ライフサイエンスコーパス: TLR2

1 ng kinase 1 (TBK1), or Toll-like receptor 2 (TLR2).

2 on upon encountering corynebacteria required TLR2.

3 substantially in their capacity to activate TLR2.

4 hrough the ubiquitination and degradation of TLR2.

5 3Cys, specific for heterodimer molecule TLR1/TLR2.

6 by human IAPP aggregation failed to activate TLR2.

7 n signaling pathway modulation downstream of TLR2.

8 eceptor for several TLRs, including TLR4 and TLR2.

9 Il-6 production was partially independent of Tlr2.

10 y and repair gene signature via the receptor TLR2.

11 ction, which is diminished in the absence of TLR2.

12 turation of DCs and was dependent in part on TLR2.

13 Remarkably, P0106-125-immunized TLR2(0/0) mice exhibited a delayed recovery as compared

14 o wild-type mice, whereas Tregs in immunized TLR2(0/0) mice were only slightly increased.

15 Immunized TLR2(0/0) mice were unable to induce OX40 and OX40L by m

16 set of donors were primed in response to the TLR2/1 agonist, Pam3CSK4, although PMN from all donors w

17 described, we hypothesized that ligation of TLR2/1 or TLR2/6 would prime PMN.

18 neuronal precursor cells and TLR2/6, but not TLR2/1, ligands.

19 eric BCAP associates with the TIR domains of TLR2/4 and MAL/TIRAP, suggesting that it is recruited to

20 e in bronchoalveolar lavage fluid, decreased TLR2/4 expression and NF-kappaB activation in the lung.

21 hich regulates inflammation through CD44 and TLR2/4 receptors.

22 oteins for their ability to activate/inhibit TLR2/4 signaling in HEK293 cell lines.

23 he number of alveolar lesions between WT and Tlr2/4(-/-) mice.

24 tumor-associated neutrophils were reduced in Tlr2/4(-/-) mice.

25 liferation and growth in WT mice, but not in Tlr2/4(-/-) mice.

26 ificantly increased in WT mice compared with Tlr2/4(-/-) mice.

27 e and mice doubly deficient in Tlr-2 and -4 (Tlr2/4(-/-)), both with an oncogenic Kras allele in lung

28 f these receptors in peritoneal macrophages (TLR2/4, C5aR) and mesothelial cells (TLR2, C5aR).

29 ere, we have shown that pericytes activate a TLR2/4- and MyD88-dependent proinflammatory program in r

30 F-, Toll-like receptor 2 (TLR2)-, TLR4-, and TLR2/4-deficient mice indicated that Acanthamoeba-induce

31 Results suggest that TLR2/4-dependent inflammatory activation and lipid oxida

32 roblasts, which responded very poorly to all TLR2/6 (PAM2CSK4, LTA, FSL-1), TLR1/2 (PAM3CSK4), and TL

33 However, the whole-blood response to the TLR2/6 agonist staphylococcal lipoteichoic acid (LTA) wa

34 hough PMN from all donors were primed by the TLR2/6 agonist, FSL-1.

35 activation, consistent with stimulation of a TLR2/6 heterodimer.

36 We demonstrate that the synthetic TLR2/6 ligand Fibroblast-stimulating lipopeptide (FSL-1)

37 ptide (WoLP) of the major nematode Wolbachia TLR2/6 ligand, peptidoglycan associated lipoprotein, ind

38 , we hypothesized that ligation of TLR2/1 or TLR2/6 would prime PMN.

39 nses to all Toll-like receptor 1/2 (TLR1/2), TLR2/6, and TLR4 agonists were impaired in the fibroblas

40 itro with fetal neuronal precursor cells and TLR2/6, but not TLR2/1, ligands.

41 ly blocked TLR4 stimulation, but not TLR1/2, TLR2/6, or TLR3 activation.

42 lear cells responded normally to all TLR1/2, TLR2/6, TLR4, TLR7, and TLR8 (R848) agonists tested, and

43 ation of Wolbachia lipoprotein by neutrophil TLR2/6.

44 s in knockout mice revealed a major role for TLR2, a lesser role for TLR4, a supplementary role for C

45 ogenic clearance and currently attributed to TLR2 activation in immune cells.

46 TLR2 activation increased p38, ERK1/2, and p65 activity

47 However, only TLR2 activation or IL-1beta treatment increased NGF prot

48 Further, IRAK-1 degradation caused by TLR2 activation was shown to inhibit ssRNA-induced IFN e

49 uding responses triggered by TLR4, TLR3, and TLR2 activation, and it is enhanced by IFN-gamma.

50 of TLR6 but not TLR1 prevented hIAPP-induced TLR2 activation, consistent with stimulation of a TLR2/6

51 lipid oxidation had a synergistic effect on TLR2 activation.

52 tiation of the HDM-allergic response through TLR2 activation.

53 JNK activity was not affected by TLR2 activation.

54 bone marrow-derived DCs compared with single TLR2 activation.

55 the anorexia and body weight loss induced by TLR2 activation.

56 Here, we show that toll-like receptor 2 (TLR2) activation by intracerebroventricular injection of

57 tory responses through Toll-like receptor 2 (TLR2) activation, and this whether they are bound to nuc

58 erstanding the challenge posed by the use of TLR2 agonist in immunotherapy.

59 he stimulation of IL-36gamma expression by a TLR2 agonist.

60 lls challenged with the TLR4 agonist LPS and TLR2 agonists lipoteichoic acid and zymosan.

61 se from human monocytes is stimulated by the TLR2 agonists Pam3CSK4 or FSL-1, as well as the TLR4 ago

62 levels of ATP, whereas cells stimulated with TLR2 agonists released high levels of ATP.

63 TLR2 agonists required pannexin-1 and P2X7 receptor acti

64 re required for mobilizing lipoproteins, the TLR2 agonists, from the staphylococcal cytoplasmic membr

65 TLR2 agonists, TLR4 agonists, or IL-1beta (control) trea

66 n a mouse model, and the combination of anti-TLR2 and antivascular endothelial growth factor receptor

67 opathology, and identifies key players, i.e. TLR2 and CTLA4, involved in this mechanism.

68 Moreover, inhibition of TLR2 and depletion of islet macrophages prevented up-reg

69 ic inflammatory markers (F4/80, MCP-1, TLR4, TLR2 and IL-1beta) and effector caspase (caspase 3 and 7

70 S. aureus abundance in a manner regulated by TLR2 and IL-1R signaling.

71 from M. tuberculosis-infected cells activate TLR2 and induce cytokine responses by uninfected macroph

72 CAP-PEs directly bind to TLR2 and induces platelet integrin alphaIIbbeta3 activat

73 fore, in this study, we examined the role of TLR2 and IRAK-1 in RV-induced IFN-beta, IFN-lambda1, and

74 TLR2 and its downstream adaptor protein MyD88 were requi

75 IL-1beta secretion in glial cells depends on TLR2 and MyD88 adapter-like/TIRAP.

76 TLR2 and NF-kappaB signaling are known to increase cytok

77 of SIR genes (Troy, Sox17, Opg, Faim2, Lpo, Tlr2 and Ptges) and a gene known to be involved in invas

78 IAPP-induced activation of TLR2 and secretion of IL-1 may be important therapeutic

79 eleton organization induced by TLR4, but not TLR2 and this correlates with increased IL4 production a

80 rane-derived lipoproteins and LPS to inhibit TLR2 and TLR4 activation, respectively.

81 Leptospira surface adhesin, Lsa21 had strong TLR2 and TLR4 activity leading to production of proinfla

82 demonstrate that CLIP170 interacts with the TLR2 and TLR4 adaptor protein TIRAP.

83 hese results indicate that Lsa21 is a potent TLR2 and TLR4 agonist that induces strong innate respons

84 F-kappaB activation in HEK-293 cells bearing TLR2 and TLR4 in MyD88 dependent manner.

85 findings reveal the influence of peritoneal TLR2 and TLR4 on PD-associated fibrosis and describe a t

86 OA synovial fluids (SF) stimulated TLR2 and TLR4 receptors and induced NF-kappaB translocat

87 ivate IL-1beta release from immune cells via TLR2 and TLR4 receptors, respectively.

88 TLR2 and TLR4 signal via the Toll/interleukin-1 receptor

89 ndings suggest that in human monocytes, both TLR2 and TLR4 signaling induce pro-IL-1beta expression,

90 ector protein TcpB that negatively regulates TLR2 and TLR4 signaling.

91 dditionally, neutralizing antibodies against TLR2 and TLR4 significantly inhibited cytokine secretion

92 IL12p70 and CXCL10 production in mDCs after TLR2 and TLR4 stimulation.

93 ctivated Toll-like receptors (TLRs), such as TLR2 and TLR4, dimerize and move laterally across the pl

94 ng confirmed that Lsa21 interacted with 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 we show that murine CD8(+) T cells can sense TLR2 and TLR7 ligands, resulting in rapid production of

98 gnificantly increased levels of TLR4 but not TLR2 and TLR9 in ONFH.

99 Neuroproliferation required TLR2 and was recapitulated in vitro with fetal neuronal

100 ir lipid chains in the hydrophobic cavity of TLR2 and, in some cases, TLR1, at the vicinity of the di

101 tion and hyperresponsiveness were reduced in TLR2(-/-) and anti-TLR2-treated mice.

102 cytokine levels were significantly lower in TLR2(-/-) and TLR4(-/-) than in wild type mouse macropha

103 GF Tlr2(-/-) and wild-type (WT) mice were indistinguishable

104 lular matrix was similarly reduced in GF WT, Tlr2(-/-) , and heterozygous Vwf(+/-) mice that are all

105 orted that ligation of Toll-like receptor 2 (TLR2) and Dectin 1 on antigen-presenting cells by zymosa

106 to dissect the role of Toll-like receptor 2 (TLR2) and programmed death-ligand 1 (PD-L1) in regulatin

107 ory markers TNF-alpha, toll-like receptor 2 (TLR2), and TLR4.

108 rotein TcpB suppresses Toll-like receptor 2 (TLR2)- and TLR4-mediated innate immune responses by targ

109 ared with cells from WT mice, but both R753Q TLR2- and WT-derived macrophages exhibited comparable ba

110 ve functional B or T cells, and in MyD88-/-, TLR2-/- and TLR4-/- mice that are defective in toll like

111 TLR2 antagonism effectively suppressed initiation and gr

112 tion of lipoglycans by Toll-like receptor 2 (TLR2) appears to be important for macrophage activation

113 the retinal pigment epithelium, and validate TLR2 as a novel therapeutic target for reducing choroida

114 PF triggered activation of NF-kappaB through TLR2, as determined using a variety of TLR-transfected h

115 naling competence, leading to impaired MyD88-TLR2 assembly, reduced phosphorylation of IRAK-1, dimini

116 ation to either M1 or M2 macrophages through TLR2, associated with impaired STATs signaling pathway.

117 ecular docking experiments suggest potential TLR2 binding modes reminiscent of bacterial lipopeptide

118 nic activities through Toll-like receptor 2 (TLR2) binding, the immunoregulatory consequences of VCAN

119 Transfer of TLR2(-/-) bone marrow into wild-type, OVA-treated C57BL/

120 pression is abolished in Toll-like receptor (TLR2)(-/-) bone marrow-derived macrophages.

121 r E3 ligase, PPP1R11, directly ubiquitinates TLR2 both in vitro and in vivo, which leads to TLR2 degr

122 Furthermore, TLR2 but not TLR4 was critical for sensing of cell wall

123 phages (TLR2/4, C5aR) and mesothelial cells (TLR2, C5aR).

124 Taken together, DNA methylation of TLR2 can modulate host innate defense mechanisms that ma

125 contrast, PPE18-mediated homodimerization of TLR2 caused poorer cytoplasmic export of nuclear IRAK3 a

126 ly, we demonstrated that RV interaction with TLR2 causes ILR-associated kinase-1 (IRAK-1) depletion i

127 Calpain exteriorization and TLR2 cleavage were critical for the control of IL-17A ex

128 thrombosis in TLR2-dependent manner and that TLR2 contributes to accelerate thrombosis in mice in the

129 R2 displayed reduced recruitment of MyD88 to TLR2, decreased NF-kappaB activation, and impaired IL-8

130 hat germ-free (GF) and Toll-like receptor-2 (Tlr2)-deficient mice have reduced thrombus growth after

131 Finally, we show that restoration of TLR2-deficient eosinophils is sufficient for protection

132 DCs from TLR2-deficient mice were additionally used to consolidat

133 icient S. aureus is similar in wild-type and TLR2-deficient mice, but TLR2 is required for protection

134 mense bone loss in wild type mice but not in Tlr2-deficient mice.

135 R2 both in vitro and in vivo, which leads to TLR2 degradation and disruption of the signaling cascade

136 lectin expression in a Toll-like receptor 2 (TLR2)-dependent manner.

137 ost inflammation via a Toll-like receptor 2 (TLR2)-dependent pathway, resulting in the suppression of

138 ly efficient manner that is mediated by both TLR2-dependent and -independent innate immune mechanisms

139 ola stimulates the innate immune system in a TLR2-dependent fashion and that PF are a key bacterial c

140 Thus, acquired anti-LTA Abs rescue TLR2-dependent immunity to staphylococcal LTA in individ

141 trated that CAP-PEs accelerate thrombosis in TLR2-dependent manner and that TLR2 contributes to accel

142 lls were shown to rapidly express IL-10 in a TLR2-dependent manner in response to S. aureus, and adop

143 th soluble but not fibrillar IAPP provided a TLR2-dependent priming stimulus for ATP-induced IL-1beta

144 n T cell response to superantigens through a TLR2-dependent, IL-10-mediated mechanism.

145 ggregation provided a Toll-like-receptor-2- (TLR2-) dependent stimulus for NF-kappaB activation in HE

146 Thus, a crucial role of TLR2 depends on agonist release by bacterial surfactants

147 lls stably transfected with YFP-tagged R753Q TLR2 displayed reduced recruitment of MyD88 to TLR2, dec

148 extent p38, but not ERK1/2 activity, blocked TLR2-driven NGF up-regulation at both the transcript and

149 n by the corynebacterial cell wall relies on TLR2-driven robust Mincle expression and the cooperative

150 as transfection agent is likely to activate TLR2 during transfection.

151 In airway epithelial cells, blocking TLR2 enhanced RV-induced expression of IFNs and CXCL-10.

152 crophages from knock-in mice harboring R753Q TLR2 expressed lower levels of TNF-alpha, IL-1beta, IL-6

153 The decreased cytokine responses in R753Q TLR2-expressing macrophages were accompanied by impaired

154 attribute this function to a cleavage of the TLR2 extracellular domain, which prevented TLR2-induced

155 determine the requirement and sufficiency of TLR2 for rhinovirus-induced airway responses.

156 Toll-like receptor 2 (TLR2) has been implicated in the orchestration of inflam

157 ine adjuvants, interacting with cell surface TLR2 heterodimers.

158 ifferentially the emergence of the different TLR2(hi) monocyte populations in the spleen.

159 Here, we have shown that Ly6C(hi)TLR2(hi) monocytes were involved in TNF-alpha and IL-12

160 -alpha and IL-12 production, whereas Ly6C(lo)TLR2(hi) monocytes were mainly committed to IL-10 and TN

161 immune system through Toll-like receptor 2 (TLR2); however, the pathogen-associated molecular patter

162 oducing bacteria also had more expression of TLR2, IL-6 and TNF in the brain than the other two group

163 XCL-10 expression was primarily dependent on TLR2/IL-1R.

164 In addition to the known role of TLR2 in detecting and restricting NMII infection, we fou

165 lls, CDK5R1 and REST in neurons and CD86 and TLR2 in monocytes.

166 These results unmask an important role of TLR2 in the development of sickness behaviors via stimul

167 ary immunopathology of chimeric mice lacking TLR2 in the hematopoietic compartment (TLR2KO-->WT) was

168 In contrast, chimeric mice deficient in TLR2 in the nonhematopoietic compartment (WT-->TLR2KO) e

169 Our data illustrate a functional role for TLR2 in the pathogenesis of choroidal neovascularization

170 vity and inflammatory cascades downstream of TLR2 in tuberculosis.

171 e inflammatory role of Toll-like receptor 2 (TLR2) in age-related macular degeneration.

172 pression of proinflammatory genes (eg, CCL8, TLR2) in the calvarial periosteum significantly increase

173 pigment epithelium cells, ligand binding to TLR2 induced robust expression of proinflammatory cytoki

174 HA dose-dependently inhibited TLR2-induced TNF-alpha production by murine bone marrow-

175 e TLR2 extracellular domain, which prevented TLR2-induced transcription of molecules essential for IL

176 ction studies revealed a critical period for TLR2 involvement in adoptive transfer EAE.

177 We have reported that TLR2 is crucial for host resistance against chronic Myco

178 TLR2 is required for early inflammatory responses induce

179 ar in wild-type and TLR2-deficient mice, but TLR2 is required for protection of mice against PSM-prod

180 Toll-like receptor 2 (TLR2) is a pattern recognition receptor that recognizes

181 We conclude, BLP acting through TLR2, is a potent inducer of inflammation with a respons

182 h our previous report, at 8 wk of infection, TLR2 knockout (TLR2KO)-->TLR2KO bone marrow chimeric mic

183 ESAT-6 but not Pam3CSK4 induced IL-6 by TLR2 knockout BMDM.

184 pretreated retina or the use of retinas from TLR2 knockout mice showed the down-regulation of inflamm

185 e effect of allergens and lipids to regulate TLR2-L-induced NF-kB/AP-1 activation in THP1 cells were

186 e of mustard lipids and PG vesicles inhibits TLR2-L-induced NF-kB/AP-1 activation in THP1 cells.

187 s a negative correlation between PPP1R11 and TLR2 levels in white blood cell samples isolated from pa

188 eninigitidis, PorB, is a naturally occurring TLR2 ligand and functions as an adjuvant.

189 e demonstrated that PSMs in combination with TLR2 ligand from S. aureus induce tolerogenic dendritic

190 ophthalmitis, counter regulation analysis of TLR2 ligand pretreated retina or the use of retinas from

191 recently reported that a microbiome-derived TLR2 ligand, Lipid 654 (L654), is present in healthy hum

192 ession both spontaneously and in response to TLR2 ligand.

193 ept we asked whether administering low-level TLR2 ligands in adoptive transfer EAE induces TLR2 toler

194 Intracellular recognition of SVLP TLR2 ligands was confirmed by observing SVLPs' associati

195 Thus, vaccines carrying hydrophobic TLR2 ligands would interact with particular DCs for effi

196 -distinct recognition of functional internal TLR2 ligands.

197 gly, DC processing in the absence of surface TLR2 ligation was defined using synthetic virus-like par

198 tion and maturation independently of surface TLR2 ligation.

199 a transmembrane glycoprotein, in regulating TLR2-linked macrophage activation and resultant proinfla

200 -27p28 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selective

201 We hypothesize that TLR2(+) macrophages are required and sufficient for rhin

202 mmatory responses induced by rhinovirus, and TLR2(+) macrophages are sufficient to confer airway infl

203 his study highlights the central role of the TLR2/Mal tandem in the distinct activity among the monoc

204 These findings establish that the TLR2-mediated hematopoietic response promotes stable con

205 Enhancing TLR2-mediated inflammation increased fibrosis in vivo Fu

206 In response to IR, TLR2(-/-) mice have increased serum beta2-GPI compared w

207 of VWF rescues defective thrombus growth in Tlr2(-/-) mice in vivo.

208 ses, whereas transfer of wild-type marrow to TLR2(-/-) mice restored them.

209 Peritoneal macrophages from TLR2(-/-) mice significantly reduced the production of T

210 All these effects were stronger in TLR2(-/-) mice than in TLR4(-/-) mice.

211 Finally, naive TLR2(-/-) mice underwent intranasal transfer of bone mar

212 , transfer of wild-type macrophages to naive TLR2(-/-) mice was sufficient for neutrophilic inflammat

213 ra experiments using OVA-treated C57BL/6 and TLR2(-/-) mice were also performed.

214 sitized and challenged C57BL/6 wild-type and TLR2(-/-) mice were infected with RV1B, followed by IgG

215 sufficient to confer airway inflammation to TLR2(-/-) mice, with the pattern of inflammation dependi

216 exudative macrophages, which was reduced in TLR2(-/-) mice.

217 microbiota and determines thrombus growth in Tlr2(-/-) mice.

218 clearance of S. epidermidis bacteremia, but TLR2(-/-)mice could still resolve a bloodstream infectio

219 signaling was blocked using a specific anti-TLR2 monoclonal antibody, serotype b-induced cytokine an

220 tion controlled by inputs from the TCR and a TLR2-MyD88-dependent PI3K signaling pathway.

221 SF in respiratory epithelial cells through a TLR2-, MyD88-, NF-kB-, and MAPK-dependent signaling path

222 us to decipher the relative contribution of TLR2 on nonhematopoietic and hematopoietic cells in resi

223 toll-like receptors (TLR) combining TLR1 and TLR2 onto a single sensor surface.

224 hage response in mice lacking TIRAP, but not TLR2 or MyD88.

225 Therefore, TLR2 or NF-kappaB inhibition may both attenuate chronic

226 ng ApoE(-/-) mice with genetic deficiency of TLR2 or TLR6 have demonstrated that oxPCCD36 contribute

227 tion independently of TLR agonist used (i.e. TLR2 or TLR9 agonists).

228 hesis by Ly6C(lo) monocytes after triggering TLR2 or TLR9.

229 t we detected in PDE, inhibited PDE-induced, TLR2- or TLR4-mediated profibrotic responses.

230 0.01) as well as significantly downregulated TLR2 (P <0.05), RAGE (P <0.01), and TNF-alpha (P <0.05)

231 s stimuli, a higher gene expression level of TLR2 (P = .02) and TLR9 (P = .02), a greater than 4-fold

232 3 (polyriboinosinic-polyribocytidylic acid), TLR2 (Pam3CSK4), and TLR9 (CpG) remained comparable with

233 he macrophages responsiveness to agonists of TLR2 (Pam3Cys), TLR4 (LPS), and TLR3 agonist Poly(I:C).

234 es, recognized intracellular exposure of the TLR2 PAMPs carried by di- and triacylated SVLP cores, wh

235 -like particles (SVLPs) carrying hydrophobic TLR2 PAMPs within di- and triacylated lipopeptide cores

236 hila T2S system dampens the signaling of the TLR2 pathway in infected human macrophages.

237 However, eliminating Toll-like receptor 2 (TLR2) permits bacterial replication, indicating that the

238 Our studies reveal that TLR2 plays a key role in platelet hyperreactivity and th

239 TLR2 plays an important role in eliciting inflammation t

240 Since TLR2 plays an important role in SA endophthalmitis, coun

241 Toll-like receptor 2 (TLR2) plays a critical role in host defenses against myc

242 and p65 NF-kappaB, suggesting that the R753Q TLR2 polymorphism alters the functions of the myeloid di

243 The R753Q TLR2 polymorphism has been associated with increased inc

244 study, we determined the impact of the R753Q TLR2 polymorphism on macrophage sensing of Mycobacterium

245 lore the plasticity of Toll-like receptor 2 (TLR2) previously described in immune response during Try

246 ere we describe a novel mechanism regulating TLR2 protein expression and subsequent cytokine release

247 a and TNF-alpha protein production following TLR2 receptor stimulation (p < 0.001).

248 Coactivating TLR2 reduced the injurious effects of dectin-1 activatio

249 ir lipopeptide interaction with cell surface TLR2, requiring degradation for PAMP recognition.

250 CD44 regulated TLR2 responses in human macrophages, whereby a reduction

251 mmatory profile and attenuated innate immune/TLR2 responses to lipopolysaccharide (LPS) challenge.

252 pected pathway in which microbiota-triggered TLR2 signaling alters the synthesis of proadhesive VWF b

253 echanisms by which this polymorphism affects TLR2 signaling are unclear.

254 Thus, the bacterial CW-TLR2 signaling axis affects fetal neurodevelopment and m

255 indicate that the R753Q polymorphism alters TLR2 signaling competence, leading to impaired MyD88-TLR

256 monstrated that IRF6 provides specificity to TLR2 signaling in oral epithelial cells.

257 n via the IL-33/ST2 signaling axis, and that TLR2 signaling limits RV-induced CXCL-10 via IRAK-1 depl

258 rial burden and granuloma integrity, whereas TLR2 signaling on nonhematopoietic cells may partly faci

259 Furthermore, TLR2 signaling played no role in the clearance of bacter

260 TLR2 signaling promoted macrophage polyploidy and suppre

261 n of the Toll-like receptor 4 (TLR4) but not TLR2 signaling restored the inflammation to normal level

262 When TLR2 signaling was blocked using a specific anti-TLR2 mo

263 TLR2 signaling was confirmed to accelerate the clearance

264 monocyte-derived macrophage polarization via TLR2 signaling, leading to dysfunctions of both M1 and M

265 n of NF-kappaB, a major downstream target of TLR2 signaling, was detected in the retinal pigment epit

266 ompared with CD44(-/-) macrophages following TLR2 stimulation (p < 0.01).

267 mma-inducible protein 10 (IP-10) response to TLR2 stimulation (P = .042).

268 Here we show that strong TLR2 stimulation depends on high-level production of phe

269 TLR2 stimulation in combination with PSMalpha3 led to in

270 TLR2 stimulation was performed on differentiated THP-1 m

271 By contrast, the absence of TLR2, STING, or the addition of TLR4 agonist has no effe

272 reased fibrosis in vivo Furthermore, soluble TLR2 (sTLR2), a negative modulator of TLRs that we detec

273 t activation by CAP-PEs includes assembly of TLR2/TLR1 receptor complex, induction of downstream sign

274 significantly downmodulated the response of TLR2-, TLR3-, TLR4-, and TLR9-expressing HEK293 cells to

275 ed from MyD88-, TRIF-, Toll-like receptor 2 (TLR2)-, TLR4-, and TLR2/4-deficient mice indicated that

276 ion, we assessed the potential of peritoneal TLR2, TLR4 and C5a receptors, C5aR and C5L2, as therapeu

277 At each time point, TLR2, TLR4, and CD86 expression on peripheral blood mono

278 In the absence of TLR2, TLR4, myeloid differentiation response gene 88, or

279 Similarly, antibody blockade of TLR2, TLR4, or C5aR differentially inhibited bacteria-in

280 Additionally, antibodies against TLR2, TLR4, or the coreceptor CD14 reduced the profibrot

281 ith and without IVH, but HA receptors--CD44, TLR2, TLR4--were elevated in the forebrain of both human

282 We detected TLR2-, TLR4-, and C5aR-mediated proinflammatory and fibr

283 TLR2-, TLR4-, MyD88-deficient and WT BALB/c mice were in

284 lergic inflammation in the murine lung via a TLR2/TLR4/MyD88-signaling pathway.

285 d IL-1R (-/-) or TLR4 (-/-) corneas, but not TLR2 (-/-), TLR5 (-/-), TLR7 (-/-), or TLR9 (-/-), were

286 oxPCCD36 induce formation of CD36/TLR2/TLR6 complex in platelets and activate downstream s

287 Stimulation of TLR2/TLR6 triggers profound decreases in ferroportin mes

288 different TLR agonists, including those for TLR2, TLR7, and TLR9.

289 Finally, our data have suggested that TLR2, TLR9, and Mal/TIRAP controlled differentially the

290 infected with RV1B, followed by IgG or anti-TLR2, to determine the requirement and sufficiency of TL

291 LR2 ligands in adoptive transfer EAE induces TLR2 tolerance and attenuates disease.

292 litogenic cells and in doing so induced both TLR2 tolerance and attenuation of EAE.

293 all peptidoglycan (CW), a universal PAMP for TLR2, traverses the murine placenta into the developing

294 nsiveness were reduced in TLR2(-/-) and anti-TLR2-treated mice.

295 e, whereas PPE18-induced homodimerization of TLR2 triggers anti-inflammatory type responses.

296 TLR2 was robustly expressed by the retinal pigment epith

297 henotype by activating Toll-like receptor 2 (TLR2), which regulates the induction of cytotoxic T-lymp

298 y observing SVLPs' association with internal TLR2, which had similar kinetics to SVLP association wit

299 Recently, we reported that stimulation of TLR2, which is preferentially expressed by human Tregs,

300 eptor dectin-1 but not Toll-like receptor-2 (TLR2), zymosan-mediated RGC regeneration is greatly redu