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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
9                             Using the Gen2.2 pDC cell line, we demonstrated that pDC-reactive opsonop
10 To avoid the deleterious effects of aberrant pDC activation, tight regulation of IRF7 is required.
11 and may add to our understanding of aberrant pDC function in cancer and autoimmune disease.
12 well as treatment with SFK inhibitors ablate pDC (but not conventional DC) responses both in vitro an
13                In this study, we asked about pDC behavior in the setting of virus-free inflammation.
14                                 Accordingly, pDC depletion after allergen challenge or during rhinovi
15                     Although the accumulated pDCs in the gut mucosae had robust cytokine responses to
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
18 tion upon TLR stimulation but did not affect pDC survival or maturation.
19                            Despite this, AGM pDC efficiently sensed SIVagm, but not heterologous HIV/
20                                 Both altered pDC-CD24(+)CD38(hi) Breg cell interactions and STAT1-STA
21 ethyltryptophan and Abs against TGF-beta and pDC, respectively.
22 b2 regulates commitment to both the cDC2 and pDC lineages through repression of Id2.
23 ors previously implicated in both B cell and pDC development to activate RAG1 and RAG2 gene transcrip
24 led allergen significantly increased mDC and pDC numbers in sputum but not in blood.
25 es the interaction of MERS-CoV with APCs and pDCs, particularly the induction of type I and III IFN s
26  of Id2, which was up-regulated in cDC2s and pDCs from conditional knockout mice.
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
30 ian numbers and frequencies of total DCs and pDCs in both SS and SR asthmatics.
31 est to those working on the roles of IFN and pDCs in HIV-1 pathogenesis in general and on the interac
32 is up-regulated on blood and sputum mDCs and pDCs after allergen inhalation.
33        The percentage of IL-17RB(+) mDCs and pDCs was significantly increased in blood and sputum 24
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-
37 pathology, the levels of NK cells, mDCs, and pDCs in the liver increased up to 3-fold.
38             In pregnant women, monocytes and pDCs exhibit an exaggerated proinflammatory immune respo
39                                    PBMCs and pDCs isolated from children with exacerbation-prone asth
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
44         The IFNalpha-producing ability of BM pDCs was similar between lupus and C57BL/6 mice, whereas
45 stemic lupus erythematosus or psoriasis, but pDCs are also involved in (anti-)tumor immunity.
46 ive role of MYC in the antiviral response by pDC.
47        IL-25 up-regulated TLR9 expression by pDCs and orchestrated the responses to TLR9 ligation.
48 dicating that sensing of the viral genome by pDCs activates cDCs in trans to cross-present capsid ant
49                  HIV-1-induced type I IFN by pDCs triggers BAFF production in both classical and inte
50 onversely restrained IFN-alpha production by pDCs via IL-10 release.
51  of BCMA and reduced the release of sBCMA by pDCs.
52 s of normal rhesus macaques, we found CD4(+) pDCs to be the subset responsible for most IFN-alpha and
53 ion, compared with relatively anergic CD4(-) pDCs.
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
58                Plasmacytoid dendritic cells (pDC) are specialized in secretion of type I interferon i
59                Plasmacytoid dendritic cells (pDC) are type I interferon-producing cells with critical
60 eport that AGM plasmacytoid dendritic cells (pDC) express extremely low levels of CD4, unlike MAC and
61 he survival of plasmacytoid dendritic cells (pDC) in such situation.
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
65 hanism between plasmacytoid dendritic cells (pDCs) and Breg cells.
66                Plasmacytoid dendritic cells (pDCs) are important in antiviral immunity and in maintai
67 lls (mDCs) and plasmacytoid dendritic cells (pDCs) are professional antigen-presenting cells.
68 HIV infection, plasmacytoid dendritic cells (pDCs) are rendered dysfunctional, as measured by their d
69                Plasmacytoid dendritic cells (pDCs) are the major producers of IFN-alpha, an antiviral
70                Plasmacytoid dendritic cells (pDCs) are the most powerful IFN-I-producing cells and pl
71                Plasmacytoid dendritic cells (pDCs) are vital to antiviral defense, directing immune r
72 transcribed in plasmacytoid dendritic cells (pDCs) in both blood and lymphoid tissue.
73 ng circulating plasmacytoid dendritic cells (pDCs) into VAT through chemokine-like receptor 1 (CMKLR1
74 r, the role of plasmacytoid dendritic cells (pDCs) is unknown.
75 n depletion in plasmacytoid dendritic cells (pDCs) led to a reduction of IFN-alpha secretion, suggest
76                Plasmacytoid dendritic cells (pDCs) produce large amounts of type I IFN in response to
77                Plasmacytoid dendritic cells (pDCs) rapidly produce large amounts of type 1 interferon
78 responses, and plasmacytoid dendritic cells (pDCs) represent a major source of these cytokines.
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
83 on in CD123(+) plasmacytoid dendritic cells (pDCs) was found only in lymphoma tissues.
84                Plasmacytoid dendritic cells (pDCs) were considered to be the major IFNalpha source in
85                Plasmacytoid dendritic cells (pDCs) were identified as the major source of IFN-Is.
86                Plasmacytoid dendritic cells (pDCs) were isolated from whole blood, stimulated with To
87 DNA) activated plasmacytoid dendritic cells (pDCs), a type of cell of the immune system linked to vir
88                Plasmacytoid dendritic cells (pDCs), prominent cells of antiviral immunity, exhibit pr
89 a responses of plasmacytoid dendritic cells (pDCs), which can be deficient in patients with allergic
90  produced from plasmacytoid dendritic cells (pDCs).
91 ly produced by plasmacytoid dendritic cells (pDCs).
92 iginating from plasmacytoid dendritic cells (pDCs).
93 +) and CD86(+) plasmacytoid dendritic cells (pDCs).
94 regulatory mechanisms in plasmacytoid cells (pDCs) still remain unclear.
95                              In chimpanzees, pDCs were transiently recruited to the liver early in in
96 rus also increases glycolysis in circulating pDCs, highlighting a previously unrecognized potential r
97 genes and transcriptomic profiling clustered pDCs more distantly from cDCs than monocytes.
98 osus (SLE), this cross-talk was compromised; pDCs promoted plasmablast differentiation but failed to
99                               In conclusion, pDC are activated alone with disease development and its
100 enge or rhinovirus infection and conditioned pDCs for proinflammatory function.
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
105 sets, myeloid DC (mDCs) and plasmacytoid DC (pDCs).
106 al of two main DC subsets: plasmacytoid DCs (pDCs) and conventional DCs (cDCs) and their dependence o
107                   Although plasmacytoid DCs (pDCs) are a primary source of IFN, the mechanisms that r
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
110 cDC) 1 and cDC2 as well as plasmacytoid DCs (pDCs) in the peripheral blood of pigs.
111 te-derived DCs (moDCs) and plasmacytoid DCs (pDCs) in two HPS2 siblings.
112                            Plasmacytoid DCs (pDCs) support antiviral immunity by linking innate and a
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
116 g with increased PD-L1, on plasmacytoid DCs (pDCs).
117           Plasmacytoid dendritic cells (DCs [pDCs]) develop from pre-pDCs, whereas two lineages of co
118                                    Defective pDC-mediated expansion of CD24(+)CD38(hi) Breg cell numb
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
124          The viral determinant for efficient pDC activation was mapped to the V1V2 region of R3A Env,
125 ted from HIV-infected subjects also enhanced pDC production of IFN in response to HIV.
126 nction of Tim-3 was investigated on enriched pDC populations from donors not infected with HIV.
127 AD and rhinovirus-induced AAD exacerbations, pDCs were recruited to the lung during inflammation and
128                             Here we examined pDC spatiotemporal dynamics during viral infection to un
129 ain containing molecule-3 (Tim-3)-expressing pDCs in the blood of HIV-infected donors.
130            The frequency of Tim-3-expressing pDCs correlated inversely with CD4 T cell counts and pos
131                             Tim-3-expressing pDCs had reduced IRF7 levels.
132                        We show that only few pDCs are capable of producing IFN-beta after virus infec
133 cific manner, which may provide insights for pDC development and functions.
134               Our findings emulate those for pDC-reactive opsonophagocytic Ab responses against coxsa
135                           sBCMA derived from pDCs might determine local availability of its high-affi
136 such as fatty acid synthesis, prevented full pDC activation.
137 which myeloid dendritic cells sense haptens, pDCs are primary sensors of imiquimod.
138                                          How pDC responses to such viral pathogens are regulated, how
139 mely low levels of CD4, unlike MAC and human pDC.
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
143 d not induce IFN-alpha or TNF-alpha in human pDC.
144 reserves the surface expression of the human pDC-specific inhibitory receptor Ig-like transcript 7.
145 e employed a knockdown technique using human pDC cell line, GEN2.2.
146                                        Human pDCs can also inhibit cryptococcal growth by a mechanism
147      During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce l
148  Src family kinases (SFK) in mouse and human pDCs.
149                            Circulating human pDCs contained BCMA protein without displaying it on the
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);
152 the innate virus-directed responses of human pDCs.
153 ficantly affects metabolism in primary human pDCs.
154 end the spectrum of BCMA expression to human pDCs.
155                       In contrast with human pDCs, murine pDCs did not express BCMA, not even after T
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
159 on when pathogens are detected by TLR 7/9 in pDC.
160                We propose that alteration in pDC-CD24(+)CD38(hi) Breg cell interaction contributes to
161 draining LNs, and gene expression changed in pDC more profoundly than in conventional DC.
162 FN-alpha increased the expression of IDO1 in pDC during AIA, and Ab-mediated depletion of pDC, either
163 cription factor; however, the role of MYC in pDC function is not well defined yet.
164 d to alter Ag-driven T cell proliferation in pDC-dependent T cell activation assays, but shifted cyto
165             Omalizumab-induced reductions in pDC FcepsilonRIalpha levels were significantly associate
166 ms of how IRF7 transcription is regulated in pDC are still elusive.
167          Among the genes most upregulated in pDC were C-type lectin receptor CLEC4E, IL-1Rs (IL-1R1 a
168 echanism by which HIV-1 induces IFN-alpha in pDCs and contributes to HIV-1 pathogenesis.
169  in the exocytic trafficking of IFN-alpha in pDCs.
170             Conditional deletion of Dusp9 in pDCs was effectively achieved in Dusp9(flox/flox); CD11c
171  TLR9 signaling is specifically essential in pDCs but not in cDCs, indicating that sensing of the vir
172 timulatory receptor, was highly expressed in pDCs.
173 y to enhance IRF7-mediated IFN expression in pDCs.
174 mmon respiratory virus, induce glycolysis in pDCs and that this metabolic pathway regulates pDC antiv
175      However, the IRF7 regulatory network in pDCs remains largely unknown.
176 c(+) cells had a cell-intrinsic reduction in pDCs and cDC2s, coupled with an increase in cDC1s.
177 ulatory mechanism of type I IFN signaling in pDCs and stage-specific function of immune cells in gene
178 ibit MyD88-dependent type I IFN signaling in pDCs.
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
181  HSV and HIV, thus functionally inactivating pDC.
182  in vivo with omalizumab treatment increases pDC antiviral IFN-alpha responses in inner-city children
183                      In healthy individuals, pDCs drive the differentiation of CD19(+)CD24(hi)CD38(hi
184  during inflammation, CD8(+) T cells induced pDC apoptosis through the perforin pathway.
185 nfluenza-induced PBMC and rhinovirus-induced pDC IFN-alpha responses in the presence of IgE cross-lin
186 ural monoamines and synthetic amines inhibit pDC activation by RNA viruses.
187 CR4) as a receptor used by amines to inhibit pDC.
188                               Using isolated pDCs and mDCs for in vitro culture with allopeptide+self
189 d CD4 and/or CCR5 expression, unlike macaque pDC.
190  stage onward and highly expressed in mature pDCs and cDC2s.
191                               In adult mice, pDC depletion predisposed to severe bronchiolitis only a
192 mall molecules targeting SFKs could modulate pDC responses in human diseases.
193  these results highlight that E2-2 modulates pDC function in a species-specific manner, which may pro
194                              IL-25 modulates pDC function through an effect on TLR9 expression.
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
197 wth by a mechanism similar to that of murine pDCs.
198          In contrast with human pDCs, murine pDCs did not express BCMA, not even after TLR9 activatio
199       We show for the first time that murine pDCs have direct activity against C. neoformans via reac
200                   Our study identified a new pDC regulatory mechanism by which the same CD28 molecule
201 ed in natural HIV infection modulated normal pDC sensing of HIV.
202 selectively expressed by macrophages but not pDCs or mDCs, block the production of cytokines.
203 undly reduced the proportion of cDCs but not pDCs.
204 regulatory T (T reg) cells in the absence of pDC-derived semaphorin 4a (Sema4a).
205                     In addition, analysis of pDC-related functions of blood-circulating mononuclear c
206      Thus, Tim-3 may serve as a biomarker of pDC dysfunction in HIV infection.
207 pDC during AIA, and Ab-mediated depletion of pDC, either during mBSA sensitization or after triggerin
208 duction of type I interferons, a hallmark of pDC activation.
209                  However, hyperactivation of pDC can cause life-threatening autoimmune diseases.
210                            This inability of pDC from 142t-IAV donors to rescue the IAV-specific CD8
211                            The high level of pDC infection by SIVagm suggests that if CCR5 paucity on
212 ingly, CD28 acted as a negative regulator of pDC IFN-I production upon TLR stimulation but did not af
213 fies CXCR4 as a potential 'on-off' switch of pDC activity with therapeutic potential.
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
216                                Activation of pDCs alleviates AHR and airway inflammation by suppressi
217                   We show that activation of pDCs through Toll-like receptor 7/8 suppresses ILC2-medi
218 lowed for the interaction and cooperation of pDCs and XCR1(+) DCs, thereby optimizing XCR1(+) DC matu
219 nd airway inflammation and that depletion of pDCs reverses this suppression.
220  implicated in regulating the development of pDCs (E2-2 and Id2) and cDC1s (Irf8, Id2, and Batf3); ho
221                         A lower frequency of pDCs expressing Tim-3 produced IFN-alpha or TNF-alpha in
222               The secretion of type I IFN of pDCs is modulated by Siglec-H, a DAP12-associated recept
223 dgkin lymphoma, possibly by the infection of pDCs and IL10 overproduction.
224 in-1 to enable the long term interactions of pDCs with Treg cells, thereby enhancing suppression of T
225       To study the function and phenotype of pDCs in lupus-prone mice we used 7 strains of lupus-pron
226 further studied to determine the presence of pDCs and correlation with inflammation.
227 luenced or even dependent on the presence of pDCs, particularly for TLR 7 and 9 ligands.
228 ve immunity demonstrated that recruitment of pDCs to the lungs is CXCR3 dependent.
229 ere associated with enhanced IFN response of pDCs, leukocyte infiltration in the intestine and mild c
230         We sought to investigate the role of pDCs in allergic airway inflammation and acute asthma ex
231 ies uncover a previously unsuspected role of pDCs in asthma exacerbations with potential diagnostic a
232             We sought to address the role of pDCs in regulating ILC2 function and ILC2-mediated airwa
233 IFN-producing cells" as a distinct subset of pDCs specialized in coordinating cellular immune respons
234 CMA was detected also on the cell surface of pDCs.
235 ey also propose the therapeutic targeting of pDCs and IL-25 for the treatment of acute asthma.
236                      The effects of IL-25 on pDCs in vitro were also assessed.
237 y mDCs and pDCs, and the effects of IL-25 on pDCs, are unknown.
238  significant effect of ERalpha deficiency on pDCs in predisease NZM2410 mice, which may represent a m
239  myeloma should consider possible effects on pDCs.
240  by Siglec-H, a DAP12-associated receptor on pDCs.
241 ssion of HLA-DR and ILT3 was also reduced on pDCs in all patients.
242 R1, cDC2 express FCER1A and FCGR2B, and only pDCs express TCF4 and NRP1 Nevertheless, despite these c
243 orms, both of which are required for optimal pDC development in vitro.
244  or transcription factor IRF7 was ablated or pDCs were depleted.
245          Consistently, in asthmatic patients pDC numbers were markedly increased during exacerbations
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
248                                       Potent pDC-activating stimuli, such as CpG, imiquimod, and Send
249 ith disease severity and greatly potentiated pDC function by triggering phagocytosis via the high-aff
250              Zeb2 was expressed from the pre-pDC and pre-cDC stage onward and highly expressed in mat
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
254                           IFN-beta-producing pDCs exhibit a distinct transcriptome profile, with high
255              Furthermore, IFN-beta-producing pDCs exhibit enhanced CCR7-dependent migratory propertie
256             Apart from IFN-alpha production, pDCs can also process Ag and induce T cell immunity or t
257 yn and Lyn as important factors that promote pDC responses, describe the mechanisms involved and high
258                      We analyzed high-purity pDCs sorted from lupus mice.
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
261 he presence of IgE cross-linking and reduced pDC surface FcepsilonRIalpha expression.
262 xpress it is co-opted to negatively regulate pDC IFN-I production and limit innate responses.
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
265  potential role for metabolism in regulating pDC immune responses to viral infections in humans.
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
270                                Specifically, pDCs upregulate neuropilin-1 to enable the long term int
271 gnature were evaluated in both BM and spleen pDC from lupus prone mice and the number of BM pDCs and
272                             Increased spleen pDC numbers were found in most lupus mice compared to C5
273                          Furthermore, spleen pDCs from MRL-lpr and NZM2410 mice showed increased resp
274 ubset (mDCs) and the plasmacytoid DC subset (pDCs).
275 r results indicate that T. gondii suppresses pDC activation by mimicking IL-10's regulatory effects t
276 ells from BAL had even greater function than pDC cells from blood (P = .008).
277  F1 and NZB mice produced more IFNalpha than pDCs from the spleens of C57BL/6 mice.
278 e Gen2.2 pDC cell line, we demonstrated that pDC-reactive opsonophagocytic IgG Ab responses against H
279                          This indicates that pDC must utilize the direct presentation pathway for thi
280                               We report that pDC survival was profoundly reduced during different non
281            The data suggest, therefore, that pDC have to be turned down during ongoing acute inflamma
282           Finally, we have demonstrated that pDCs, cDCs, and macrophages were required for generating
283 dermatitis with the distinctive feature that pDCs are the primary sensors, leading to an IL-23/TH17 d
284                                We found that pDCs accumulated at sites of CD8(+) T cell antigen-drive
285 cine DC subsets to TLR ligands revealed that pDCs are by far the most important source of TNF-alpha,
286        Taken together, our results show that pDCs inhibit C. neoformans growth in vitro via the produ
287                         We further show that pDCs suppress cytokine production and the proliferation
288                                          The pDC and mDC subsets varied according to clinical immunit
289              When we knocked down MYC in the pDC cell line, production of IFN-stimulated genes was dr
290 However, the function of at least one of the pDC or CD8alpha(+) DC subsets is required for survival o
291                                   Therefore, pDC infection and efficient sensing are not prerequisite
292 ronic HIV-1 infection depletes ILC3s through pDC activation, induction of IFN-I, and CD95-mediated ap
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 igenic rechallenge prevents inflammation via pDC.
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
299 general and on the interaction of HIV-1 with pDCs in particular.
300 ar in skin lesions that are infiltrated with pDCs.

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