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1 antly faster diffusion of CD14 compared with TLR2.
2  a RING E3-ubiquitin ligase, associates with TLR2.
3 om knockout mice for NE (ela(-/-)), TLR4, or TLR2.
4 entiation and function through engagement of TLR2.
5 y and repair gene signature via the receptor TLR2.
6 r, through the TLR4/MD2 receptor complex and TLR2.
7 corresponding to HLA-DQA1, HLA-DQA2, OLR1 or TLR2.
8 was demonstrated to be partially mediated by TLR2.
9                                          The TLR2/1 agonist PAM3CSK4 (PAM3) induces human and murine
10 bers and 5-HT levels, whereas treatment with TLR2/1 agonist upregulates 5-HT production in irradiated
11  line (BON-1 cells) release higher 5-HT upon TLR2/1 agonist via NF-kappaB pathway.
12 locks TLR2 dimerization that is critical for TLR2/1 and TLR2/6 heterodimer signaling to blunt inflamm
13 N may be due to differential localization of TLR2/1 signaling.
14 morphism rs5743618 (1805G/T) as a marker for TLR2/1 specificity.
15    We found that the TLR2/6 heterodimer, not TLR2/1, is responsible for CDT recognition, and that gen
16        In summary, Mtb LAM activates PMN via TLR2/1, resulting in the production of cytokines but doe
17 mmatory cytokine production and release in a TLR2/1-dependent manner, using the TLR1 single-nucleotid
18                Heterozygous genotypes of the TLR2 2029C/T and TLR3 1377C/T and -7C/A SNPs may serve a
19             The heterozygous genotype of the TLR2 2029C/T SNP was more common in patients with AAA th
20 volunteers were screened for the presence of TLR2 (2029C/T and 2258G/A), TLR3 (1377C/T, 1234C/T, and
21 cells, IL-12 and CCL2 responses as evoked by TLR2, 3, 4, 5, and 8, as well as IL-12 responses evoked
22 n, initiating local gut inflammation through TLR2/4 activation, resulting in the activation of proinf
23                       Following LPS-mediated TLR2/4 activation, TNF-alpha and IL-1beta self-regulated
24 overexpression attenuated inflammation after TLR2/4 activation.
25 induction of proinflammatory mediators after TLR2/4 activation.
26 omotes ubiquitination and degradation of the TLR2/4 adaptor protein TIRAP and TLR2 in macrophages and
27 stimulating astrocytes with potent exogenous TLR2/4 agonist, bacterial lipopolysaccharide (LPS).
28 ollected from 12- to 14-week-old TLR2, TLR4, TLR2/4 double knock-out (KO) mice using a MiSeq platform
29                      Autophagy induction was TLR2/4 independent because the receptor blockade did not
30                        In addition, TLR4 and TLR2/4 KO mice demonstrated a significant increase in th
31 n the present study, we examined the role of TLR2/4 signaling on various astrocyte functions (i.e., p
32 he number of alveolar lesions between WT and Tlr2/4(-/-) mice.
33 , Toll-like receptor (TLR)2, TLR4, and both (TLR2/4) to the maintenance of neutrophil homeostasis in
34  Low lnc-IL7R expression in COPD may augment TLR2/4-mediated inflammation and be associated with acut
35 onal antibodies against TNF-alpha suppressed TLR2/4-mediated upregulation of astrocyte proliferation,
36  is overcome by intranasal installation of a TLR2/6 agonist and a MAIT cell antigen.
37 s including NF-kappaB and MAPK downstream of TLR2/6 are upregulated in mice with intact TLR2/6 signal
38 dimerization that is critical for TLR2/1 and TLR2/6 heterodimer signaling to blunt inflammation in a
39                            We found that the TLR2/6 heterodimer, not TLR2/1, is responsible for CDT r
40            We demonstrate that the synthetic TLR2/6 ligand Fibroblast-stimulating lipopeptide (FSL-1)
41 f TLR2/6 are upregulated in mice with intact TLR2/6 signaling during CDI.
42 nses to all Toll-like receptor 1/2 (TLR1/2), TLR2/6, and TLR4 agonists were impaired in the fibroblas
43 ly blocked TLR4 stimulation, but not TLR1/2, TLR2/6, or TLR3 activation.
44 lear cells responded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and
45 s in knockout mice revealed a major role for TLR2, a lesser role for TLR4, a supplementary role for C
46                     Tlr2 (-/-) mice and anti-TLR2 Ab-treated mice infected with enteric parasite, Tri
47                    We previously showed that TLR2 activates both a cytoplasmic and an endosome-depend
48                     Recently, we showed that TLR2 activation contributes to limitation of rhinovirus
49 both JNK and p38 activation is linked to the TLR2 activation only.
50 with the structural features that facilitate TLR2 activation.
51  lipid oxidation had a synergistic effect on TLR2 activation.
52 tory responses through Toll-like receptor 2 (TLR2) activation, and this whether they are bound to nuc
53 and N-terminal modification generally lowers TLR2 activity.
54 ties in Pam(2)Cys-conjugated lipopeptides on TLR2 activity.
55   We examined whether deficiency of maternal TLR2 affects the normal development of oral tolerance an
56             Spinal cord GT1b functions as an TLR2 agonist and induces proinflammatory microglia activ
57 al cells showed attenuated IL-8 responses to TLR2 agonist despite expressing TLR2 similar to normal,
58         Colonic LMMP of germ-free mice given TLR2 agonist had increased neuronal numbers compared wit
59 rd microglia, but the responsible endogenous TLR2 agonist has not been identified.
60 d from the colonic LMMP, incubation with the TLR2 agonist increased the percentage of neurons origina
61 erm-free mice were given drinking water with TLR2 agonist or without (controls).
62                                              TLR2 agonist rapidly recruited myeloid cells to the CP,
63               We described a detailed SAR in TLR2 agonistic scaffolds and also covered the design and
64                     Thus, the development of TLR2 agonists is attractive in the search of potential i
65 lls challenged with the TLR4 agonist LPS and TLR2 agonists lipoteichoic acid and zymosan.
66 se from human monocytes is stimulated by the TLR2 agonists Pam3CSK4 or FSL-1, as well as the TLR4 ago
67 levels of ATP, whereas cells stimulated with TLR2 agonists released high levels of ATP.
68                                              TLR2 agonists required pannexin-1 and P2X7 receptor acti
69       The approaches involved in delivery of TLR2 agonists such as lipidation of antigen, conjugation
70  design and chemistry for the conjugation of TLR2 agonists to antigens, carbohydrates, polymers, and
71 cific comparison with the purified synthetic TLR2 agonists, Pam(3)CSK(4) and FSL-1.
72                        Toll-like receptor 2 (TLR2) agonists are lipopeptides possessing the S-[2,3-bi
73 n a mouse model, and the combination of anti-TLR2 and antivascular endothelial growth factor receptor
74 atory effects of LCBs were dependent on host TLR2 and CD14.
75 ophages to employ multiple receptors such as TLR2 and CD36 to recognize a single ligand, as in this c
76 or-associated macrophages (TAMs) through the TLR2 and MyD88 pathway, and recruits p62 to activate the
77 holine, inhibited downstream S100A9-elicited TLR2 and NF-kappaB activation.
78 Here we explore the interactions of CDT with TLR2 and the impact on host immunity during CDI.
79 al cells, demonstrating robust expression of TLR2 and TLR3.
80 in epidermal keratinocytes, soy PG inhibited TLR2 and TLR4 activation and inflammatory mediator expre
81 rane-derived lipoproteins and LPS to inhibit TLR2 and TLR4 activation, respectively.
82  inflammatory mediator expression induced by TLR2 and TLR4 activators as well as NFkappaB activation
83  that volatile anesthetics directly bound to TLR2 and TLR4 and attenuated their functions.
84                                      Loss of TLR2 and TLR4 increased the nuclear abundance of the cel
85 he combined, but not the individual, loss of TLR2 and TLR4 increased the replication of beta cells, b
86 t study we show that the toll-like receptors TLR2 and TLR4 inhibited the diet-induced replication of
87 ge in the oral microbial composition in both TLR2 and TLR4 KO mice demonstrate that these TLRs contri
88 tor alpha and interleukin-6 mediated through TLR2 and TLR4 signaling.
89 e-exposed Toll-like receptors (TLRs) such as TLR2 and TLR4 survey the extracellular environment for p
90          Furthermore, CCN1 binds directly to TLR2 and TLR4 to activate MyD88-dependent signaling, cyt
91 n-mediated regulation of Toll-like receptor (TLR2 and TLR4) signaling in dendritic cells, but not in
92 ctivated Toll-like receptors (TLRs), such as TLR2 and TLR4, dimerize and move laterally across the pl
93 ive enteric neural precursor cells expressed TLR2 and TLR4.
94  recombinant S100A9 functioning through both TLR2 and TLR4.
95 y contributes to OA progression, mediated by TLR2 and TLR4.
96 s (Toll-like receptors), we demonstrate that TLR2 and TLR6 are required for the activation of human a
97 e human embryonic kidney (HEK) cells through TLR2 and TLR6 but not TLR1.
98                  In this study, we show that TLR2 and TLR7 ligands potently lower the Ag threshold fo
99 ir lipid chains in the hydrophobic cavity of TLR2 and, in some cases, TLR1, at the vicinity of the di
100                              TLR2-deficient (Tlr2 (-/-)) and Myd88 (-/-) mice express lower EC cell n
101 ate PD-L1 expression on normal IMC; IMC from Tlr2(-/-) and Tlr7(-/-) mice demonstrated similar result
102  levels of key immune mediators in milk from TLR2(-/-) and WT mothers were also examined.
103 lular matrix was similarly reduced in GF WT, Tlr2(-/-) , and heterozygous Vwf(+/-) mice that are all
104 recognition receptors, toll-like receptor-2 (TLR2) and -4 (TLR4).
105 er host chitin-binding Toll-like receptor 2 (TLR2) and CD14 are required for the anti-inflammatory ef
106 to dissect the role of Toll-like receptor 2 (TLR2) and programmed death-ligand 1 (PD-L1) in regulatin
107 engage human and mouse Toll-like receptor 2 (TLR2) and to inhibit mouse osteoblast differentiation an
108    The level of toll-like receptor 4 (TLR4), TLR2, and erythropoietin-producing hepatoma A2 (EphA2) e
109 matory responses were partially inhibited in TLR2- and TLR4-deficient mice compared to those of wild-
110                                              TLR2 antagonism effectively suppressed initiation and gr
111 excretory-secretory products is abrogated by TLR2 antagonist.
112  and the transmembrane toll-like receptor 2 (TLR2) are important receptors in the plasma membrane of
113 und to be dependent on Toll-like receptor 2 (TLR2), as evident by reduced expression of IRE1alpha and
114 PF triggered activation of NF-kappaB through TLR2, as determined using a variety of TLR-transfected h
115 antibodies against Toll-like receptor (TLR)1/TLR2, as well as small interfering RNA targeting TLR1/TL
116                       Thus, the St3gal2-GT1b-TLR2 axis may offer a novel therapeutic target for the t
117                                    Moreover, TLR2 block prior to DENV infection of peripheral blood m
118  effect was abolished by treatment with anti-TLR2 blocking antibody.
119 d C57BL/6 mice, which are reconstituted with Tlr2 (-/-) bone marrow cells, and in germ-free mice.
120                                 Furthermore, TLR2 but not TLR4 was critical for sensing of cell wall
121                                              TLR2-, but not TLR7-mediated costimulation, can enhance
122 xia in mice with or without functional TRL2 (TLR2(+/+), C57BL/6-Tyrc-Brd-Tg(Tlr2-luc/gfp)Kri/Gaj;TLR2
123 +), C57BL/6-Tyrc-Brd-Tg(Tlr2-luc/gfp)Kri/Gaj;TLR2(-/-),C57BL/6-Tlr2tm1Kir).
124                         Expression of CD206, TLR2, CD16/CD32, MHC class II, and CD86 was higher in CD
125  control of lesion size and parasite load in Tlr2(-/-) compared with wild-type infected mice.
126         Together, the results establish that TLR2 controls neutrophil-driven immunopathology during i
127                                 Importantly, TLR2 costimulation increases the percentage of polyfunct
128 is was prevented by cross-fostering onto WT (TLR2(+/+)) dams.
129 R2(+/-) pups that were born to and nursed by TLR2(-/-) dams exhibited impaired oral tolerance.
130 zygous TLR2(+/-) pups from wild-type (WT) or TLR2(-/-) dams were fed either by their biologic dam or
131                                              TLR2 deficiency also affected milk content of insulin-li
132                                              TLR2-deficient (Tlr2 (-/-)) and Myd88 (-/-) mice express
133                               Neither sex of TLR2-deficient mice showed anti-inflammatory effects whe
134 ogression was observed in wild-type, but not TLR2-deficient, NOD mice.
135  OmpU-treated macrophages, p38 activation is TLR2 dependent, but JNK activation happens through a sep
136 to stimulate host cell Toll-like receptor 2 (TLR2)-dependent signaling and interleukin-1beta (IL-1bet
137 eus Cell wall components of S. aureus elicit TLR2-dependent cellular responses, but the exact signali
138                        Importantly, monocyte TLR2-dependent endosomal signaling enabled immune escape
139 eus infection of human monocytes activates a TLR2-dependent endosomal signaling pathway, leading to I
140                                         This TLR2-dependent IFN-I signaling originates from the cell
141 culosis (Mtb LAM) would prime human PMN in a TLR2-dependent manner and investigated this with specifi
142 ferentiation, respectively, most likely in a TLR2-dependent manner.
143 feration in an antigen receptor-independent, TLR2-dependent manner.
144                       These results reveal a TLR2-dependent mechanism in human monocytes whereby S. a
145 sponsive cathelicidin expression through the TLR2-dependent p38-MAPK-CYP27B1-VDR signaling pathway.
146                                              TLR2-dependent signaling did not play a major role in ea
147 normal, COPD cells failed to show RV-induced TLR2-dependent SIRT-1 expression.
148 phosphorylation and this was associated with TLR2-dependent SIRT-1 expression.
149  glycine lipid classes were shown to promote TLR2-dependent tumor necrosis factor alpha (TNF-alpha) r
150 ed a TLR2 trans-membrane peptide that blocks TLR2 dimerization that is critical for TLR2/1 and TLR2/6
151 estigated responses to Toll-like receptor 2 (TLR2)-driven extracellular signal-related kinase (ERK) s
152  structure of Diprovocim in a complex with a TLR2 ectodomain, which revealed, unexpectedly, two Dipro
153 the ligand binding pocket formed between two TLR2 ectodomains.
154 ct signaling pathways activated by S. aureus-TLR2 engagement and the consequences of their activation
155 meras and immunohistology, we identified the TLR2-expressing cells involved in this early neutrophil
156    The decreased cytokine responses in R753Q TLR2-expressing macrophages were accompanied by impaired
157 n together, our data show a crucial role for TLR2-expressing nonhematopoietic skin cells in the recru
158 , which is associated with downregulation of TLR2 expression but not TLR1 or TLR4.
159                                              TLR2 expression on CD14 + + classical monocytes isolated
160 roduction, which mechanistically depended on Tlr2 Finally, we found that TRIM58 mRNA and protein expr
161               Mice given an antibody against TLR2 had prolonged whole gut transit times; their coloni
162                      Among the various TLRs, TLR2 has a special place due to its ability to sense the
163 stimulation of the Toll-like receptor (TLR)1-TLR2 heterodimer (referred to herein as TLR1/2), TLR7 or
164  in human APCs by signaling through the TLR1/TLR2 heterodimer.
165 ine adjuvants, interacting with cell surface TLR2 heterodimers.
166 rmation of TLR2/TLR1 heterodimers as well as TLR2 homodimers in vitro.
167  immune system through Toll-like receptor 2 (TLR2); however, the pathogen-associated molecular patter
168 In this study, we identify a pivotal role of TLR2 in 5-HT production in the gut.
169 ce higher 5-HT production in BON-1 cells via TLR2 in a dose-dependent manner, whereby the effect of e
170   Altogether, these data identify a role for TLR2 in DENV infection and provide insights into the com
171  cascades triggered by stroke and a role for TLR2 in injury, we also used direct TLR2 stimulation as
172 tion of the TLR2/4 adaptor protein TIRAP and TLR2 in macrophages and microglial cells.
173 ndosomal TLR7, -9, and -13, and cell surface TLR2 in MHV68 detection.
174 ndings not only suggest an important role of TLR2 in mucosal 5-HT production in the gut by resident m
175    Our results underline a critical role for TLR2 in regulating milk components that are essential fo
176 ary immunopathology of chimeric mice lacking TLR2 in the hematopoietic compartment (TLR2KO-->WT) was
177 ation on the potential benefits of targeting TLR2 in various gut disorders that exhibit aberrant 5-HT
178 egarding its lipid binding and activation of TLR2 indicate that it could participate in the initiatio
179       Existing SAR studies of Pam(2)Cys with TLR2 indicate that the structural requirements for activ
180  pigment epithelium cells, ligand binding to TLR2 induced robust expression of proinflammatory cytoki
181             Here we reveal that DA inhibited TLR2-induced NF-kappaB activation and inflammation via t
182 promoted proteasome-dependent degradation of TLR2, inhibiting its signaling activity.
183                     In summary, we show that TLR2 is required for limiting RV-induced IFNs, and this
184 ssarily colocalization, between Dectin-1 and TLR2 is required for their synergistic regulation of mac
185                        Toll-like receptor 2 (TLR2) is an innate immune receptor implicated in regulat
186                                 We show that TLR2 knockout (TLR2KO) mice infected with M. tuberculosi
187 ssion of IRE1alpha and Xbp1 mRNA splicing in TLR2 knockout mouse retina.
188 PHHs are able to sense HBV particles through TLR2, leading to an activation of anti-HBV immune respon
189  cytokine expression in response to TLR4 and TLR2 ligand challenge.
190                           Stimulation with a TLR2 ligand modulated TRIM58 synthesis in myeloid cells.
191 pression and release in response to TLR4 and TLR2 ligand stimulation but not for TLR-independent stim
192 lar to that induced by toll-like receptor 2 (TLR2) ligand Pam3Cys, but different from those induced b
193 sis (Mtb), were covalently conjugated to the TLR2-ligand Pam(2)Cys to generate a self-adjuvanting lip
194                 Here, we report that diverse TLR2 ligands induce an IFN-I response in human monocyte-
195 In this study, we show that in normal cells, TLR2 limits RV-induced IFN responses by attenuating STAT
196 -27p28 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selective
197 ctional TRL2 (TLR2(+/+), C57BL/6-Tyrc-Brd-Tg(Tlr2-luc/gfp)Kri/Gaj;TLR2(-/-),C57BL/6-Tlr2tm1Kir).
198               Infection in siTLR2-treated or tlr2(-/-) macrophages reduced the survival of LprE (Mtb)
199 STAT1/STAT2 phosphorylation, indicating that TLR2 may limit RV-induced IFN responses via SIRT-1.
200                                    Enhancing TLR2-mediated inflammation increased fibrosis in vivo Fu
201 the IRE1alpha/XBP1 pathway as a regulator of TLR2-mediated protective innate immune responses in S au
202 t with an HBV entry inhibitor attenuated the TLR2-mediated response to HBV, suggesting a receptor bin
203                                              Tlr2 (-/-) mice and anti-TLR2 Ab-treated mice infected w
204  findings suggest that resistance to KIM5 in TLR2(-/-) mice is dependent on early immune cell traffic
205 sely, restoring early neutrophil presence in Tlr2(-/-) mice through injection of wild-type neutrophil
206 tion of bone marrow-derived macrophages from TLR2(-/-) mice.
207 ver was greater and earlier in KIM5-infected TLR2(-/-) mice.
208 ming these species in CO92 Deltapgm-infected TLR2(-/-) mice.
209 microbiota and determines thrombus growth in Tlr2(-/-) mice.
210 nstrate that Toll-like receptor 2-deficient (TLR2(-/-)) mice are resistant to septicemic infection by
211 -8 in respiratory epithelial cells through a TLR2-, NF-kB- and MAPK-dependent signalling pathway.
212 mpare the diffusion coefficients of CD14 and TLR2 on the apical and basal membranes of macrophages us
213 toll-like receptors (TLR) combining TLR1 and TLR2 onto a single sensor surface.
214  mice were given a blocking antibody against TLR2 or a TLR4 inhibitor.
215                               The absence of TLR2 or TLR13 did not affect lytic viral titers.
216 culture (ALI) model was used to test whether TLR2 or TLR3 stimulation alters epithelial barrier funct
217                           Antibodies against TLR2 or TLR4 did not block the increases in IL1B or TNF
218 ation into healthy mouse JE does not require TLR2 or TLR4.
219 t we detected in PDE, inhibited PDE-induced, TLR2- or TLR4-mediated profibrotic responses.
220                   Our findings implicate the TLR2 pathway as a potential regulator of esophageal epit
221 e a significantly improved anti-inflammatory TLR2 peptide and critical insights in its mechanism of a
222                    We show that although the TLR2 peptide treatment ameliorated colitis, it allowed r
223                        Toll-like receptor 2 (TLR2) plays a key role in innate immune response recogni
224 and p65 NF-kappaB, suggesting that the R753Q TLR2 polymorphism alters the functions of the myeloid di
225                                    The R753Q TLR2 polymorphism has been associated with increased inc
226                                     Blocking TLR2 prior to DENV infection in vitro abrogates NF-kappa
227                             rs111200466 is a TLR2 promoter insertion/deletion polymorphism with contr
228                    In the adult mouse colon, TLR2 promotes colonic neurogenesis, regulated by intesti
229 y and associated with enhanced expression of TLR2 protein and proinflammatory cyto/chemokine producti
230 s, which showed constitutive upregulation of TLR2 protein, overreacted to a proinflammatory milieu (T
231                                 Heterozygous TLR2(+/-) pups from wild-type (WT) or TLR2(-/-) dams wer
232                                 Heterozygous TLR2(+/-) pups that were born to and nursed by TLR2(-/-)
233 a and TNF-alpha protein production following TLR2 receptor stimulation (p < 0.001).
234 tdTomato mice and incubated with agonists of TLR2 (receptor for gram-positive bacteria), TLR4 (recept
235    Previous work from our lab has shown that TLR2 recognizes CDT to induce inflammation.
236 well as small interfering RNA targeting TLR1/TLR2, reduced the expression of RALDH2 in PN-stimulated
237 othelium, suggesting a potential role of the TLR2-responses in vascular integrity.
238 e-nucleotide polymorphisms (SNPs) rs5743708 (TLR2), rs4986791 (TLR4), rs361525 (TNFA), rs2430561 (IFN
239  and B. licheniformis PGA both elicited more TLR2 signal than B. anthracis PGA, but only responses to
240 an macrophages responded to S. aureus EVs by TLR2 signaling and activation of NLRP3 inflammasomes thr
241 ins exhibited an increased ability to induce TLR2 signaling and IL-1beta production.
242 ion in an arthritic mouse model dependent on TLR2 signaling and in a CSS mouse model dependent on TLR
243 echanisms by which this polymorphism affects TLR2 signaling are unclear.
244 , we identified the functional importance of TLR2 signaling in this process.
245      Our findings reveal that the outcome of TLR2 signaling includes an IFN-I response in human monoc
246 milar to normal, indicating dysregulation in TLR2 signaling pathway.
247 obiotic approaches directed towards specific TLR2 signaling processes might be developed for treatmen
248                    Therapeutic modulation of TLR2 signaling represents an underutilized opportunity t
249 EV-associated lipoproteins not only mediated TLR2 signaling to initiate the priming step of NLRP3 act
250                                              TLR2 signaling was induced with Pam(3)Cys-Ser-Lys(4), an
251 activation of human macrophages, but not for TLR2 signaling.
252 e immune control and mucosal homeostasis via TLR2 signaling.
253 usly demonstrated that toll-like receptor 2 (TLR2) signaling is critical for nerve injury-induced act
254 ce arises from Toll-like receptor (TLR) 4 or TLR2 signalling and, in the case of protease allergens,
255 responses to TLR2 agonist despite expressing TLR2 similar to normal, indicating dysregulation in TLR2
256  glycine lipids and that these lipids engage TLR2 similarly to the previously reported serine-glycine
257 uced gene expression could be neutralized by TLR2-specific antibodies.
258                                              TLR2-stimulated monocytes produced modest IFNbeta levels
259 ompared with CD44(-/-) macrophages following TLR2 stimulation (p < 0.01).
260 role for TLR2 in injury, we also used direct TLR2 stimulation as an independent injury model.
261 , the impact of ERK signaling in response to TLR2 stimulation differs between macrophages and DCs, po
262                                              TLR2 stimulation increased TEER (1.28- to 1.31-fold) and
263 onula occludens-1 were upregulated following TLR2 stimulation, and ChIP assay demonstrated altered hi
264  of myeloid cells diverged between tMCAO and TLR2 stimulation, in both models, disruption of CX3CR1-C
265 3CR1 and CCR2 receptors, or following direct TLR2 stimulation.
266 ation and associated tissue damage following TLR2-stimulation, while ERK-mediated induction of IL-12/
267 reased fibrosis in vivo Furthermore, soluble TLR2 (sTLR2), a negative modulator of TLRs that we detec
268 ed that neuroinflammation and the microglial TLR2-system may act as a core process at the intersectio
269 ally, the modulatory role for the functional TLR2-system was suggested in aetiology of depressive, an
270              This resistance is dependent on TLR2, the route of infection, and the isoform of YopJ.
271  potent, synthetic small molecule agonist of TLR2/TLR1 and has shown significant adjuvant activity in
272 first light into the activation mechanism of TLR2/TLR1 by a noncanonical agonist.
273 und that Diprovocim induced the formation of TLR2/TLR1 heterodimers as well as TLR2 homodimers in vit
274 e investigated how Diprovocim interacts with TLR2/TLR1 through in vitro biophysical, structural, and
275 rity to the canonical lipopeptide ligands of TLR2/TLR1, we investigated how Diprovocim interacts with
276 obtained here may be exploited to manipulate TLR2/TLR1-dependent signaling.
277                In addition to TLR9 agonists, TLR2, TLR3, or TLR4 agonists, as well as TNF-alpha, IL-6
278 tokine production triggered by various TLRs (TLR2, TLR3, TLR4, and TLR7), C-type lectin receptors (De
279  development, we determined the frequency of TLR2, TLR3, TLR4, and TLR9 single-nucleotide polymorphis
280 falpha(-/-), Il1alpha(-/-)/Il1beta(-/-), and Tlr2(-/-)/Tlr4(-/-) mice as well as Sprague Dawley rats
281                            In the absence of TLR2, TLR4, myeloid differentiation response gene 88, or
282              Similarly, antibody blockade of TLR2, TLR4, or C5aR differentially inhibited bacteria-in
283             Additionally, antibodies against TLR2, TLR4, or the coreceptor CD14 reduced the profibrot
284 oral swabs collected from 12- to 14-week-old TLR2, TLR4, TLR2/4 double knock-out (KO) mice using a Mi
285                                              TLR2-, TLR4-, MyD88-deficient and WT BALB/c mice were in
286                                     However, TLR2/TLR4 double deficiency substantially diminished the
287  and suggest that selective targeting of the TLR2/TLR4 pathways may reverse beta cell failure in pati
288 lergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway.
289 d IL-1R (-/-) or TLR4 (-/-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were
290            oxPCCD36 induce formation of CD36/TLR2/TLR6 complex in platelets and activate downstream s
291  different TLR agonists, including those for TLR2, TLR7, and TLR9.
292 ed the contribution of Toll-like receptor 2 (TLR2) to host resistance against Mycobacterium tuberculo
293                    Here, we demonstrate that TLR2, together with its co-receptors CD14 and TLR6, is a
294 mmunoproteasome proteolysis, by treatment of TLR2 (Toll-like receptor 2)-engaged and TLR7 (Toll-like
295                     In this study, we used a TLR2 trans-membrane peptide that blocks TLR2 dimerizatio
296                                 Furthermore, TLR2 triggering by L. major phosphoglycans is critical f
297                                 We show that TLR2 triggering by Leishmania major is required for thei
298                                              TLR2 was robustly expressed by the retinal pigment epith
299  immune responses triggered predominantly by TLR2 when their centroid-to-centroid proximity is <500 n
300   Various scaffolds are reported to activate TLR2, which include naturally occurring lipoproteins, sy

 
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