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1 s) and fungal C-type lectin receptors (e.g., dectin-1).
2 oides brasiliensis include TLR-2, TLR-4, and dectin-1.
3 es activation of the fungal pattern receptor dectin-1.
4 inflammatory responses mediated by IL-17 and Dectin-1.
5 n domains of complement receptor 3 (CR3) and dectin-1.
6 surface pathogen recognition receptor called Dectin-1.
7 at-killed C cladosporioides was dependent on Dectin-1.
8 alter the immune response through binding to Dectin-1.
9 rface of the spores and increased binding to Dectin-1.
10 ich tyrosine kinase 2, and in the absence of Dectin-1.
11 ized by the immune system by their receptor, Dectin-1.
12 on CD18, but not on the beta-glucan receptor dectin-1.
13 hilic inflammation independent of IL-17A and Dectin-1.
14 ucans on their surface and were able to bind Dectin-1.
15 ne system through the innate immune receptor Dectin-1.
16 t-labile serum component(s) independently of Dectin-1.
17 n of yeasts by the host beta-glucan receptor Dectin-1.
18 ht determine whether it can be recognized by Dectin-1.
19                                  The role of Dectin-1, a beta-1,3-glucan receptor, critical for funga
20                                              Dectin-1, a beta-glucan receptor, contributes to host an
21 zonensis infection occurs upon engagement of Dectin-1, a C-type lectin receptor that signals via sple
22 ed by hyphae but not spores and depends upon Dectin-1, a C-type lectin receptor.
23                  Detection of C. albicans by Dectin-1, a C-type signaling lectin specific for beta-(1
24 uring P. carinii infection the expression of Dectin-1, a critical receptor for recognition and cleara
25 ward the fungal pathogen, we aimed to target Dectin-1, a pattern-recognition receptor expressed on mo
26 t and autophagy were offset in vitro through Dectin-1, a receptor that elicits TREM2-like intracellul
27                             Phagocytosis via dectin-1 acted as a sensor of microbe size and prevented
28 s TNFSF15 and OX40L, which are essential for dectin-1-activated DC-induced Th9 cell priming.
29                         Our results identify dectin-1-activated DCs as a powerful inducer of Th9 cell
30 hat depends on Th9 cells and IL-9 induced by dectin-1-activated DCs in vivo.
31 re, immunization of tumour-bearing mice with dectin-1-activated DCs induces potent antitumour respons
32                             Mechanistically, dectin-1 activates Syk, Raf1 and NF-kappaB signalling pa
33  a florid macrophage reaction; however, only dectin-1 activation causes macrophage-mediated demyelina
34 vating TLR2 reduced the injurious effects of dectin-1 activation.
35 rface topology are correlated with increased Dectin-1 adhesion and decreased cell wall elasticity.
36  and binding affinity did not correlate with Dectin-1 agonism, antagonism, or potency.
37  were able to identify a laminarin that is a Dectin-1 agonist and a laminarin that is Dectin-1 antago
38                                    In vivo a Dectin-1 agonist as adjuvant was sufficient to induce TH
39  principle to a strong synergism between the dectin-1 agonist curdlan and an inflammatory growth fact
40               DCs become unresponsive to the dectin-1 agonist curdlan and fail to phosphorylate Syk a
41 eir Th9-polarizing capability in response to dectin-1 agonist curdlan.
42 up-regulated after exposure to GM-CSF or the Dectin-1 agonist zymosan.
43                   Particulate beta-glucan (a DECTIN-1 agonist) induced mast cell degranulation in mes
44 combinations of TLR agonists with or without Dectin-1 agonist.
45 , there are reports that laminarin is also a Dectin-1 agonist.
46  albicans, live C. albicans, or the specific Dectin-1 agonists curdlan or whole glucan particles.
47          Here, we show that DCs activated by dectin-1 agonists potently promote naive CD4(+) T cells
48                                              Dectin-1 agonists represent a promising TH1 adjuvant for
49 arins were Dectin-1 antagonists and two were Dectin-1 agonists.
50 mmalian target of rapamycin (mTOR) through a dectin-1-Akt-HIF-1alpha (hypoxia-inducible factor-1alpha
51       Coactivation of neonatal moDCs through Dectin-1 allows TLR-mediated IL-12p70 secretion and TH1
52                        GPs are recognized by Dectin-1 and are potent complement activators.
53 activating myeloid-specific CTLRs, including Dectin-1 and CLEC-2, and consist of a single tyrosine si
54 y, we examined the relative contributions of Dectin-1 and complement to GP phagocytosis and Ag-specif
55 phobin RodA as a virulence factor that masks Dectin-1 and Dectin-2 recognition of conidia, resulting
56 in ligase CBLB directs polyubiquitination of dectin-1 and dectin-2, two key pattern-recognition recep
57 he parent G10 strain, which was dependent on Dectin-1 and Dectin-2.
58 ntrol of innate immune responses mediated by dectin-1 and dectin-2.
59 gh lipocalin 2 production was observed to be Dectin-1 and IL-22 dependent, lipocalin 2-deficient mice
60 SCs through the pattern recognition receptor Dectin-1 and its downstream adaptor protein CARD9.
61 tern recognition receptors for fungi include dectin-1 and mannose receptor, and these mediate phagocy
62 preparations were bound by recombinant human Dectin-1 and mouse Dectin-1, but the affinity varied con
63 to LT-deficient cells restored expression of dectin-1 and PU.1, as well as dectin-1 responsiveness.
64 re, IL-8 secretion was partially mediated by Dectin-1 and required SYK, MAPKs, and the transcription
65 riming requires the beta-1,3-glucan receptor dectin-1 and the noncanonical Raf-1 pathway.
66 e training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway.
67                         The combined loss of dectin-1 and TLR2 completely blocks the proregenerative
68                                              Dectin-1 and TLR9 play distinct roles in the recognition
69            Simultaneous coactivation through Dectin-1 and TLRs induced robust secretion of IL-12p70 b
70      Subcutaneous immunization of wild-type, Dectin-1(-/-), and C3(-/-) mice with GP-OVA resulted in
71 eptors, such as Toll-like receptors 1 and 2, dectin 1, and dendritic cell-specific intercellular adhe
72  recognition receptors, such as pentraxin 3, dectin-1, and Toll-like receptors, leads to complement a
73 their downstream kinase SYK, thus inhibiting dectin-1- and dectin-2-mediated innate immune responses.
74 as IL-17A- and Dectin-1-independent, whereas Dectin-1- and IL-17A-dependent pathways were protective
75 a demonstrate that laminarin can be either a Dectin-1 antagonist or agonist, depending on the physico
76 s a Dectin-1 agonist and a laminarin that is Dectin-1 antagonist, both of which are relatively pure p
77                The remaining laminarin was a Dectin-1 antagonist, but when the low m.w. moieties were
78 -beta-glucan that is widely reported to be a Dectin-1 antagonist, however, there are reports that lam
79 h human and mouse cells, two laminarins were Dectin-1 antagonists and two were Dectin-1 agonists.
80 macrophages by fluorescent anti-CR3 and anti-dectin-1 antibodies, respectively, and to stimulate phag
81 es when both an intact complement system and Dectin-1 are present.
82 onses generated via the beta-glucan receptor Dectin-1 are required for lung defense during acute, inv
83 relatively short mimetics to bind to CR3 and dectin-1, as compared to the greater degree of polymeriz
84 9 after receptor ligation and localized with Dectin-1 at the cell membrane.
85 naling and cytokine production downstream of Dectin-1 because of an increased expression and sustaine
86 osyl lipid adjuvant aqueous formulation) and Dectin-1 (beta-glucan peptide) acted synergistically in
87         Studies using beta-glucans and other Dectin-1 binding components have demonstrated the potent
88  the physical properties, structure, purity, Dectin-1 binding, and biological activity of five differ
89 cans yeast and hyphae is limited to isolated Dectin-1-binding sites.
90                                              Dectin-1 binds to beta-glucans in fungal cell walls and
91                            The C-type lectin Dectin-1 binds to yeasts and signals either in an autono
92 ficient for the pattern recognition receptor dectin-1 but not Toll-like receptor-2 (TLR2), zymosan-me
93 ound by recombinant human Dectin-1 and mouse Dectin-1, but the affinity varied considerably, and bind
94                                  Ligation of Dectin-1 by fungal glucans elicits a Th17 response that
95 milar DC profile was obtained by stimulating Dectin-1 (C-type lectin family member) on Rictor(-/-) DC
96                                We found that dectin 1 can ligate the lectin galectin 9 in mouse and h
97 s with defects affecting segments of innate (dectin-1, CARD9, IL12RB1) or adaptive immunity (interleu
98 n candidiasis, involves a well-characterized Dectin-1/caspase-associated recruitment domain adaptor 9
99  associated with resolution of inflammation, Dectin-1, CD206 (mannose receptor), and IL-4R.
100                                              Dectin-1 (Clec7a) is a paradigmatic C-type lectin recept
101 we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe fo
102 sults indicate that the beta-glucan receptor Dectin-1 contributes to lung inflammation and immunopath
103 ther, these results define the importance of dectin-1, CR3, and caspase-8, in addition to the canonic
104 gal recognition and immunity such as Mincle, dectin-1, dectin-2, and pentraxin 3 are strongly upregul
105 ethal dose of C. albicans, and deficiency of dectin-1, dectin-2, or both in Cblb(-/-) mice abrogates
106 nal invasion during systemic infection, with dectin-1 deficiency associating with impaired fungal cle
107 on this response seems to be redundant since dectin-1 deficiency in mice does not affect intestinal i
108                                  Remarkably, dectin-1 deficiency increased the expansion of regulator
109                                              Dectin-1 deficiency led to aberrant NET release and NET-
110 ing from different immune defects, including dectin-1 deficiency, CARD9 deficiency, or chronic granul
111                 We assessed the responses of dectin-1 deficient macrophages to the intestinal microbi
112  in response towards the intestinal flora in dectin-1 deficient macrophages, during intestinal inflam
113 his microbiota were significantly reduced in dectin-1 deficient macrophages.
114  in the course of inflammation were found in dectin-1 deficient mice compared to wild type mice.
115 ic Helicobacter hepaticus induced colitis in dectin-1 deficient mice.
116  collected from both A. fumigatus-challenged Dectin-1-deficient and IL-22-deficient mice had compromi
117 liensis infection reinforced the tendency of dectin-1-deficient macrophages to express an M2 phenotyp
118                           Here, we show that Dectin-1-deficient mice demonstrated significantly reduc
119 eas bone marrow-derived dendritic cells from Dectin-1-deficient mice failed to produce IL-23 in respo
120                                           In Dectin-1-deficient mice, A. versicolor exposure resulted
121 r in lung cells from A. fumigatus-challenged Dectin-1-deficient mice, whereas bone marrow-derived den
122  rescued IL-22 production by lung cells from Dectin-1-deficient mice.
123 eg3g mRNA expression was not lower in either Dectin-1-deficient or IL-22-deficient mice.
124 or leukotriene B(4) receptor 1 (BLT1) direct dectin-1-dependent binding, ingestion, and cytokine prod
125                                  In summary, Dectin-1-dependent IL-17A production in the lungs during
126             In contrast, we observed robust, Dectin-1-dependent IL-22 production by unfractionated lu
127  defense against A. fumigatus is mediated by Dectin-1-dependent IL-22 production.
128 ic lung digests ex vivo further demonstrated Dectin-1-dependent IL-22 production.
129  Candida albicans-containing phagosomes in a Dectin-1-dependent manner in GM-CSF-derived bone marrow
130 icitation of TNF-alpha from macrophages in a Dectin-1-dependent manner.
131 , IFN-gamma, and IL-17A, but not IL-22, in a Dectin-1-dependent manner.
132 ific CD4(+) and CD8(+) T cell responses in a dectin-1-dependent manner.
133 lood mononuclear cells and macrophages via a Dectin-1-dependent mechanism.
134 mes containing Candida albicans also require Dectin-1-dependent Syk activation for phagosomal maturat
135                             However, whether dectin-1 directs DCs to prime antitumour Th9 cells remai
136                                     Further, Dectin-1 directs the recruitment of LC3II to phagosomes,
137 t mice deficient in the beta-glucan receptor Dectin-1 displayed increased susceptibility to Aspergill
138 7a-the gene encoding dectin 1-or blockade of dectin 1 downstream signaling was protective.
139                                  Loss of the dectin-1 downstream effector caspase recruitment domain
140                      SHIP-1 colocalized with Dectin-1 during phagocytosis of zymosan in a hemITAM-dep
141                  Here, we show that TLR2 and Dectin 1 engagement by zymosan promotes regulatory T-cel
142                                              Dectin-1 engagement triggers a plethora of activating ev
143                               In conclusion, dectin-1 exerts an important protective role in pulmonar
144                                 Mice lacking Dectin-1 exhibited increased susceptibility to chemicall
145 investigated the role of LTB(4) signaling in dectin-1 expression and responsiveness in macrophages.
146 nses to fungal glucans correlated with lower dectin-1 expression in macrophages from leukotriene (LT)
147 is showed that H. polygyrus bakeri decreases dectin-1 expression on the intestinal DC subsets that dr
148 ecognition receptor dectin-1; restoration of dectin-1 expression recovered innate cytokine production
149 nhances Th17 differentiation, independent of Dectin-1 expression, in A. fumigatus-infected mice.
150  of the transcription factor responsible for dectin-1 expression, PU.1, and PU.1 small interfering RN
151 ll interfering RNA abolished LTB(4)-enhanced dectin-1 expression.
152 hagosomes expressing a signaling incompetent Dectin-1 failed to mature as demonstrated by prolonged D
153 , and precoating the surface of zymosan with Dectin-1:Fc can reduce cytokine production by macrophage
154                                          All Dectin-1:Fc variants showed specificity of binding to th
155 matory properties by assembling a galectin-3-Dectin-1-FcgammaRIIB receptor complex that activated bet
156 lec7a(-/-) mice support the critical role of Dectin-1 for inflammasome activation, restriction of par
157 isting of the carbohydrate binding domain of Dectin-1 fused to the Fc regions of the 4 subtypes of mu
158                       Upon disruption of the dectin 1-galectin 9 axis, CD4(+) and CD8(+) T cells, whi
159                               The absence of dectin-1 has also impaired the production of T-helper ty
160 urthermore, non-pathogen-derived ligands for dectin 1 have not been characterized.
161 ic cells (DCs) via Dectin-1 using anti-human Dectin-1 (hDectin-1)-HA1 recombinant fusion proteins.
162                            In the absence of Dectin-1, heat-killed spores induced a predominantly TH2
163 row chimeric mice revealed a requirement for dectin-1 in both retina-resident immune cells and bone m
164 3)-glucan, which leads to greater binding by Dectin-1 in both yeast and hyphal forms.
165                                Abrogation of dectin-1 in DCs completely abolishes their Th9-polarizin
166 production of IL-22, we examined the role of Dectin-1 in IL-22 production, as well as the role of IL-
167  by the non-TLR pattern recognition receptor Dectin-1 in murine bone marrow-derived dendritic cells a
168 that activation of a C-type lectin receptor, dectin-1, in MDSC differentially modulates the function
169  in a CD1d-restricted, MyD88-independent and dectin-1-independent fashion.
170 ncreased after exposure to A. fumigatus in a dectin-1-independent manner.
171 sponse to C. cladosporioides was IL-17A- and Dectin-1-independent, whereas Dectin-1- and IL-17A-depen
172  contrast, clustering the hemi-ITAM receptor Dectin-1 induced signaling that did not require LynA or
173                               Restoration of dectin-1-induced Rac1 activation and phagocytosis by res
174 ructure and activity relationships of glucan/Dectin-1 interactions.
175                                              Dectin 1 is an innate immune receptor crucial for anti-f
176                                We found that dectin 1 is highly expressed on macrophages in pancreati
177                                              Dectin-1 is a pattern recognition receptor that is impor
178                                              Dectin-1 is a receptor for the major fungal cell wall ca
179                                              Dectin-1 is a widely expressed pattern recognition recep
180                                              Dectin-1 is also present on blood-derived myeloid cells
181                                              Dectin-1 is an innate pattern recognition receptor essen
182                     Our results suggest that Dectin-1 is crucial for macrophage recognition and the m
183                               Thus, in mice, dectin-1 is essential for controlling systemic infection
184            Here, we demonstrate that in mice dectin-1 is essential for the control of gastrointestina
185                               In the retina, dectin-1 is expressed by microglia and dendritic cells,
186                               Thus, although Dectin-1 is necessary for optimal phagocytosis of GPs in
187                                              Dectin-1 is specifically recruited to the macrophage-hyp
188 cognition receptors, such as TLR4, CD14, and dectin 1, is now known to induce the activation of calci
189 migatus conidia, beta-glucan recognition via Dectin-1 led to the induction of multiple proallergic (M
190                 Intraocular injection of the dectin-1 ligand curdlan [a particulate form of beta(1, 3
191 thermore, priming of Xiap(-/-) mice with the dectin-1 ligand curdlan alone resulted in XLP-2-like syn
192 was also observed after stimulation with the Dectin-1 ligand Curdlan.
193 LR engagement as a direct target gene of the Dectin-1 ligand Zymosan.
194 homa 10 (BCL10)-mediated innate responses to dectin-1 ligands but did not affect responses to various
195  administration of IL-17 family cytokines or Dectin-1 ligands promoted regeneration.
196                                              Dectin 1 ligation accelerated the progression of PDA in
197 ndrome had reduced TNF-alpha responses after Dectin-1 ligation but in part used a Raf-1-mediated path
198                                              Dectin-1 ligation is required for gammadeltaT cells to p
199 ut Th17 cell responses due to the absence of Dectin-1 ligation.
200 nificantly decreased TNF-alpha release after Dectin-1 ligation.
201 t polarized surviving M-MDSCs toward CCR7(+) Dectin-1(-)M1 cells, accompanied by IFN-gamma production
202  This prevalent antiinflammatory activity of dectin-1(-/-) macrophages resulted in impaired fungicida
203 y, production of IFN-gamma on stimulation of dectin-1, mannose, and Toll-like receptors with Candida
204                                       Hence, dectin-1 may be involved in the pathogenesis of IBD.
205  responses through a mechanism that required Dectin-1-mediated expression of interleukin-6 (IL-6) by
206  in the absence of Dectin-1, suggesting that Dectin-1-mediated IL-22 production potentiated responses
207 tant for triggering phagocytosis, killing or Dectin-1-mediated inflammatory cytokine production, it f
208                                              Dectin-1-mediated spleen tyrosine kinase activation is r
209  macrophages was comparable in wild-type and Dectin-1(-/-) mice and was not inhibited by the soluble
210 n-1-sufficient mice, the fungal infection of dectin-1(-/-) mice was more severe and resulted in enhan
211 comparable to zymosan in WT mice, but not in dectin-1(-/-) mice.
212 atitis model using C57BL/6, Mincle(-/-), and Dectin-1(-/-) mice.
213 stitution inflammatory syndrome (IRIS), both Dectin-1:mIgG1 and Dectin-1:mIgG2a Fc reduced hypoxemia
214 vivo challenge model, systemic expression of Dectin-1:mIgG1 Fc significantly reduced ascus burden in
215 ory syndrome (IRIS), both Dectin-1:mIgG1 and Dectin-1:mIgG2a Fc reduced hypoxemia despite minimal eff
216                                              Dectin-1:mIgG2a Fc was able to reduce the viability of P
217 ogether, these results support a model where Dectin-1 not only controls internalization of beta-1,3-g
218                                           In dectin-1-null mutant (knock-out) mice, dieback of cortic
219  ligation of Toll-like receptor 2 (TLR2) and Dectin 1 on antigen-presenting cells by zymosan results
220 ted, or "masked," from immune recognition by Dectin-1 on dendritic cells (DCs) and other innate immun
221 cilitating the recruitment of Syk to the CLR dectin-1 or the adaptor FcRgamma, through its N-SH2 doma
222 on by macrophages from C57BL/6, but not from Dectin-1(-/-) or Dectin-2(-/-) mice.
223 , but not lectin-like oxidized-LDL receptor, Dectin-1, or DC-specific ICAM-3-grabbing nonintegrin fav
224  complement receptor 3 (CD11b/CD18), but not Dectin-1, or ROS.
225                                         Upon Dectin-1- or RIG-I-mediated activation, Rubicon dynamica
226 whereas deletion of Clec7a-the gene encoding dectin 1-or blockade of dectin 1 downstream signaling wa
227 ive to Histoplasma infection than wild-type, Dectin-1-/-, or interleukin 1 receptor-deficient (IL-1R-
228 ticles (WGP; a ligand to engage and activate dectin-1, oral treatment in vivo) significantly decrease
229 RE formed a transient complex with the known Dectin-1 pathway components phosphorylated spleen tyrosi
230          Innate immune signaling through the Dectin-1 pathway was assessed in both PBMCs from patient
231 trafficking, is recruited directly by LC3 to Dectin-1 phagosomes.
232 nd that both complement receptor 3 (CR3) and dectin-1 play a crucial role in coordinating beta-glucan
233 7-producing gammadeltaT cells or deletion of Dectin-1 prevented development of regenerative phenotype
234               In addition, LTB(4) effects on dectin-1, PU.1, and cytokine production were blunted in
235 nd to DCs and macrophages independent of the dectin-1 receptor and did not activate DCs.
236 ubclasses, showing that vaccine targeting to Dectin-1 receptor can benefit from augmentation and immu
237 ritic cells (DCs) following detection by the Dectin-1 receptor, but the effects of beta-glucan-induce
238    Focusing on CLEC7A, which encodes for the dectin-1 receptor, flow analysis showed that H. polygyru
239 lucans and was mediated by activation of the Dectin-1 receptor.
240 lement activation pathway but independent of dectin-1 receptor.
241 mulated cells were mTOR-independent and used Dectin-1 receptor.
242             This effect was dependent on the dectin-1 receptor.
243 umigatus and C. albicans phagosomes requires Dectin-1 recognition.
244                         The receptor protein Dectin-1 recognizes structures found on cancerous cells,
245                                 In addition, Dectin-1 regulates TLR9-dependent gene expression.
246  expression of dectin-1 and PU.1, as well as dectin-1 responsiveness.
247 pression of the pattern recognition receptor dectin-1; restoration of dectin-1 expression recovered i
248                            Ligand binding to Dectin-1 resulted in the following: 1) activation of Src
249 ailed to mature as demonstrated by prolonged Dectin-1 retention, presence of Rab5B, failure to acquir
250 ased cytokine production after inhibition of dectin 1 revealed that this receptor plays a major role
251    In addition, AFM tips functionalized with Dectin-1 revealed that the forces of binding of Dectin-1
252                                 Mutations in dectin-1 (rs7309123) and DC-SIGN (rs11465384 and rs72486
253 s employed to show binding and activation of Dectin-1 signal transduction pathway by the beta-glucan-
254            These data suggest that targeting dectin 1 signaling is an attractive strategy for develop
255                       SOCS1 did not modulate Dectin-1 signaling but affected TLR signaling, leading t
256                  In this study, we show that Dectin-1 signaling in macrophages and bone marrow-derive
257                  AIRE can participate in the Dectin-1 signaling pathway, indicating a novel extrathym
258 be, Tang et al. (2015) show that suppressing Dectin-1 signaling protects mice from experimental colit
259  further dependent on pathways downstream of Dectin-1 signaling, notably reactive oxygen species (ROS
260 ng to define a more precise picture of early Dectin-1 signaling, we explored the interactome of the i
261                                              Dectin-1 signalling in dendritic cells (DCs) has an impo
262 oluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate bet
263  that SCIMP is strongly phosphorylated after Dectin-1 stimulation and that it participates in signal
264                                     Notably, dectin-1 stimulation of DCs upregulates TNFSF15 and OX40
265 ular pathways triggered by combined TLR plus Dectin-1 stimulation was determined by using pharmacolog
266 aling downstream of Toll-like receptor 2 and dectin-1 stimulation.
267                This fact motivated us to use dectin-1-sufficient and -deficient mice to investigate t
268                                Compared with dectin-1-sufficient mice, the fungal infection of dectin
269 mmatory responses observed in the absence of Dectin-1, suggesting that Dectin-1-mediated IL-22 produc
270 ainst live C. albicans that was dependent on Dectin-1, Syk, and NADPH oxidase.
271 s increased oxidative burst was dependent on Dectin-1, Syk, PI3K, phosphoinositide-dependent protein
272                             Our studies link Dectin-1/Syk kinase signaling with autophagy-dependent m
273       Additionally, our data reveal that the dectin-1/Syk pathway is redundant and that TLR2 has an i
274     Thus, we reported that activation of the Dectin-1/Syk/ROS/NLRP3 pathway during L. amazonensis pha
275                                              Dectin-1, the innate immune receptor that recognizes bet
276  We adapted the pattern-recognition receptor Dectin-1 to activate T cells via chimeric CD28 and CD3-z
277 tin-1 revealed that the forces of binding of Dectin-1 to all of the strains were similar, but the fre
278 of acidification results in retention of GFP-Dectin-1 to phagosome membranes highlighting the require
279 or Syk results in prolonged retention of GFP-Dectin-1 to the phagosome signifying a link between Syk
280                                              Dectin-1, Toll-like receptor 2, and Toll-like receptor 4
281 CAM-3-grabbing nonintegrin (DC-SIGN, CD209), Dectin-1, Toll-like receptors (TLRs), complement recepto
282 1 signaling as an unrecognized controller of dectin-1 transcription via GM-CSF and PU.1 that is requi
283                             We show that GFP-Dectin-1 translocates to the fungal phagosome, but its s
284  via a new, NF-kappaB-independent pathway in Dectin-1-triggered murine BMMs and influences TLR cross
285 rates that recognition of beta-1,3 glucan by Dectin-1 triggers TLR9 trafficking to beta-1,3 glucan-co
286   Following beta-1,3-glucan recognition, GFP-Dectin-1 undergoes tyrosine phosphorylation by Src kinas
287 1 was delivered to dendritic cells (DCs) via Dectin-1 using anti-human Dectin-1 (hDectin-1)-HA1 recom
288 g required Syk tyrosine kinase activity, but dectin-1 was dispensable for both of them.
289            A macrophage cell line expressing Dectin-1 was employed to show binding and activation of
290 risingly, however, following oral infection, dectin-1 was not required for the control of mucosal col
291           Laminarin, a beta-glucan ligand of Dectin-1, was incorporated into the original beta-mannan
292 hese receptors, ligands specific for TLR2 or dectin-1 were microinjected, alone or in combination, in
293  proinflammatory responses in the absence of Dectin-1 were not associated with changes in Ido (IDO),
294 onidia involves integrin CD11b/CD18 (and not dectin-1), which triggers a PI3K-dependent nonoxidative
295 r molecules like the C-type signaling lectin Dectin-1, which is found on macrophages, neutrophils, an
296 two pathogen recognition receptors, TLR2 and dectin-1, which recognize the same microbial stimulus (z
297 regulated expression of CCL20 and ligands of Dectin-1, which was associated with recruitment and acti
298 ngagement of ITAM-coupled beta2 integrins or Dectin-1 with TLR4 did not affect TLR4-induced direct ac
299 trigger innate receptors (e.g., TLRs, Rig-I, Dectin-1) within APCs, with the consequential induction
300                                 Studies with dectin-1(-/-)/WT reciprocal bone marrow chimeric mice re

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