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1 attributed to platelet Toll-like receptor 7 (TLR7).
2 ular Y. pestis by host Toll-like receptor 7 (TLR7).
3 m-TLR7 adjuvant effect requires a functional TLR7.
4 to particularly deleterious effects, such as TLR7.
5 f microRNAs to the 3' untranslated region of TLR7.
6  ligands for Toll-like receptor 4 (TLR4) and TLR7.
7 ecreased recruitment of the adaptor MyD88 to TLR7.
8  TLR7 antagonist or genetically deficient in TLR7.
9 -type lectin (trehalose-6,6-dibehenate), and TLR7/8 (R848) greatly enhanced caspase-1 and NF-kappaB a
10 e mice a Western diet or by applying topical TLR7/8 (Toll-like receptor) agonists.
11                             We observed that TLR7/8 activation leads to a furin-dependent proteolytic
12     Therapeutic approaches aimed at blocking TLR7/8 activation would be predicted to increase phagocy
13 triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spared the polyinosin
14 of this inhibitory activity was confirmed on TLR7/8 activity in human peripheral blood mononuclear ce
15 n therapy with intratumoral, tissue-retained TLR7/8 agonist and checkpoint blockade in metastatic can
16            However, some TLR ligands such as TLR7/8 agonist imidazoquinolines do not efficiently adso
17 rimental allergic asthma have shown that the TLR7/8 agonist resiquimod (R848) is a potential inhibito
18 n of a small-molecule imidazoquinoline-based TLR7/8 agonist to 50-nm-sized degradable polymeric nanog
19 orm also enables PD-1-targeted delivery of a TLR7/8 agonist to the tumor microenvironment, increasing
20  in mice have shown that relative to soluble TLR7/8 agonist, imidazoquinoline-ligated nanogels induce
21  were immunized with NPs containing TLR4 and TLR7/8 agonists mixed with soluble recombinant SIVmac239
22                               The ability of TLR7/8 agonists to reverse mMDSC-mediated immune suppres
23 r patients can be reversed by treatment with TLR7/8 agonists, which induce human mMDSC to differentia
24     We further found that the combination of TLR7/8 and TLR9 agonists was associated with the release
25                                We identified TLR7/8 as mediators of monocyte differentiation and M2 M
26 ges, but not by monocytes and DCs, through a TLR7/8 dependent mechanism; this leads to chloroquine se
27 specific for Toll-like receptor 4 (TLR4) and TLR7/8 encapsulated in poly(lactic-co-glycolic) acid (PL
28  potential for off-target effects of AMOs on TLR7/8 function, which should be taken into account in t
29 d patients, we found increased expression of TLR7/8 in circulating monocytes that was associated with
30 ogels the potency of the agonist to activate TLR7/8 in in vitro cultured dendritic cells is largely r
31 nuated this expression, suggesting roles for TLR7/8 in induction of fibrocytes in HCV infection.
32  a lipid-based nanosuspension of a synthetic TLR7/8 ligand (3M-052) that facilitates adsorption to al
33                In contrast, stimulation with TLR7/8 ligand protected MDCs but not MDDCs from IAV infe
34                 In T cell cocultures without TLR7/8 ligand, macrophages were the primary source of IL
35 n, even after stimulation with virus-encoded TLR7/8 ligand.
36 er, we demonstrated that HCV ssRNA and other TLR7/8 ligands promote MPhi polarization and generation
37                          After engagement of TLR7/8 or TLR9, BCMA was detected also on the cell surfa
38 n via Macrophage-inducible C-type lectin and TLR7/8 representing a novel approach to enhance the effi
39 rferon gamma response to TLR4 (P = .038) and TLR7/8 stimulation (P = .035), a reduced interleukin 6 r
40 = .035), a reduced interleukin 6 response to TLR7/8 stimulation (P = .037), and reduced IFN-gamma-ind
41                                    Following TLR7/8 stimulation by its agonist R848, chemical inhibit
42 on strategies should target the induction of TLR7/8 stimulation in APCs in order to establish potent
43 gut mucosae had robust cytokine responses to TLR7/8 stimulation in vitro, pDC gut migration occurred
44 stimulated monocytes while not doing so upon TLR7/8 stimulation.
45 4 (TLR4) and by poly(I.C) of TLR3 but not of TLR7/8 with imiquimod.
46 ll-like receptor pathways (TLR1/2, TLR4, and TLR7/8) and influenza virus-and mapped expression quanti
47 y, we show that upon Toll-like receptor 7/8 (TLR7/8)-mediated inflammation of mesenteric veins, plate
48 s were analyzed after stimulation with TLR4, TLR7/8, and retinoic acid-inducible gene I agonists.
49 onizing endosomal toll-like receptors (TLR3, TLR7/8, and TLR9), proteins involved in innate immune si
50 nsiveness was attributed to the finding that TLR7/8, but not TLR4, stimulation markedly inhibited vit
51                      Rolipram inhibited both TLR7/8- and TLR9-induced IFN regulatory factor 5 and NF-
52 l responses, it consistently fails to modify TLR7/8- or RSV-stimulated innate cytokine production, ev
53  and IFN-alpha together restored function in TLR7/8-activated macrophages.
54                                              TLR7/8-activated neutrophils promoted cleavage of FcgRII
55 D86, and MHC class I in response to TLR3 and TLR7/8-agonists.
56 e IL6 from tumor-associated macrophages in a TLR7/8-dependent manner, which in turn promoted liposarc
57 CD14(+) monocytes were stimulated with TLR4, TLR7/8-selective ligands, or respiratory syncytial virus
58                                              TLR7/8-stimulated pDC, mDC and macrophages all produced
59  and that such proliferation is blocked by a TLR7/8/9 inhibitor, by DNase, and by the PDE4 inhibitor
60 f the virus-recognizing receptors TLR3/MDA5, TLR7/-8, and TLR9 and found that this treatment elicits
61 ntially decreases IFN-alpha production after TLR7/9 activation with different types of CpG oligodeoxy
62 eficient in Unc93b, a chaperone required for TLR7/9 endosomal localization, fail to produce autoantib
63  indicator for caution in clinical trials of TLR7/9 inhibitors for MYD88(L265P) B-cell malignancies.
64 alized upon receptor-mediated endocytosis of TLR7/9 ligands to allow high IFN-alpha production.
65 e large amounts of type I IFN in response to TLR7/9 ligands.
66 D88), a downstream adapter of TLRs including TLR7, abolished the RNA-induced MIP-2 production.
67                                              TLR7 activation by PapMV in the absence of C3 induced hi
68      CXCL13 production by monocytes required TLR7 activation of plasmacytoid dendritic cells and secr
69 induced OX40L expression on myeloid APCs via TLR7 activation.
70 lating the production of IFN-alpha following TLR7 activation.
71            Finally, we demonstrate that Alum-TLR7 adjuvant effect requires a functional TLR7.
72 we demonstrate here that a combined TLR4 and TLR7 adjuvant signals via the appropriate receptors and
73                                              TLR7 agonist administration led to innate immune stimula
74 ed a new type of vaccine adjuvant based on a TLR7 agonist adsorbed to alum (Alum-TLR7), which is high
75 sly reported that SLE neutrophils exposed to TLR7 agonist autoantibodies release interferogenic DNA,
76    In this study, we show that the selective TLR7 agonist GS-9620 induced HIV in peripheral blood mon
77 Using a murine model of psoriasis induced by TLR7 agonist imiquimod (IMQ), we show that VISTA deficie
78  by injecting IL-23 or by application of the TLR7 agonist imiquimod.
79 ion induced by topical administration of the TLR7 agonist imiquimod.
80              GSK2245035 is a novel selective TLR7 agonist in pharmaceutical development.
81  in response to either administration of the TLR7 agonist R848 or infection with Citrobacter rodentiu
82  to the MLN after oral administration of the TLR7 agonist R848, it was not required for the steady-st
83                                      R848, a TLR7 agonist, decreased host vulnerability in NS4B-P38G-
84        Here, we show that a highly selective TLR7 agonist, GS-9620, activated HIV from peripheral blo
85 5-7 d-long application of imiquimod (IMQ), a TLR7 agonist, to the skin of mice triggers a psoriasis-l
86 plex, and 1V270 is a phospholipid-conjugated TLR7 agonist.
87 lated with a toll-like receptor 7-dependent (TLR7) agonist recently designed and developed in our lab
88 from Treml4(-/-) mice were hyporesponsive to TLR7 agonists and failed to produce type I interferons d
89 tigen and adjuvant, benzonaphthyridine (BZN) TLR7 agonists are chemically modified with phosphonates
90 ed IFN-alpha or TNF-alpha in response to the TLR7 agonists imiquimod and Sendai virus and to the TLR9
91                                          The TLR7 agonists R-837 and R-848 were used to mimic a viral
92                                    Localized TLR7 agonists without systemic exposure can afford good
93 fied as a new series of potent and selective TLR7 agonists.
94 ng adaptor MyD88 upon receptor triggering by TLR7 agonists.
95         Small molecule Toll-like receptor 7 (TLR7) agonists have been used as vaccine adjuvants by en
96  (pDC) stimulated with Toll-like receptor 7 (TLR7) agonists, Erk1/2 activation is very weak relative
97                                         Alum-TLR7 also drives antibody response towards Th1 isotypes.
98 ' and 3' stems (TAR microRNAs) bound best to TLR7 and -8 and none to PKR.
99 ules of the imidazoquinoline family activate TLR7 and 8 and are being developed as therapeutic agonis
100 his same mechanism may explain inhibition of TLR7 and 9 signaling by hydroxychloroquine (Plaquenil; S
101  skin, mucosa, and glands, and expression of TLR7 and DDX58 receptor genes correlated with upregulati
102 -) mice were attributed to overexpression of Tlr7 and IFN-stimulated gene-56 expression, whereas redu
103  development with subsequent upregulation of Tlr7 and Ifna1 Together, these data suggest that T1 B ce
104 , mediated through CD21, triggered endosomal TLR7 and led to the secretion of interferon (IFN) alpha
105 roduction and AP activation through specific TLR7 and MyD88 signaling.
106                                        Human TLR7 and TLR8 and mouse TLR7 recognize viral ssRNA motif
107 initiate an anti-HCV immune response through TLR7 and TLR8 in various antigen presenting cells.
108 -29a binds and activates dendritic cells via TLR7 and TLR8, resulting in the activation of the NF-kap
109  CLL cell proliferation induced by synthetic TLR7 and TLR9 agonists, as well as TLR agonist-induced c
110                           The endosomal TLRs TLR7 and TLR9 are critical for generation of Abs targeti
111                                              TLR7 and TLR9 function as innate sensors of viral infect
112 criptional program, robust responsiveness to TLR7 and TLR9 ligands, and a propensity for IgG2a/c prod
113 e large amounts of type I IFN in response to TLR7 and TLR9 ligands, whereas conventional DCs (cDCs) p
114    B cells activated by nucleic acid-sensing TLR7 and TLR9 proliferate and secrete immune globulins.
115  required for IL-10 production downstream of TLR7 and TLR9 signaling in multiple immune cell types.
116 d NZM2410 mice showed increased responses to Tlr7 and Tlr9, respectively.
117 fusion, and initiated signaling through both TLR7 and TLR9, which was not utilized in the absence of
118 recognition that relies on the expression of TLR7 and TLR9.
119 nt (Apoe (-/-)) mice and produced Apoe (-/-) Tlr7 (-/-) and Apoe (-/-) Tlr7 (+/+) littermates, follow
120 express the putative receptor for imiquimod, TLR7, and as such are stimulated by imiquimod through a
121  differentiation that appears independent of TLR7, and they provide a preclinical indicator for cauti
122 ponded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and to IL-1beta.
123                            Six SNPs of TLR3, TLR7, and TLR8 were genotyped to determine their associa
124 lved in the toll-like receptor system (TLR4, TLR7, and TLR8) and inflammasome complex pathway (NLRP3,
125 uimod, and CpG oligodeoxynucleotide for BCR, TLR7, and TLR9, respectively, alone or in combination fo
126 rent TLR agonists, including those for TLR2, TLR7, and TLR9.
127                 Lastly, BMS-986126 inhibited TLR7- and TLR9-dependent responses using cells derived f
128 rated synergy with prednisolone in assays of TLR7- and TLR9-induced IFN target gene expression using
129                                            A TLR7 antagonist may mitigate atherosclerosis.
130 as partially inhibited in cells treated with TLR7 antagonist or genetically deficient in TLR7.
131 in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the same in TLR3- or Trif-
132 n together, our data support the use of Alum-TLR7 as adjuvant for glycoconjugate vaccines.
133 ion of Toll-like receptor (TLR) 3, TLR4, and TLR7, but not TLR2 or TLR9, reduced primary microglial C
134   Furthermore, like the type I IFN response, TLR7 contributed to the lethality of septicemic plague a
135                                   Therefore, TLR7 contributes to atherogenesis in Apoe (-/-) mice by
136 ter cell assays, we verified that potency at TLR7 correlates with IFN-alpha/beta production in human
137                                              TLR7 deficiency also reduced aortic arch SMC loss and le
138                                     However, TLR7 deficiency did not affect aortic wall elastin fragm
139                            In severe asthma, TLR7 deficiency drives impaired innate immune responses
140 ion of TLR7 in atherosclerosis, we crossbred TLR7-deficient (Tlr7 (-/-)) mice with apolipoprotein E-d
141 of wild-type, TLR7-expressing platelets into TLR7-deficient mice caused a drop in platelet count and
142         Although these effects were strictly TLR7 dependent, RNAdjuvant-mediated augmentation of vacc
143       The induction of toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from
144  single autoreactive B cell clone drives the TLR7-dependent activation, expansion, and differentiatio
145  demonstrate that C1q deficiency impairs the TLR7-dependent chemokine production by pristane-primed p
146 1b(+) Ly6C(high) inflammatory monocytes in a TLR7-dependent fashion.
147 ediated knockdown found 43 regulators of the TLR7-dependent IRF5 signaling pathway.
148 ient HIV-1 induced upregulation of CD1d in a TLR7-dependent manner.
149       Collectively, these data indicate that TLR7-dependent recognition of RNA is pivotal for IFN-alp
150 ypothesis that reduced Toll-like receptor 7 (TLR7)-derived signaling drove the impaired IFN responses
151 autoantigens, which are commonly targeted in TLR7-dominated systemic erythematosus lupus-prone mice.
152 eriments revealed NXF1 selectively regulates TLR7-driven IRF5 transcriptional activity, suggesting a
153 he BALB/c pristane model recapitulates other TLR7-driven spontaneous models of SLE and is negatively
154 ing Y. pestis infection and suggest that the TLR7-driven type I IFN response plays an important role
155 cations include an increased accumulation of TLR7-expressing Ly6C(hi) inflammatory monocytes at the s
156                    Transfusion of wild-type, TLR7-expressing platelets into TLR7-deficient mice cause
157 isruption, potentially through regulation of TLR7 expression and beta-catenin activation.
158                             Reduced TLR3 and TLR7 expression and TLR downstream-signaling molecules i
159 ad3(+/-) mice, with a three-fold increase in TLR7 expression compared to controls.
160 sulted in induced IFN-stimulated gene-56 and Tlr7 expression following WNV infection.
161  highlight the importance of conventional DC-TLR7 expression for kidney pathogenesis in a murine mode
162                                    Increased TLR7 expression in human atherosclerotic lesions suggest
163                         Here we demonstrated TLR7 expression in macrophages, smooth muscle cells (SMC
164     In these systems normalization of B-cell TLR7 expression or temporal depletion of plasmacytoid de
165  report that differences in codon bias limit TLR7 expression relative to TLR9.
166 x vivo knockdown of these microRNAs restored TLR7 expression with concomitant augmentation of virus-i
167 an myeloid DCs to IFN-alpha or Flu increases TLR7 expression, suggesting they may have a role in self
168 which we showed were able to directly reduce TLR7 expression.
169 bundant in mice with high copy number of the Tlr7 gene.
170          We found that in a mouse model Alum-TLR7 greatly improved potency of a CRM197-MenC vaccine i
171 eated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists showed decreased proliferation
172            To test a direct participation of TLR7 in atherosclerosis, we crossbred TLR7-deficient (Tl
173             Here we found that engagement of TLR7 in CD4(+) T cells induced intracellular calcium flu
174 ectively, the data point to a major role for TLR7 in the response to self-antigens in this model of e
175              Furthermore, we found that Alum-TLR7 increases anti-polysaccharide immune response even
176                        Codon optimization of Tlr7 increases protein levels as well as responses to li
177                                Imiquimod has TLR7-independent activities that are mechanistically une
178   The results provide further evidence for a TLR7-independent role of imiquimod in the epithelial imm
179  directly associated with TLR8, but not with TLR7, indicating a novel role for TLR8 regulation of SOC
180                             Mechanistically, TLR7 induced PI3K/mammalian target of rapamycin signalin
181  CD4(+) T cells, we investigated the role of TLR7-induced anergy in HIV-1 infection.
182 HIV-1-induced CXCL13 secretion-one caused by TLR7 induction of type I IFN by plasmacytoid dendritic c
183 rferi RNA could be completely abrogated by a TLR7 inhibitor, IRS661.
184  vaccines in humans, we investigated if Alum-TLR7 is able to improve immunogenicity of this class of
185                               Although mouse TLR7 is cleaved in endosomes by acidic proteases, hTLR7
186 ave shown that conventional DC expression of TLR7 is essential for severe autoimmunity in the Sle1Tg7
187                        Toll-like receptor 7 (TLR7) is expressed on multiple types of cells.
188 increase of the innate Toll-like receptor 7 (TLR7) is sufficient for the development of nephritis.
189 ace that was attenuated in MyD88-knockout or TLR7-knockout mice, respectively.
190                                Activation of TLR7 leads to the production of several stimulatory cyto
191                             Stimulation with TLR7 ligand enhances formation of IRF5-NXF1 protein comp
192  studies demonstrate that treatment with the TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, re
193  poly (I: C) of TLR3 ligand and imiquimod of TLR7 ligand, along with inactivated PRRSV antigen.
194 XCL1, and IL-6 when stimulated in vitro with TLR7 ligand.
195 ation of the FOXO3A pathway, TLR3, TLR4, and TLR7 ligands activated FOXO3A as indicated by decreased
196 eral dose combinations of synthetic TLR4 and TLR7 ligands are potent adjuvants for recombinant influe
197                       Combining the TLR4 and TLR7 ligands balances Th1 and Th2-type immune responses
198                           Combining TLR4 and TLR7 ligands balances Th1- and Th2-type immune responses
199 antiproliferative effects of TLR3, TLR4, and TLR7 ligands correlated with significant downregulation
200 all-molecule Toll-like receptor 4 (TLR4) and TLR7 ligands is a potent adjuvant for recombinant influe
201 of synthetic Toll-like receptor 4 (TLR4) and TLR7 ligands is a potent adjuvant for recombinant influe
202 hat murine CD8(+) T cells can sense TLR2 and TLR7 ligands, resulting in rapid production of IFN-gamma
203 roduced Apoe (-/-) Tlr7 (-/-) and Apoe (-/-) Tlr7 (+/+) littermates, followed by feeding them an athe
204                                            A TLR7-luciferase reporter construct was created to evalua
205                                 Silencing of TLR7 markedly decreased the frequency of HIV-1-infected
206 port that TLR8 coupling with SOCS-1 inhibits TLR7-mediated antiviral immunity during WNV infection in
207  very low doses led to local upregulation of TLR7-mediated cytokines (IP-10).
208 ng during pDC development in vitro inhibited TLR7-mediated IFN-alpha production by human pDCs, which
209 F5 protein into human primary pDCs increased TLR7-mediated IFN-alpha secretion.
210 lation of STAT3 signaling is responsible for TLR7-mediated inhibition of Th17 cells due to induction
211 (DCs), as well as both B cells and DCs, in a TLR7-mediated model of autoimmunity, similar to systemic
212                                              TLR7-mediated suppression of Th17 cells does not require
213                                              TLR7 mediates innate immune responses to viral RNA in en
214                        Toll-like receptor 7 (TLR7) mediates autoantigen and viral RNA-induced cytokin
215                       Compared to Apoe (-/-) Tlr7 (+/+) mice, Apoe (-/-) Tlr7 (-/-) mice showed reduc
216        Reduced atherosclerosis in Apoe (-/-) Tlr7 (-/-) mice did not affect lesion macrophage-positiv
217 ed to Apoe (-/-) Tlr7 (+/+) mice, Apoe (-/-) Tlr7 (-/-) mice showed reduced aortic arch and sinus les
218 therosclerosis, we crossbred TLR7-deficient (Tlr7 (-/-)) mice with apolipoprotein E-deficient (Apoe (
219 ation, which was significantly attenuated in TLR7(-/-) mice.
220 cing IFN-beta [TRIF] responsive), C/EBPbeta (TLR7-MyD88 responsive), and JunB (all responsive).
221 at exRNA induces cytokine production through TLR7-MyD88 signaling.
222 arapsilosis-mediated induction of IL-27 in a TLR7-, MyD88-, and NOD2-dependent manner.
223 define a novel link between C. parapsilosis, TLR7, NOD2, IFN-beta, and IL-27, and we have identified
224  this review, we take a specific look at how TLR7, non-coding RNA, and SSA/Ro60 can contribute to cli
225 opposing effects of TLR9 and TLR3, TLR4, and TLR7 on the key angiogenic pathways, Fli1 and FOXO3A.
226                          Genetic deletion of TLR7 or MyD88, but not TLR3, and inhibition of the MAPKs
227 oduction was abolished in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the
228 erentiation into MPhis could be prevented by TLR7 or TLR8 knockdown.
229                                 Furthermore, TLR7 or TLR8 stimulation, independent of HCV, caused mon
230 heral blood human B cells were stimulated by TLR7 or TLR9 ligands, with or without IFN-alpha, and com
231 ining fragments with resultant activation of TLR7 or TLR9, respectively.
232  upon stimulation with ligands that activate TLR7 or TLR9.
233 /-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were more susceptible to P. a
234 generated Mer(-/-) mice with a global MyD88, TLR7, or TLR9 deficiency and cell type-specific MyD88 de
235 n monocytes exposed to HCV, and knockdown of TLR7 partially attenuated this expression, suggesting ro
236 y, our results suggest that dysregulation of TLR7 partially contributes to impaired innate and adapti
237                 Coactivation of the TLR3 and TLR7 pathways synchronizes the interaction of IRF1, JunB
238     Situations that tilt this balance toward TLR7 promote inappropriate responses, including autoimmu
239 iptional assays confirm Smad3 binding at two TLR7 promoter SBE sites.
240                Human TLR7 and TLR8 and mouse TLR7 recognize viral ssRNA motifs and induce antiviral i
241  responses mediated by Toll-like receptor 7 (TLR7) remain to be fully elucidated.
242 alpha in the upper airways via activation of TLR7 represents a novel immunomodulatory approach to the
243 FN-beta is required for optimal survival and TLR7 responses of transitional B cells in the spleen and
244 rs and TLR polymorphisms (TLR2 rs3804100 and TLR7 rs179012) also were associated with set point, expl
245                       The "G-G" haplotype of TLR7 rs3853839 and TLR8 rs3764880 increased risk of SLE
246 h a phosphorothioate backbone also inhibited TLR7 sensing in a sequence-dependent manner, demonstrati
247 d a subset of sequences highly inhibitory to TLR7 sensing in mouse macrophages.
248 a identify TREML4 as a positive regulator of TLR7 signaling and provide insight into the molecular me
249                    In addition, we show that TLR7 signaling can suppress Th1 cell development and fun
250                                     Impaired TLR7 signaling in old mice led to dendritic cell (DC) an
251 s article, we demonstrate that activation of TLR7 signaling in T cells can inhibit Th17 cell differen
252                                     Enhanced TLR7 signaling in Vsir (-/-) dendritic cells (DCs) led t
253 her, these data demonstrate that an atypical TLR7 signaling pathway contributes to type I IFN express
254 combined adjuvant is dependent upon TLR4 and TLR7 signaling via myeloid differentiation primary respo
255 roduced substantial amounts of IFN-alpha via TLR7 signaling when cocultured with infected cells.
256 tivates endosomal NOX2 oxidase and restricts TLR7 signaling, and that an endosomal NOX2 inhibitor dec
257 c93b1(3d/3d) mutation, which blocks TLR9 and TLR7 signaling, or Tlr9 deficiency suppressed MYD88(L265
258 und that HIV-induced IFN production required TLR7 signaling, receptor-mediated entry, fusion, and vir
259 trategy to manipulate Th17/Th1 cells through TLR7 signaling, with important implications for successf
260 TREML4 as an essential positive regulator of TLR7 signaling.
261 e production and leukocyte migration through TLR7 signaling.
262 ished when gene encoding nucleic acid sensor TLR7, signaling adaptor MyD88, or transcription factor I
263                        In vivo activation of TLR7 significantly increased IFNa4 and IL-1ra expression
264 ion lead to higher IFN-alpha production upon TLR7 stimulation in females and provide novel targets fo
265                            Finally, platelet-TLR7 stimulation is independent of thrombosis and has im
266  The combination of Ad26/MVA vaccination and TLR7 stimulation resulted in decreased levels of viral D
267 Cs) from females produce more IFN-alpha upon TLR7 stimulation than pDCs from males, yet the mechanism
268  MNECs, and HNECs within 15 minutes of local TLR7 stimulation.
269 ed dysregulated responses to TLR4, TLR8, and TLR7 stimulation.
270 madelta(+) and CD4(+) Th17 T cells following TLR7 stimulation.
271                        Toll-like receptor 7 (TLR7) stimulation in the airways may reduce responses to
272 hich is the only known signaling adaptor for TLR7, suggesting that a noncanonical mechanism occurs in
273 tors of endosomal Toll-like receptors (TLR9, TLR7) that activate MYD88.
274 all-molecule ligand of Toll-like receptor-7 (TLR7) that is licensed for the treatment of viral infect
275 nocyte-specific pattern recognition receptor TLR7, the Langerhans cell chemoattractant CCL20, and pro
276              Destruction of YxxPhi abolished TLR7, TLR8, and TLR9 activity toward nucleic acids in hu
277 es TRAILshort production are type I IFNs and TLR7, TLR8, and TLR9 agonists.
278 acellular PRRs such as endosomal TLRs (TLR3, TLR7, TLR8, and TLR9) and cytoplasmic proteins (absent i
279 4-diamine was found to be a very potent dual TLR7/TLR8 agonist.
280                                         Dual TLR7/TLR8 agonists markedly upregulate CD80 expression i
281          In an effort to identify novel dual TLR7/TLR8-active compounds, we undertook structure-activ
282 hese studies identify a non-MyD88 pathway of TLR7/ TLR9 signaling in neurons and provide a mechanism
283 ple adjuvant combination, TLR4/TLR9 and TLR4/TLR7/TLR9, for further evaluation and found that both co
284  we identified the mechanism responsible for TLR7/TLR9-mediated neuronal apoptosis.
285                                          The TLR7 to TLR9 blocker hydroxychloroquine has been in use
286 ars, but oligonucleotide-based inhibitors of TLR7 to TLR9, despite showing promise in animal models o
287 upus by blocking BAFF, type I interferon, or TLR7 to TLR9.
288 ated gene 5 (MDA5) and Toll-like receptor 7 (TLR7) to induce transcription of type I interferon.
289 cinia Ankara (MVA) boost) and stimulation of TLR7 (Toll-like receptor 7) improves virologic control a
290                                We then chose TLR7, transcription factor p65 (RelA), gamma interferon
291                           Mouse and human (h)TLR7 undergo proteolytic cleavage, resulting in the gene
292 e the effect of B cell-intrinsic deletion of TLR7 versus TLR9 in parallel lupus models.
293                  In the murine plague model, TLR7 was a significant contributor to the expression of
294                                 In contrast, TLR7 was important for defense against disease in the lu
295 otably, mortality in the absence of Mavs and Tlr7 was independent of viral load or MyD88-dependent si
296                            The expression of TLR7 was significantly reduced in severe asthma AMs and
297 d resistance due to deficiencies in Mavs and Tlr7, we found an elevated respiratory bacterial burden.
298 probably signaling via Toll-like receptor 7 (TLR7) were critical for sensing of MERS-CoV by pDCs.
299 sed on a TLR7 agonist adsorbed to alum (Alum-TLR7), which is highly efficacious at enhancing immunoge
300 ion of innate immunity through engagement of TLR7 with papaya mosaic virus (PapMV)-like nanoparticles

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