ライフサイエンスコーパス: TLR6

1 ur of these genes (COL1A1, COL7A1, MMP7, and TLR6).

2 ce (TIR) deletion mutants of TLR1, TLR2, and TLR6.

3 hat this could be blocked by the presence of TLR6.

4 that human platelets express TLR2, TLR1, and TLR6.

5 EDN activates TLR2 independently of TLR1 or TLR6.

6 ting that the functional heterodimer is TLR2/TLR6.

7 TLR1, whereas the latter are favored by TLR2/TLR6.

8 pression of TLR4 or TLR2 with either TLR1 or TLR6.

9 econdary to deficient expression of TLR2 and TLR6.

10 s enhanced upon coexpression of TLR1 but not TLR6.

11 y TLR2 or co-expression of TLR2 with TLR1 or TLR6.

12 heir responses to ligands for TLR2, TLR1 and TLR6.

13 er component, bacterial lipopeptide, without TLR6.

14 inflammatory cytokines (IL-1a and IL-6), and TLR6.

15 RI and TLR2 as well as its partners TLR1 and TLR6.

16 hich forms a heterodimer with either TLR1 or TLR6.

17 ation was enhanced by TLR1 and suppressed by TLR6.

18 ial-derived agonists shared by TLR1, but not TLR6.

19 -like receptor (TLR) family members TLR2 and TLR6.

20 Our results identify CD36-TLR4-TLR6 activation as a common molecular mechanism by which

21 For example, clinical data indicate that TLR6 activation exerts protective effects in asthma.

22 Together, our data demonstrate that TLR6 activation is critical for IL-23 production and Th1

23 ed that signals generated following TLR2 and TLR6 activation were important for controlling viral rep

24 Thus, therapeutics targeting TLR6 activity might prove efficacious in the treatment o

25 ), TLR5 (aGMR, 1.19; 95% CI, 1.01-1.41), and TLR6 (aGMR, 1.20; 95% CI, 1.04-1.38).

26 clusively activates epithelial cells through TLR6 and -2 but not through TLR1 and -2.

27 In addition to TLR2, TLR6 and CD14 expression were essential for GBS-F respon

28 that acts through TLR2 and its co-receptors TLR6 and CD14.

29 ated with asthma, as well as 4p14 near TLR1, TLR6 and TLR10 (rs2101521, P=5.3x10(-21)); 6p21.33 near

30 ammals from an ancestral gene also shared by TLR6 and TLR10.

31 TLR6 and TLR2 both are recruited to the macrophage phago

32 s) assayed in 4 TLR genes (TLR1, TLR2, TLR4, TLR6) and 2 adaptor molecules (TIRAP, MyD88) were associ

33 l variants in 4 TLR genes (TLR1, TLR2, TLR4, TLR6) and the adaptor molecule TIRAP between 205 African

34 ted by Toll-like receptors 2 and 6 (TLR2 and TLR6) and which induces hypoferremia in mice injected wi

35 lex composed of Toll-like receptor 4 (TLR4), TLR6, and CD36 induced by fibrillary Abeta peptides, the

36 n polymorphisms (indels) within bovine TLR2, TLR6, and PGLYRP1, thereby facilitating future TLR signa

37 TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adapto

38 ne phosphorylation, hetero-dimerization with TLR6, and recruitment of Mal and MyD88.

39 tyrosine phosphorylation, dimerization with TLR6, and recruitment of Mal and MyD88.

40 ILC2s expressed TLR1, TLR4, and TLR6, and TLR stimulation induced IL-5 and IL-13 product

41 Immunogenetic analysis showed that TLR1, TLR6, and TLR10 single-nucleotide polymorphisms modulate

42 a broad range of TLRs, including TLR2, TLR3, TLR6, and TLR7/8, in addition to a previously identified

43 7 and TLR9 infrequent, and TLR1, TLR3, TLR5, TLR6, and TLR8 expressed in selective patterns.

44 ining adaptor-inducing IFN-beta, TLR2, TLR4, TLR6, and TLR9 had no defect in their ability to respond

45 Polymorphisms in TLR1, TLR2, and TLR6 are associated with increased susceptibility to cSS

46 -like receptors (TLRs) TLR1, TLR2, TLR4, and TLR6 are evolutionarily conserved, highly homologous, an

47 ike receptors), we demonstrate that TLR2 and TLR6 are required for the activation of human and murine

48 affected the heterodimerization of TLR2 with TLR6 as well as the homodimerization of TLR4 as determin

49 Moreover, we shed new light on TLR4-TLR6 assembly and localization and show the potential of

50 Inhibition of TLR4-TLR6 assembly was associated with reduced secretion of p

51 d; TLR2-TLR2 association increased, but TLR2-TLR6 association diminished.

52 veals that TLR10 is most related to TLR1 and TLR6, both of which mediate immune responses to a variet

53 ted response to this modulin was enhanced by TLR6 but inhibited by TLR1, indicating a functional inte

54 Blockade of TLR6 but not TLR1 prevented hIAPP-induced TLR2 activatio

55 ombinations (chimeras with TLR1+TLR2 or TLR2+TLR6 but not TLR1+TLR6) resulted in LPS responsiveness,

56 acid replacements encoded by bovine TLR2 and TLR6, but not PGLYRP1, resulted in the confident predict

57 phagocytes via Toll-like receptor (TLR)2 and TLR6, but that GBS cell walls activate cells independent

58 from three to ten, including SNPs in or near TLR6, C11orf30, STAT6, SLC25A46, HLA-DQB1, IL1RL1, LPP,

59 However, the assembly site of TLR4-TLR6-CD36 and the domains participating in Abeta-induced

60 ding to their extracellular domain, the TLR4-TLR6-CD36 complex assembly has been suggested to be indu

61 Furthermore, the pair of TLR2+TLR6 chimera required approximately 10-fold less LPS to

62 ges expressing TLR4/TLR1, TLR4/TLR2, or TLR4/TLR6 chimeras.

63 oxPCCD36 induce formation of CD36/TLR2/TLR6 complex in platelets and activate downstream signal

64 ession in monocytes via engagement of a TLR4/TLR6 complex.

65 By activating TLR2:TLR6 complexes and inducing TNF-alpha secretion by myelo

66 s expressing the chimeric TLR2/TLR1 and TLR2/TLR6 complexes, we report the selectivity of PorB bindin

67 Tlr6-/- DCs generated less IL-23 upon activation with li

68 demonstrated using purified neutrophils from TLR6 deficient mice.

69 Lungs from TLR1- and TLR6-deficient mice had diminished CXCL1 and CXCL2 produ

70 ne marrow-derived macrophages from TLR1- and TLR6-deficient mice produced lower amounts of interleuki

71 TLR6 dependency of Wolbachia and WoLP NETosis was demons

72 lture and in BALB/c mice; the protection was TLR6 dependent and IL-12 dependent, and it was accompani

73 on and show the potential of inhibiting TLR4-TLR6 dimerization as a treatment of Alzheimer's disease.

74 Our findings support TLR4-TLR6 dimerization induced by Abeta.

75 By interfering with TLR4-TLR6 dimerization using a TLR4-derived peptide, we show

76 Our results support the idea that TLR1 and TLR6 diverged during evolution to differentially recogni

77 Unravelling the molecular basis of TLR1 and TLR6-driven heterodimerization upon LPA binding underlin

78 Furthermore, in the presence of TLR6, exposure to PDG resulted in trophoblast NF-kappaB

79 We observed coregulation of TLR2 and TLR6 expression correlating with local processing of ver

80 those of TLR2 dimerization partners TLR1 and TLR6 extensively.

81 t of functional cooperation between TLR2 and TLR6 for all these TLR2 ligands.

82 quirement of the auxiliary receptor, TLR1 or TLR6, for recognition by TLR2.

83 We suggest that CD14 and TLR2 and TLR6 function as coreceptors for secreted microbial prod

84 l that the transmembrane domains of TLR4 and TLR6 have an essential role in receptor dimerization and

85 -/-) mice with genetic deficiency of TLR2 or TLR6 have demonstrated that oxPCCD36 contribute to accel

86 novel diacylated lipopeptide ligand for TLR2-TLR6 heterodimer, induces IL-12-dependent, inducible NO

87 ated, have the ability to stimulate the TLR2/TLR6 heterodimer.

88 ligands for the Toll-like receptor 2 (TLR2)-TLR6 heterodimer.

89 de insight into the mechanisms by which TLR2-TLR6 heterodimers recognize diacylated liporoteins, wher

90 gulated mRNA and protein expression of TLR1, TLR6, IL-25, and IL-33 in human atopic dermatitis skin l

91 DFE activated the expression of TLR1, TLR6, IL-25, and IL-33 in human primary keratinocytes an

92 nputs" such as cell surface receptors (e.g., TLR6, IL-7Ralpha) and functional "outputs" such as infla

93 on when TLR2 was co-transfected with TLR1 or TLR6 in 293T cells, but not when TLR1, 2, 3, 5, 6, or 9

94 r with TLR1 or TLR6 in mice and TLR1 but not TLR6 in humans.

95 iated by TLR4 and TLR2 together with TLR1 or TLR6 in mice and TLR1 but not TLR6 in humans.

96 e is functional interaction between TLR2 and TLR6 in the cellular response to STF and OspA-L in addit

97 er, our results demonstrate the role of TLR2/TLR6 in the host's inflammatory response to F. tularensi

98 By coexpressing TLR1 or TLR6 in TLR2-transgenic HEK293 cells or silencing tlrs g

99 es, the expression of TLR1 and TLR2, but not TLR6, increased; TLR2-TLR2 association increased, but TL

100 macrophages, in keeping with mouse-specific TLR6 induction.

101 Dominant negative constructs of TLR2 or TLR6 inhibit the responses of STF and OspA-L as well as

102 Knockdown of TLR6 inhibited DFE-induced upregulation of IL-25 or IL-3

103 nd O. volvulus filaria are dependent on TLR2-TLR6 interactions and are mediated by adaptor molecules

104 TLR2, together with TLR1 and TLR6, is essential for detecting lipopeptides and bacter

105 including TLR2 and its coreceptors TLR1 and TLR6, is mediated by a number of specific ligands.

106 tion, peritoneal macrophages from wild-type, TLR6 knockout, and TLR1 knockout mice, but not TLR2 knoc

107 Interestingly, polymorphisms in TLR6 led to decreased cytokine production after C. burne

108 CSK4 (a TLR1/TLR2 ligand), and Fsl-1 (a TLR2/TLR6 ligand) but not that by poly(I:C) (a TLR3 ligand) o

109 bisacycloxypropylcysteine (BPPcysMPEG; TLR2-TLR6 ligand) reduced L. major number in L. major-infecte

110 Furthermore, the expression of TLR6 may be a key factor in determining whether the resp

111 ound that DFE-induced activation of TLR1 and TLR6 may cause polarization toward a T helper type 2 imm

112 ed the mechanism or mechanisms through which TLR6 mediates this effect using mouse models of Aspergil

113 TLR2, in cooperation with either TLR1 or TLR6, mediates responses to a wide variety of microbial

114 Tlr6(-/-) mice did not show DFE-induced upregulation of

115 nd TLR4(-/-) mice, but not from TLR2(-/-) or TLR6(-/-) mice.

116 Impaired IL-23 generation in Tlr6-/- mice also corresponded with lower levels of expr

117 Exogenous IL-23 treatment of asthmatic Tlr6-/- mice restored IL-17A production and substantiall

118 Tlr6-/- mice with fungal- or HDM antigen-induced asthma

119 en compared with that in untreated asthmatic Tlr6-/- mice.

120 ith immune response (TRAF1, RIPK3, BAT2, and TLR6), mitogen-activated protein kinase (MAPK) signaling

121 rrelated with no increase in hepatic TLR1 or TLR6 mRNA.

122 RAK1 mutation), 2 TLR2 (one with concomitant TLR6 mutation), 1 IRAK1, and 1 TLR5.

123 TLR6, not TLR1, was shown to be involved in mediating th

124 Toll-like receptor 1 (TLR1), TLR2, TLR4, TLR6, nucleotide-binding oligomerization domain receptor

125 omain of TLR2 can form functional pairs with TLR6 or TLR1, and this interaction leads to cytokine ind

126 TLR2-dependent activators that utilize TLR1, TLR6, or both as co-receptors.

127 in TLR1 (S248N and R80T), TLR2 (P631H), and TLR6 (P249S) were associated with an increased susceptib

128 during systemic infection, whereas the TLR2/TLR6 receptor complex induced IL-10(+) regulatory T cell

129 TLR2, with TLR1 and TLR6, recognizes structurally diverse bacterial products

130 lthough TLR2 forms heterodimers with TLR1 or TLR6, recognizing different ligands, differences in the

131 Similarly, a deficiency of either TLR4 or TLR6 reduced levels of MP TF activity.

132 TLR1 and TLR2, or a combination of TLR2 and TLR6 responded to PAO1.

133 y showing LPS pretreatment boosts subsequent TLR6 responses in mouse but not human macrophages, in ke

134 Transgenic expression of TLR2 and TLR6 restored responsiveness to phenol soluble modulin a

135 ras with TLR1+TLR2 or TLR2+TLR6 but not TLR1+TLR6) resulted in LPS responsiveness, indicating functio

136 of protein domain architectures for TLR2 and TLR6 revealed six regions of leucine-rich-repeat pattern

137 Among African Americans, the TLR6 rs5743810 T allele significantly decreased endometr

138 095, the CC genotype for TLR2 rs3804099, the TLR6 rs5743810 T allele, and the CC genotype for TIRAP r

139 secondary aims (PTX3, CLEC7a, CD209, CXCL10, TLR6, S100B, IFNG, PLG, TNFR1), with hazard ratios rangi

140 A) or TLR2-shRNA administration reduced, but TLR6-shRNA increased L. major infection in BALB/c mice.

141 out mice, we have demonstrated that TLR2 and TLR6 signaling in leukocytes can activate innate immunit

142 tein) is an adaptor in TLR1, TLR2, TLR4, and TLR6 signaling, whereas MyD88 is an adaptor for all TLRs

143 domain (TMD)-derived peptides from TLR2 and TLR6 specifically inhibit TLR2 activation.

144 HT-29) were analyzed for expression of TLR2, TLR6, TLR1, and Toll inhibitory protein (Tollip) mRNA by

145 Two of the four loci (TLR6-TLR1 and HLA-DQA1-HLA-DQB1) identified in all three

146 Three SNPs located in the TLR6-TLR1 locus had the lowest P-values and Q-values < 0

147 The TLR6-TLR1 locus is likely to have a central role in the

148 the highest Neandertal ancestry, we find the TLR6-TLR1-TLR10 cluster, which also contains functional

149 For example, Toll-like receptor 1 (TLR1)/TLR6/TLR10 gene cluster showed a strong signal of adapti

150 ied several immune pathways, among them TLR1/TLR6/TLR10, as being shaped by convergent evolution in t

151 Finally, we show that TLR6, TLR2, and TLR1 are recruited to macrophage phagoso

152 Leukocytes express TLRs, including TLR2, TLR6, TLR3, TLR4, and TLR7, that can interact with RSV a

153 ) and Toll-like receptors (TLRs), only TLR2, TLR6, TLR7, and TLR9 contribute to the NF-kappaB-depende

154 proteolytic degradation is extended to TLR3, TLR6, TLR7, TLR8, TLR9, and TLR10, whereas the cellular

155 normal responses in mice lacking Tlr1, Tlr3, Tlr6, Tlr7, Tlr9, Tlr11 or the interleukin-18 receptor (

156 as observed for polymorphisms in TLR2, TLR4, TLR6, TLR8, ITGAV, ITGB3, ITGAM, and TIRAP.

157 -helix ubiquitous kinase, IRAK1, TLR1, TLR4, TLR6, TLR8, TLR9, and TNFR-associated factor 6) were dow

158 idemia were observed for SNPs in TLR2, TLR4, TLR6, TLR9, MyD88, or TIRAP.

159 b(R)LD, but not Sb(S)LD, interacts with TLR2/TLR6 to induce IL-10 by exploiting p50/c-Rel subunits of

160 TLR6 with the LRR derived from TLR1 enables TLR6 to recognize TUL4, FTT1103, and triacylated lipopep

161 cooperation with other TLRs, namely TLR1 and TLR6, to mediate cell signaling.

162 that two members of the TLR family, TLR2 and TLR6, together coordinate macrophage activation by Gram-

163 Stimulation of TLR2/TLR6 triggers profound decreases in ferroportin messenge

164 on TLR2 expression, hetero-dimerization with TLR6, tyrosine phosphorylation, and recruitment of myelo

165 66; 95% confidence interval [CI] 0.52-0.85), TLR6 V427A (OR = 5.20; CI 1.77-15.3), SELPLG M264V (OR =

166 ls of IL-23 and IL-17 were markedly lower in Tlr6-/- versus WT asthmatic mice.

167 phenol-soluble modulin mediated by TLR2 and TLR6 was more refractory to inhibition by TLR1 than one

168 ivated macrophages independently of TLR2 and TLR6, whereas a response to the secreted GBS-F was not o

169 Substitution of the corresponding LRR of TLR6 with the LRR derived from TLR1 enables TLR6 to reco