                                        Thus, pDCs act as positive feedback amplifiers of neutrophil e
292                                   Tlr7 (-/-) pDC responded similarly to WT.
293 roperties that were previously attributed to pDC.
294 L mononuclear cells showed function equal to pDC from blood and greater than blood monocytes.
295 ne model to deliver antigens specifically to pDCs, we have demonstrated that pDC-targeted vaccination
296       However, we found that in Unc93b (-/-) pDC, as well as in Tlr7 (-/-) Tlr9 (-/-) double-knockout
297 o cDCs was mediated by previously unreported pDC-derived exosomes (pDCexos), that were also produced
298 t cDC2s were required for cross-priming upon pDC-targeted vaccination, suggesting that cDC1s played a
299 age-related Sema4a-mediated pathway by which pDCs and microbial colonization induce T reg cell expans
300           Naive T cells were cocultured with pDCs in specific strain combinations and analyzed for Fo

 
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