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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
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
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
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
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
32 a lipid-based nanosuspension of a synthetic TLR7/8 ligand (3M-052) that facilitates adsorption to al
36 er, we demonstrated that HCV ssRNA and other TLR7/8 ligands promote MPhi polarization and generation
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
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
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
52 l responses, it consistently fails to modify TLR7/8- or RSV-stimulated innate cytokine production, ev
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
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.
72 we demonstrate here that a combined TLR4 and TLR7 adjuvant signals via the appropriate receptors and
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
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
85 5-7 d-long application of imiquimod (IMQ), a TLR7 agonist, to the skin of mice triggers a psoriasis-l
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
96 (pDC) stimulated with Toll-like receptor 7 (TLR7) agonists, Erk1/2 activation is very weak relative
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
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
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.
117 fusion, and initiated signaling through both TLR7 and TLR9, which was not utilized in the absence of
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.
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
128 rated synergy with prednisolone in assays of TLR7- and TLR9-induced IFN target gene expression using
131 in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the same in TLR3- or Trif-
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
136 ter cell assays, we verified that potency at TLR7 correlates with IFN-alpha/beta production in human
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
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
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
161 highlight the importance of conventional DC-TLR7 expression for kidney pathogenesis in a murine mode
164 In these systems normalization of B-cell TLR7 expression or temporal depletion of plasmacytoid de
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
171 eated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists showed decreased proliferation
174 ectively, the data point to a major role for TLR7 in the response to self-antigens in this model of e
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
182 HIV-1-induced CXCL13 secretion-one caused by TLR7 induction of type I IFN by plasmacytoid dendritic c
184 vaccines in humans, we investigated if Alum-TLR7 is able to improve immunogenicity of this class of
186 ave shown that conventional DC expression of TLR7 is essential for severe autoimmunity in the Sle1Tg7
188 increase of the innate Toll-like receptor 7 (TLR7) is sufficient for the development of nephritis.
192 studies demonstrate that treatment with the TLR7 ligand imiquimod can inhibit Th1 and Th17 cells, re
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
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
206 port that TLR8 coupling with SOCS-1 inhibits TLR7-mediated antiviral immunity during WNV infection in
208 ng during pDC development in vitro inhibited TLR7-mediated IFN-alpha production by human pDCs, which
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
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 (
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.
227 oduction was abolished in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the
230 heral blood human B cells were stimulated by TLR7 or TLR9 ligands, with or without IFN-alpha, and com
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
238 Situations that tilt this balance toward TLR7 promote inappropriate responses, including autoimmu
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
246 h a phosphorothioate backbone also inhibited TLR7 sensing in a sequence-dependent manner, demonstrati
248 a identify TREML4 as a positive regulator of TLR7 signaling and provide insight into the molecular me
251 s article, we demonstrate that activation of TLR7 signaling in T cells can inhibit Th17 cell differen
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
262 ished when gene encoding nucleic acid sensor TLR7, signaling adaptor MyD88, or transcription factor I
264 ion lead to higher IFN-alpha production upon TLR7 stimulation in females and provide novel targets fo
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
272 hich is the only known signaling adaptor for TLR7, suggesting that a noncanonical mechanism occurs in
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
278 acellular PRRs such as endosomal TLRs (TLR3, TLR7, TLR8, and TLR9) and cytoplasmic proteins (absent i
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
286 ars, but oligonucleotide-based inhibitors of TLR7 to TLR9, despite showing promise in animal models o
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
295 otably, mortality in the absence of Mavs and Tlr7 was independent of viral load or MyD88-dependent si
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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