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1 pDC are specialized in type I IFN (IFN-I) secretion to c
2 pDC depletion ablated interferon production and increase
3 pDC that expressed the GM-CSF receptor were increased in
4 pDCs are key players in various type I IFN-driven autoim
5 pDCs are rapidly activated during HIV-1 infection and ar
6 pDCs express Fyn and Lyn and their activating residues a
7 pDCs may play a protective role in asthma and are key pl
8 pDCs were key mediators of the immunoinflammatory cascad
10 To avoid the deleterious effects of aberrant pDC activation, tight regulation of IRF7 is required.
12 well as treatment with SFK inhibitors ablate pDC (but not conventional DC) responses both in vitro an
16 highly pathogenic R3A efficiently activated pDCs to induce robust IFN-alpha production, while the le
17 ed the mechanism through which HIV-activated pDCs produce IFN as well as how both monoclonal HIV-spec
23 ors previously implicated in both B cell and pDC development to activate RAG1 and RAG2 gene transcrip
25 es the interaction of MERS-CoV with APCs and pDCs, particularly the induction of type I and III IFN s
27 l and plasmacytoid dendritic cells (cDCs and pDCs, respectively) resident in the steady-state thymus
28 +)CADM1(+)CD115(+)wCD11R1(+)CD1(+) cells and pDCs are CD4(+)CD135(+)CD172a(+)CD123(+)CD303(+) cells.
29 cleic acids by endosomal TLRs in B cells and pDCs is thought to be an important step in the pathogene
31 est to those working on the roles of IFN and pDCs in HIV-1 pathogenesis in general and on the interac
34 ens on the expression of IL-17RB by mDCs and pDCs, and the effects of IL-25 on pDCs, are unknown.
35 efficient Ag cross-presentation by mDCs and pDCs, leading to strong ex vivo activation of HA-1-speci
36 ential for in vivo Ag delivery into mDCs and pDCs, thereby using the specialized functions and cross-
40 ments pDC IFN-alpha responses and attenuates pDC FcepsilonRIalpha protein expression and provide evid
41 indicate that omalizumab treatment augments pDC IFN-alpha responses and attenuates pDC FcepsilonRIal
42 mechanism by which sex differences in basal pDC IRF5 expression lead to higher IFN-alpha production
43 C from lupus prone mice and the number of BM pDCs and their ability to produce IFNalpha gradually dec
48 dicating that sensing of the viral genome by pDCs activates cDCs in trans to cross-present capsid ant
52 s of normal rhesus macaques, we found CD4(+) pDCs to be the subset responsible for most IFN-alpha and
54 ucing cells in the spleen as a CCR9(+)CD9(-) pDC subset that is localized exclusively within the T/B
55 that transient plasmacytoid dendritic cell (pDC) depletion during primary Pneumovirus infection alon
56 for B cell and plasmacytoid dendritic cell (pDC) development, but its molecular function(s) in early
57 rker, CD14; the plasmacytoid dendritic cell (pDC) marker, BDCA4, identifying neuropilin-1 (NRP1); and
60 eport that AGM plasmacytoid dendritic cells (pDC) express extremely low levels of CD4, unlike MAC and
62 We show that plasmacytoid dendritic cells (pDC) of natural hosts display reduced CD4 and/or CCR5 ex
63 agonist CpGA, plasmacytoid dendritic cells (pDC) produced type 1 IFNs, which, through an autocrine t
64 TGF-beta, and plasmacytoid dendritic cells (pDC) were neutralized by 1-methyltryptophan and Abs agai
68 HIV infection, plasmacytoid dendritic cells (pDCs) are rendered dysfunctional, as measured by their d
73 ng circulating plasmacytoid dendritic cells (pDCs) into VAT through chemokine-like receptor 1 (CMKLR1
75 n depletion in plasmacytoid dendritic cells (pDCs) led to a reduction of IFN-alpha secretion, suggest
79 l depletion of plasmacytoid dendritic cells (pDCs) slow progression; however, the critical cell that
80 that activates plasmacytoid dendritic cells (pDCs) through FcgammaRIIa would be associated with contr
81 monocytes and plasmacytoid dendritic cells (pDCs) to influenza A virus infection in 21 pregnant and
82 nventional and plasmacytoid dendritic cells (pDCs) under low and high doses, respectively, through CD
87 DNA) activated plasmacytoid dendritic cells (pDCs), a type of cell of the immune system linked to vir
89 a responses of plasmacytoid dendritic cells (pDCs), which can be deficient in patients with allergic
96 rus also increases glycolysis in circulating pDCs, highlighting a previously unrecognized potential r
98 osus (SLE), this cross-talk was compromised; pDCs promoted plasmablast differentiation but failed to
101 macytoid DC Ag-1(high)B220(+)CD11c(int)) DC (pDC) populations during steady-state conditions revealed
102 etween interferon-producing plasmacytoid DC (pDC) and antigen-presenting classical DC (cDC) is contro
103 share surface markers with plasmacytoid DC (pDC) but have distinct functional properties that were p
104 DC) and macrophages but not plasmacytoid DC (pDC) had suppressed capacity to stimulate CD4 T cell pro
106 al of two main DC subsets: plasmacytoid DCs (pDCs) and conventional DCs (cDCs) and their dependence o
108 dendritic cells (cDCs) and plasmacytoid DCs (pDCs) are required for the crosspriming of capsid-specif
109 hat shares properties with plasmacytoid DCs (pDCs) but potently activates T cells, thus redefining pD
113 and internalized by human plasmacytoid DCs (pDCs) that express the TIM1 phosphatidylserine receptor,
114 myeloid DCs (mDCs) but not plasmacytoid DCs (pDCs) was observed in the blood of SR as compared to SS
115 A3+(high) mDC2s and BDCA2+ plasmacytoid DCs (pDCs) were identified and expressions of CD86, immunoglo
119 this study, we show that Siglec-H-deficient pDCs produce more of the type I IFN, IFN-alpha, in vitro
120 duced AAD exacerbations were used to dissect pDC function in vivo and unwind the potential mechanisms
121 sNP, but CD45(+) CD11c(-) CD303(+) HLA-DR(+) pDCs were only elevated in NPs compared to control UT.
122 cf4 was required for its upregulation during pDC differentiation, revealing a positive feedback loop.
123 e that Tim-3 is a biomarker of dysfunctional pDCs and may negatively regulate IFN-alpha, possibly thr
127 AD and rhinovirus-induced AAD exacerbations, pDCs were recruited to the lung during inflammation and
140 In conclusion, S1PR4 agonists block human pDC activation and may therefore be a promising tool to
141 novel immunomodulatory role of MYC in human pDC and may add to our understanding of aberrant pDC fun
142 he role of transcription factor MYC in human pDC, we employed a knockdown technique using human pDC c
144 reserves the surface expression of the human pDC-specific inhibitory receptor Ig-like transcript 7.
147 During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce l
150 us failed to activate freshly isolated human pDCs, these cells produced substantial amounts of IFN-al
151 The display of BCMA on the surface of human pDCs was accompanied by release of soluble BCMA (sBCMA);
156 presentation pathway by coating the 142t-IAV pDC with IAV peptide epitopes restores their ability to
157 stine in terms of draining LNs, and identify pDC as active sentinels of colonic inflammation and/or m
158 y in pDCs, and its deletion in mice impaired pDCs development and led to the expansion of non-canonic
162 FN-alpha increased the expression of IDO1 in pDC during AIA, and Ab-mediated depletion of pDC, either
164 d to alter Ag-driven T cell proliferation in pDC-dependent T cell activation assays, but shifted cyto
171 TLR9 signaling is specifically essential in pDCs but not in cDCs, indicating that sensing of the vir
174 mmon respiratory virus, induce glycolysis in pDCs and that this metabolic pathway regulates pDC antiv
177 ulatory mechanism of type I IFN signaling in pDCs and stage-specific function of immune cells in gene
179 ng Tcf4 isoform is expressed specifically in pDCs, and its deletion in mice impaired pDCs development
180 n progenitors and was further upregulated in pDCs, correlating with stage-specific activity of multip
182 in vivo with omalizumab treatment increases pDC antiviral IFN-alpha responses in inner-city children
185 nfluenza-induced PBMC and rhinovirus-induced pDC IFN-alpha responses in the presence of IgE cross-lin
193 these results highlight that E2-2 modulates pDC function in a species-specific manner, which may pro
195 comparing gene expression profiles of murine pDCs and conventional DCs, we found that CD28, a prototy
196 The anticryptococcal activity of murine pDCs is independent of opsonization but appears to requi
207 pDC during AIA, and Ab-mediated depletion of pDC, either during mBSA sensitization or after triggerin
212 ingly, CD28 acted as a negative regulator of pDC IFN-I production upon TLR stimulation but did not af
214 therapeutic opportunity for the treatment of pDC-associated autoimmune diseases, such as lupus or pso
215 ective role for the microbiome, treatment of pDC-depleted neonates with the microbial-derived metabol
218 lowed for the interaction and cooperation of pDCs and XCR1(+) DCs, thereby optimizing XCR1(+) DC matu
220 implicated in regulating the development of pDCs (E2-2 and Id2) and cDC1s (Irf8, Id2, and Batf3); ho
224 in-1 to enable the long term interactions of pDCs with Treg cells, thereby enhancing suppression of T
229 ere associated with enhanced IFN response of pDCs, leukocyte infiltration in the intestine and mild c
231 ies uncover a previously unsuspected role of pDCs in asthma exacerbations with potential diagnostic a
233 IFN-producing cells" as a distinct subset of pDCs specialized in coordinating cellular immune respons
238 significant effect of ERalpha deficiency on pDCs in predisease NZM2410 mice, which may represent a m
242 R1, cDC2 express FCER1A and FCGR2B, and only pDCs express TCF4 and NRP1 Nevertheless, despite these c
246 ) cells and myeloid (mDCs) and plasmacytoid (pDCs) dendritic cells on control of virus replication an
247 nserved subset-specific transcripts, porcine pDCs differed from the species described so far in many
249 ith disease severity and greatly potentiated pDC function by triggering phagocytosis via the high-aff
251 endritic cells (DCs [pDCs]) develop from pre-pDCs, whereas two lineages of conventional DCs (cDCs; cD
252 shows that S1P stimulation of human, primary pDCs substantially decreases IFN-alpha production after
253 nctive characteristics of IFN-beta-producing pDCs are independent of the type I IFNR-mediated feedbac
257 yn and Lyn as important factors that promote pDC responses, describe the mechanisms involved and high
259 e receptor 9 (TLR9) in the adipose-recruited pDCs by transporting extracellular DNA through receptor
260 potently activates T cells, thus redefining pDCs; a new subdivision within the CD1C(+) subset of DCs
263 fections, and IFN-I also negatively regulate pDC survival during the course of viral infections.
264 Cs and that this metabolic pathway regulates pDC antiviral functions, including IFN-alpha production
266 n pDCs decrease in circulation and remaining pDC produce lower amounts of IFN-alpha in response to vi
267 y, cell-intrinsic CD28 expression restrained pDC (and systemic) IFN-I production during in vivo RNA a
268 CD34(+) CD123(+) progenitors with restricted pDC, cDC, and monocyte potential, whereas Delta-like1 si
269 The expression of Tcf4 and the resulting pDC differentiation were selectively sensitive to the in
271 gnature were evaluated in both BM and spleen pDC from lupus prone mice and the number of BM pDCs and
275 r results indicate that T. gondii suppresses pDC activation by mimicking IL-10's regulatory effects t
278 e Gen2.2 pDC cell line, we demonstrated that pDC-reactive opsonophagocytic IgG Ab responses against H
283 dermatitis with the distinctive feature that pDCs are the primary sensors, leading to an IL-23/TH17 d
285 cine DC subsets to TLR ligands revealed that pDCs are by far the most important source of TNF-alpha,
290 However, the function of at least one of the pDC or CD8alpha(+) DC subsets is required for survival o
292 ronic HIV-1 infection depletes ILC3s through pDC activation, induction of IFN-I, and CD95-mediated ap
296 ne responses to TLR7/8 stimulation in vitro, pDC gut migration occurred after infection and detection
297 ilar between lupus and C57BL/6 mice, whereas pDCs from the spleens of NZB/W F1 and NZB mice produced
298 age-related Sema4a-mediated pathway by which pDCs and microbial colonization induce T reg cell expans
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