ライフサイエンスコーパス: IL-1R

1 IL-1R (-/-) corneas also showed down-regulation of IL-6

2 IL-1R was detected on T(H)17 cells but not on type 1 hel

3 IL-1R(-/-) mice fail to develop protective immunity but

4 IL-1R, IL-1alpha, and IL-1beta were required for neutrop

5 IL-1R-associated kinase (IRAK) 1 is an important compone

6 IL-1R-associated kinase 1 (IRAK1) was depleted rapidly (

7 IL-1R-associated kinase-M (IRAK-M), a MyD88-dependent in

8 HVPG and interleukin (IL)-1beta (P=0.0052); IL-1R-alpha (P=0.0085); Fas-R (P=0.0354), and serum VCAM

9 tors (TLRs) and receptors for interleukin 1 (IL-1Rs) and to whole pathogens.

10 the inflammasome pathway defined by the IL-1-IL-1R interaction between dendritic cells (DC) and CD4(+

11 ficient in MyD88; NLRP3, ASC, and caspase-1; IL-1R; or IL-18.

12 ria of IFNAR1(-/-) mice produced less IL-10, IL-1R antagonist, and IL-27 compared with WT MPs.

13 studies indicate that caspase-8, caspase-11, IL-1R-associated kinases (IRAK), and receptor-interactin

14 ment of an autocrine loop through IL-1alpha, IL-1R, and MyD88 leading to phosphorylation of IkappaBal

15 ry phenotype in fibroblasts via an IL-1alpha/IL-1R-dependent signaling pathway.

16 IL-1beta also increased IL-1beta, IL-1R-1, PANX1 and CASP1 expression.

17 In the absence of IL-1beta-IL-1R or MyD88 signaling, there is a selective reduction

18 IL-1beta/IL-1R actions account for oedema and neutrophil recruitm

19 CFA immunization requires MyD88 and IL-1beta/IL-1R signaling.

20 TB4 production and further PGE2 via IL-1beta/IL-1R signalling.

21 18BP is consistently most similar to IL-1R9 (IL-1R accessory protein-like 2), another member of the I

22 s involved upregulation of IL-1beta, IL-1RN (IL-1R antagonist), and NLRP3 transcripts, de novo protei

23 sion by knocking down Pellino 2 in human 293-IL-1R cells and primary bone marrow macrophages.

24 antially affected in Pellino 2 knockdown 293-IL-1R cells and primary macrophages, respectively.

25 Anakinra, an IL-1R antagonist, blocked the IL-31 effects on skin diff

26 at intra-articular injection of Anakinra, an IL-1R antagonist, improved range of movement and pain in

27 n of cardiac fibroblasts was abrogated by an IL-1R antagonist and an IL-1alpha-blocking Ab.

28 iggers inflammasome formation and elicits an IL-1R-dependent inflammation in mice.

29 this increased expression is dependent on an IL-1R-MyD88 pathway.

30 in-1 receptor (IL-1R), and treatment with an IL-1R antagonist during the repopulation phase impaired

31 nd IL-1R signaling; it was abrogated with an IL-1R antagonist or with IL-1-neutralizing Abs, whereas

32 e nucleotide polymorphisms (SNP) of IL-1 and IL-1R family genes with Vogt-Koyanagi-Harada (VKH) and B

33 Correspondingly, IL-1beta and IL-1R knockout aortas had decreased inflammatory cytokin

34 Genetic deletion of IL-1beta and IL-1R significantly decreased thoracic aortic dilation (

35 trolled colitis progression through MD-2 and IL-1R signaling via MyD88, and we identify commensally i

36 dilation (IL-1beta knockout=54.2+/-16.8% and IL-1R knockout=62.6+/-17.2% versus WT TAA=104.7+/-23.8%;

37 ion of myeloid differentiation factor 88 and IL-1R-associated kinase 4, which are required for NF-kap

38 monocyte migration toward stressed cells and IL-1R-associated kinase 1 phosphorylation.

39 ontribution of peripheral myeloid cells, and IL-1R signaling participates in this restorative prolife

40 rophages, NLRP3 inflammasome components, and IL-1R in the lethality caused by sterile hemolysis.

41 NF-signaling pathway, NLRP3 inflammasome and IL-1R signaling are required to provoke skin inflammatio

42 IRF6 and IL-1R-associated kinase 1 also regulated the stimulation

43 IL-1beta knockout and IL-1R knockout aortas demonstrated preserved elastin and

44 uate the collective contribution of PRRs and IL-1R signalling to RSV immunity, we generated Myd88/Tri

45 eficient in signalling by all TLRs, RLRs and IL-1R, as well as other cytokine receptors such as IL-18

46 was dependent on reactive oxygen species and IL-1R signaling; it was abrogated with an IL-1R antagoni

47 D88 is the main adaptor molecule for TLR and IL-1R family members.

48 TLR and IL-1R responses are weak but not abolished in mice lacki

49 POP1 expression was regulated by TLR and IL-1R signaling, and we propose that POP1 provides a reg

50 t on MyD88, a key adaptor protein of TLR and IL-1R signaling, but the basal lamina represents the fin

51 sically known as an adaptor, linking TLR and IL-1R to downstream signaling pathways in the innate imm

52 abundance in a manner regulated by TLR2 and IL-1R signaling.

53 rial lipoproteins are required for TLR2- and IL-1R-associated kinase-4-mediated inflammatory response

54 most TLR (except for TLR3 and some TLR4) and IL-1R signaling in both leukocytes and fibroblasts.

55 data demonstrated the importance of TLRs and IL-1R signaling events for the establishment of an effec

56 on of immune pathways downstream of TLRs and IL-1R.

57 way following Toll-like receptor, TNFR1, and IL-1R stimulation.

58 tion and uncouples the activation of TLR and IL-1Rs from the initiation of proinflammatory signaling

59 redundant role downstream from both TLRs and IL-1Rs in leukocytes.

60 Upon ligand binding, TLRs and IL-1Rs recruit adaptor proteins, such as myeloid differe

61 a, and IL-6, as well as the antiinflammatory IL-1R antagonist.

62 ncrease in inflammatory dendritic cells, are IL-1R independent.

63 s critical for signaling by TLR5, as well as IL-1Rs and IL-18Rs, major downstream mediators of the Na

64 to block the inflammasome-IL-1alpha/IL-beta-IL-1R system in kidney disease should be further explore

65 Thus, the inflammasome-IL-1alpha/IL-beta-IL-1R system is a central element of kidney inflammation

66 fere with the inflammasome-IL-1alpha/IL-beta-IL-1R system, ranging from recently described small mole

67 ent of BM that could be reversed by blocking IL-1R or IL-6R.

68 Importantly, blocking IL-1R with IL-1R antagonist (IL-Ra) inhibited tumor grow

69 Both IL-1R-associated kinase (IRAK) 1 and IRAK4 are critical

70 orneal surface glycosylation is modulated by IL-1R and Pseudomonas aeruginosa challenge but is insuff

71 ated in human cells following stimulation by IL-1R and Toll-like receptor agonists, which can be bloc

72 d in pDC were C-type lectin receptor CLEC4E, IL-1Rs (IL-1R1 and -2), proinflammatory cytokines (IL-1a

73 n-1-/-, or interleukin 1 receptor-deficient (IL-1R-/-) mice.

74 this signaling cascade by rapidly degrading IL-1R-associated kinase-1, leading to induction of the a

75 ompared with the significantly less diseased IL-1R-deficient or wild-type mice treated with the IL-1R

76 Separately, WT mice pretreated with either IL-1R antagonist anakinra (100 mg/kg per day) or vehicle

77 e to hapten challenge, indicating a need for IL-1R signaling for the localization or activation, or b

78 appreciated Trim24-dependent requirement for IL-1R expression on TH2 cells and an important nonredund

79 Experiments using leukocytes from IL-1R-associated kinase-4-deficient patients and a mouse

80 nly a few small tumors in orthotopic grafts, IL-1R-deficient RAS-expressing keratinocytes retain the

81 a to produce CXCR2 ligands, and loss of host IL-1R signaling in vivo reduces melanoma growth.

82 alpha and IL-1beta, can stimulate the type I IL-1R.

83 (IL-1R8, also known as single immunoglobulin IL-1R-related receptor, SIGIRR, or TIR8) is a member of

84 In IL-1R KO mice exposed to OVA+SEB, attraction of CD4+ cel

85 Clinical EAE is significantly attenuated in IL-1R-deficient and IL-1beta-deficient mice, and IL-1bet

86 se we observed augmented bacterial burden in IL-1R and IL-18 knockout mice.

87 er metastases generated by the same cells in IL-1R knockout animals, confirming that tumor-secreted I

88 y, the expression of ICAM-1 was decreased in IL-1R-deficient and anakinra-treated mice injected with

89 of TLR4, TLR5, and IL-1R1, with decreases in IL-1R-associated kinase 1 and an inhibitor of NF-kappaB,

90 ssociated factor 6, a common intermediate in IL-1R and TLR-dependent signaling.

91 of microRNA-146a, and greater reductions in IL-1R-associated kinase 1 and TRAF6 levels following LOS

92 1, and inhibition of downstream signaling in IL-1R- or IL-18R-null mice, all resulted in enhanced bac

93 induced allergic inflammation was studied in IL-1R knockout (KO) mice exposed to OVA+SEB.

94 y downregulated pathways in LS skin included IL-1R/TLR signaling, type I and II cytokine receptor sig

95 Nine, including IL-1R antagonist (IL-1RN), are present at a single locus

96 Despite increased infection, IL-1R-deficient mice had significantly reduced oviduct p

97 itor treatment, and consequently, inhibiting IL-1R or CXCR2 signaling in vivo enhanced the efficacy o

98 e used to detect S1P receptors, interleukin (IL) 1R, IL17RA, and nitrosative stress in multiple scler

99 ctivation through modulation of interleukin (IL)1R/IL1Ra signaling.

100 hibited aberrant activation of the intrinsic IL-1R/MYD88/NF-kappaB signaling pathway and MYD88-depend

101 ling adaptor MyD88 and its downstream kinase IL-1R-associated kinase 1, but independent of TNFR-assoc

102 The serine/threonine kinase IL-1R-associated kinase (IRAK)4 is a critical regulator

103 (-/-)), and interleukin-1 receptor knockout (IL-1R(-/-)) mice treated with vehicle or aldosterone (60

104 In this study, we report that mice lacking IL-1R or MyD88 are less sensitive to topical skin carcin

105 Compared with control mice, IL-1R-deficient mice displayed delayed clearance and inc

106 he possible function of the adaptor molecule IL-1R-associated kinase (IRAK)-4 against this pathogen h

107 y TLR4-dependent activation of the FAK/MyD88/IL-1R-associated kinase 4 signaling pathway.

108 rimed wild type CD8 T cell transfer to naive IL-1R(-/-) mice did not result in T cell activation in r

109 ndritic cells from wild type donors to naive IL-1R(-/-) mice resulted in decreased numbers of the den

110 MyD88(-/-)) and germ-free (GF) mice, but not IL-1R(-/-) mice, exhibit impairment in IL-1beta inductio

111 infection, NK cells required MyD88, but not IL-1R, for optimal expansion.

112 The IL-18R pathway, but not IL-1R, was required for early innate and subsequent cell

113 This process was dependent on MyD88, but not IL-1R-associated kinase 1/4.

114 -1 is essential downstream from TLRs but not IL-1Rs in fibroblasts, whereas it plays a redundant role

115 recombinant form of the naturally occurring IL-1R antagonist (IL-1Ra), which blocks IL-1R1, is broad

116 Blockade or absence of IL-1R negated the impact of aerobic glycolysis on intrac

117 ase was completely blocked in the absence of IL-1R.

118 at NLRP3 inflammasome, through activation of IL-1R, is critically involved in the deleterious vascula

119 so known as SIGIRR or Tir8) or activation of IL-1R, leads to up-regulation of the mTOR pathway and in

120 LPS caused MyD88-dependent activation of IL-1R-associated kinase 4.

121 ld be reversed by systemic administration of IL-1R antagonist (anakinra).

122 However, blockage of IL-1R signaling did not abolish the deleterious effects

123 Bacteria adherent to the corneas of IL-1R (-/-) or TLR5 (-/-) mice penetrated beyond the epi

124 (IL-1R), or harboring a targeted deletion of IL-1R are significantly less prone to develop bone tumor

125 ation of the NF-kappaB pathway downstream of IL-1R, TNFR1, and TLRs.

126 ments indicated that IRF6 acts downstream of IL-1R-associated kinase 1 to stimulate the expression of

127 ause no activation of NLRP3 or enrichment of IL-1R family genes in bronchial brushings or biopsy spec

128 During macrophage activation, expression of IL-1R-associated kinase (IRAK)-M is induced to suppress

129 CD16 also upregulated the expression of IL-1R-associated kinase M and IL-1 receptor antagonist,

130 Pharmacological inhibition of IL-1R activation by Anakinra corrects transcriptional ch

131 tic deletion and pharmacologic inhibition of IL-1R in Scnn1b-Tg mice and determined effects on airway

132 ibition using chloroquine or an inhibitor of IL-1R-associated kinases 1 and 4 in normal differentiate

133 Lack of IL-1R had no effect on epithelial necrosis and elevated

134 minent phenotype associated with the lack of IL-1R signaling in mice and support further investigatio

135 ng ocular inflammation and show that loss of IL-1R signaling confers protection from experimental aut

136 e copy numbers were detected in the lungs of IL-1R(-/-) mice at 14 days postinfection.

137 rect IL-18R signaling in T cells, but not of IL-1R, phenocopied the absence of the MyD88 pathway, ind

138 e accompanied by impaired phosphorylation of IL-1R-associated kinase 1 (IRAK-1), p38, ERK1/2 MAPKs, a

139 D14 expression and by the phosphorylation of IL-1R-associated kinase 1, a well-known MyD88-dependent

140 of TLR1/2 caused an increased recruitment of IL-1R-associated kinase (IRAK)1, MyD88, and protein kina

141 Thus, RABGEF1-mediated regulation of IL-1R/MYD88 signaling might represent a potential therap

142 The role of IL-1R signaling during 2, 4 dinitro-1-fluorobenezene (DN

143 The roles of IL-1R-associated kinase (IRAK)2 and IRAK1 in cytokine pr

144 n, inflammasome-derived IL-1beta upstream of IL-1R is a critical regulator of GM-CSF production by T

145 se findings indicate the possible utility of IL-1R-blocking agents for the treatment of ocular inflam

146 reover, secretion of GM-CSF was dependent on IL-1R under both IL-12- and IL-23-induced stimulatory co

147 Microbiota-induced IL-1beta acts directly on IL-1R-expressing T cells to drive the generation of sT(H

148 In contrast, mice deficient in IL-25R or IL-1R showed minimal differences as compared with wild-t

149 nd IL-18, by other TLRs/inflammasome- and/or IL-1R/IL-18R-mediated signaling.

150 primary neurons depleted with either CBS or IL-1R, IL-1beta-induced loss of PSD95 was rescued along

151 Correspondingly, IRF4- or IL-1R-deficient mast cells exhibit a strong impairment i

152 MyD88(-/-) or IL-1R(-/-) keratinocytes expressing oncogenic RAS are hy

153 t be recapitulated by deficiencies in TLR or IL-1R signaling.

154 IL-1R9 and the related IL-1R8, but not other IL-1R family members, exhibit an amino acid sequence sim

155 second domain (D2) is unique among the other IL-1R family members, which presumably distinguishes the

156 However, knocking out IL-1R did not affect any of the features of allergic air

157 anti-inflammatory cytokines, in particular, IL-1R antagonist (IL-1Ra), to ensure the correct develop

158 egulates proinflammatory signaling pathways, IL-1R antagonist (IL-1Ra) adheres to the same receptor a

159 a steadily increased IL-33 and its receptor IL-1R-like 1 expression in the liver during the first we

160 -1beta (IL-1beta knockout) or IL-1 receptor (IL-1R knockout; n=10 each).

161 bserved that mice lacking the IL-1 receptor (IL-1R) (IL1r(-/-)) or deficient in IL1-beta developed mu

162 through TRAF6 in the interleukin 1 receptor (IL-1R) and toll-like receptor (TLR) pathways, we sought

163 m24(-/-) T cells have reduced IL-1 receptor (IL-1R) expression, are refractory to IL-1beta-mediated a

164 e receptor (TLR) and interleukin-1 receptor (IL-1R) families transduce signals via a canonical pathwa

165 compared with MMAs, including IL-1 receptor (IL-1R) family and nucleotide-binding oligomerization dom

166 Members of the IL-1 Receptor (IL-1R) family include six receptor chains forming four s

167 Interleukin-1 (IL-1) and the IL-1 receptor (IL-1R) family play an important role in the pathogenesis

168 e receptor (TLR) and interleukin 1 receptor (IL-1R) mediated signaling pathways.

169 e receptor (TLR) and interleukin 1 receptor (IL-1R) signaling against mycobacteria.

170 s bystander response required IL-1 receptor (IL-1R) signaling during early pulmonary infection.

171 of the Toll-like and interleukin-1 receptor (IL-1R) signaling pathways, controls intestinal inflammat

172 key role for T cell-specific IL-1 receptor (IL-1R) signals in the accumulation and survival of patho

173 -like receptor (TLR)/interleukin-1 receptor (IL-1R) superfamily, IL-1beta production, NLRP3 inflammas

174 and IL-1beta ligate the same IL-1 receptor (IL-1R) that is present on nearly all cells inside and ou

175 Surprisingly, the interleukin-1 receptor (IL-1R) was required for an AEC chemokine response to Pne

176 ignaling through the interleukin 1 receptor (IL-1R) was required for productive priming of CD8(+) T c

177 cell signaling by binding the IL-1 receptor (IL-1R) whereas IL-1Ra acts as an antagonist, blocking re

178 high amounts of the interleukin-1 receptor (IL-1R), and treatment with an IL-1R antagonist during th

179 ne receptors such as interleukin 1 receptor (IL-1R), have been implicated in responses to RNA viruses

180 e receptor 4 (TLR4), interleukin-1 receptor (IL-1R), or interferon-gamma receptor (IFN-gammaR) but in

181 Interleukin-1 receptor (IL-1R)-associated kinase (IRAK) 1 is modified first by K

182 We identified interleukin-1 receptor (IL-1R)-associated kinase 1 (IRAK1) as a potential target

183 ing was reduced and patchy on IL-1 receptor (IL-1R)-knockout mouse corneas (P < 0.05, ANOVA).

184 ago as a mediator of interleukin-1 receptor (IL-1R)-mediated activation of NFkappaB, TRAF6 has since

185 Thus, our observation that IL-1 receptor (IL-1R)-mediated signals were still required to initiate

186 oll-like receptors (TLRs) and IL-1 receptor (IL-1R).

187 IL-1beta are mediated through IL-1 receptor (IL-1R).

188 rough members of the interleukin-1 receptor (IL-1R)/Toll-like receptor superfamily.

189 nist of the interleukin (IL)-1beta receptor (IL-1R), or harboring a targeted deletion of IL-1R are si

190 L-1beta binds to its high-affinity receptor, IL-1R, and upregulates proinflammatory signaling pathway

191 , a negative regulator of Toll-like receptor/IL-1R signaling, are associated with susceptibility to t

192 eceptors (TLRs) and Interleukin-1 receptors (IL-1Rs) with downstream signaling molecules.

193 eceptors (TLRs) and interleukin-1 receptors (IL-1Rs).

194 stribution of surface glycosylation requires IL-1R, but not MyD88, and is not sufficient to prevent b

195 DNFB-sensitized IL-1R(-/-) mice had low CHS responses to hapten challeng

196 Decreased CD8 T cell priming in sensitized IL-1R(-/-) mice was associated with marked decreases in

197 okine activation and abrogated by a specific IL-1R antagonist.

198 of human monocytes into a refractory state: IL-1R-associated kinase-M, NFkB2/p100, and hypoxia-induc

199 Strikingly, IL-1R antagonist inhibition, pharmacologic or genetic su

200 dependent of bacterial infection and suggest IL-1R as a novel target for antiinflammatory therapy in

201 Our work demonstrates that IL-1R is required for GM-CSF production after both TCR-

202 These results indicate that IL-1R signaling is required at multiple steps during the

203 The IL-1R family member IL-33R mediates Fcepsilon-receptor-I

204 Although the IL-1R type 1 (IL-1R1) receptor for IL-1 shares downstrea

205 nce of inflammasome-derived IL-1beta and the IL-1R/MyD88 signaling axis in the regulation of GM-CSF p

206 Blocking the IL-1R or IL-6R reversed cytokine impairment.

207 ficient in the IL-1 receptor Type I, but the IL-1R-/- mice were fully protected from lethal rechallen

208 DCs into the MLN is in part governed by the IL-1R family/TLR signaling adaptor molecule MyD88.

209 infection clearance, mice deficient for the IL-1R antagonist cleared infection at a faster rate.

210 Mice lacking the IL-1R or the inflammasome components NLRP3 and caspase-1

211 tal or keratinocyte-specific deletion of the IL-1R and IL-36R signaling adaptor Myd88.

212 se (IRAK) 1 is an important component of the IL-1R and TLR signaling pathways, which influence Th cel

213 Expression of NLRP3 and of the IL-1R family genes was validated in the Airway Disease E

214 ssory protein-like 2), another member of the IL-1R family.

215 he adaptor molecule MyD88 and members of the IL-1R-associated kinase family (IRAK-1, 2, M and 4).

216 Importantly, we demonstrate that the IL-1R antagonist anakinra significantly reduces CHS resp

217 tal videomicroscopy, we demonstrate that the IL-1R type 1 governs the firm adhesion of neutrophils to

218 uction of IL-1beta, or signaling through the IL-1R would be less reactogenic in vivo, but would retai

219 Thus, the IL-1R-MyD88 pathway is implicated in inhibiting granulom

220 or dying cells, achieves its effects via the IL-1R family member ST2L.

221 s both IL-1alpha and IL-1beta signal via the IL-1R, we examined immune responses in mice lacking eith

222 hich occurs in response to signaling via the IL-1R.

223 Treatment of adult Scnn1b-Tg mice with the IL-1R antagonist anakinra had protective effects on neut

224 deficient or wild-type mice treated with the IL-1R antagonist anakinra or anti-IL-1beta.

225 rleukin-1alpha (IL-1alpha) signaling through IL-1R and MyD88 in both stromal and immune cells drive i

226 a or IL-1beta, both of which signals through IL-1R, instigates skin inflammation and systemic disease

227 nt component of the Toll-like receptor (TLR)/IL-1R signaling cascade.

228 on of developmentally regulated genes by TLR/IL-1R (TIR) signaling and/or indigenous microbes.

229 that Pellino 2 plays a critical role for TLR/IL-1R-mediated post-transcriptional control.

230 wn cells, implicating MAPK activation in TLR/IL-1R-induced mRNA stabilization.

231 this study, we investigated the role of TLR/IL-1R signaling pathways including the common adaptor My

232 l TCPs, potently augments suppression of TLR/IL-1R signaling.

233 each Pellino member distinctly regulates TLR/IL-1R signaling by modulating IRAK1 ubiquitination.

234 trate KSHV-encoded miRNAs regulating the TLR/IL-1R signaling cascade at two distinct points and sugge

235 be regulating a second component of the TLR/IL-1R signaling cascade, resulting in a stronger phenoty

236 echanism of action in downregulating the TLR/IL-1R transducer, MyD88.

237 Upon ligand binding, TLR/IL-1Rs hetero- or homodimerize and recruit MyD88 through

238 0 expression was primarily dependent on TLR2/IL-1R.

239 flammatory state, through cell surface TLR4, IL-1R-associated kinase-1, and the Toll-interacting prot

240 10(-/-) DCs expressed larger numbers of TLR4/IL-1R molecules and had enhanced IL-1beta production.

241 hese data show complex roles for TLR4, TLR5, IL-1R and CD11c+ cells in constitutive epithelial barrie

242 TLR2(-/-), TLR3(-/-), TLR4(-/-), TLR9(-/-), IL-1R(-/-), and IL-18(-/-) mice, we found that, while th

243 sponses downstream of IgE/FcepsilonRI, TLRs, IL-1R, and IL-33R.

244 factor receptor/interleukin-1 receptor, TNFR/IL-1R in mammals) is indispensable for intestinal immuni

245 hat bone marrow-derived cells contributed to IL-1R-dependent barrier function.

246 Signaling via TLR4 and its adaptor Toll-IL-1R domain-containing adapter inducing IFN-beta (TRIF)

247 n primary response protein (MyD88), and Toll-IL-1R domain-containing adapter inducing IFN-beta (TRIF)

248 MyD88, TLR4, or Toll-IL-1R domain-containing adapter-inducing IFN-beta (TRIF)

249 Yersinia infection and to proapoptotic Toll-IL-1R domain-containing adapter inducing IFN-beta signal

250 s was mediated by overexpression of the Toll-IL-1R domain-containing adapter inducing IFN-beta in epi

251 ring the death domain and the other the Toll-IL-1R domain.

252 Toll/IL-1R (TIR) domain-containing adapter-inducing IFN-beta

253 Toll/IL-1R resistance (TIR) domain-containing adapter-inducin

254 Structural data suggest that 1) Toll/IL-1R (TIR) domain-containing regulators (BCAP, SIGIRR,

255 ptor mechanism, involving the TLR4/MD-2/Toll/IL-1R domain-containing adapter inducing IFN-beta-mediat

256 g the first 5 d postinfection through a Toll/IL-1R domain-containing adapter inducing IFN-beta-depend

257 MPs) constitutively produced IFN-1 in a Toll/IL-1R domain-containing adapter-inducing IFN-beta-depend

258 ember of this family, sterile alpha and Toll/IL-1R domain-containing 1 (SARM), is unclear.

259 es derived from TLR4-mediated MyD88 and Toll/IL-1R domain-containing adapter inducing IFN-beta pathwa

260 in a manner dependent on both MyD88 and Toll/IL-1R domain-containing adaptor inducing IFN-beta, where

261 f septic insult by targeting MyD88- and Toll/IL-1R domain-containing adaptor inducing IFN-beta-depend

262 activation of adaptor protein MyD88 and Toll/IL-1R domain-containing adaptor-inducing IFN-beta.

263 t IFN-I induction by TLR3 or TLR4 (both Toll/IL-1R domain-containing adapter-inducing IFN-beta depend

264 he fifth, most evolutionarily conserved Toll/IL-1R adaptor, sterile alpha and HEAT/Armadillo motif-co

265 ue is highly conserved in the cytosolic Toll/IL-1R signaling domains of human TLRs.

266 her TLR agonists that are selective for Toll/IL-1R domain-containing adapter inducing IFN-beta (polyi

267 The four Toll/IL-1R domain-containing adaptor proteins MyD88, MAL, TRI

268 The MyD88-independent Toll/IL-1R domain-containing adapter inducing IFN-beta-IFN re

269 signaling through the adaptor molecule Toll/IL-1R domain-containing adapter inducing IFN-beta and do

270 The TLR adaptor molecule, Toll/IL-1R domain-containing adaptor inducing IFN (TRIF), fac

271 Whereas MyD88, Toll/IL-1R adaptor protein, and TNFR-alpha-associated factor

272 pro-memory" signals were MyD88, but not Toll/IL-1R domain-containing adapter inducing IFN-beta, depen

273 tudy investigates the role of Zn(2+) on Toll/IL-1R domain-containing adapter inducing IFN-beta (TRIF)

274 deficient in the TLR-3 adaptor protein Toll/IL-1R domain-containing adaptor molecule-1 (TRIF) did no

275 e BANK1 contains an N-terminal putative Toll/IL-1R receptor domain, we used mouse Bank1(-/-) splenic

276 he plasma membrane to NF-kappaB via the Toll/IL-1R (TIR) adaptor protein MyD88 requires the TIR sorti

277 EFIR structure resembles closest to the Toll/IL-1R domain of TLR10 with low sequence homology, substa

278 only IRAK1 is partially required in the Toll/IL-1R domain-containing adapter inducing IFN-beta pathwa

279 retion was hardly affected, because the Toll/IL-1R domain-containing adapter-inducing IFN-beta (TRIF)

280 Four of the five members of the Toll/IL-1R domain-containing adaptor family are required for

281 croarray experiments indicated that the Toll/IL-1R domain-containing adaptor inducing IFN-beta/ TNFR-

282 onferred by minimal determinants of the Toll/IL-1R domain.

283 We found that TLRs signaling through Toll/IL-1R domain-containing adapter inducing IFN-beta promot

284 Aspergillus conidia activated the TLR4/Toll/IL-1R domain-containing adapter inducing IFN-beta-depend

285 o CD11b(+) DCs in association with TLR4/Toll/IL-1R domain-containing adapter-inducing IFN-beta activa

286 ow that DCs sense CyaA through the TLR4/Toll/IL-1R domain-containing adapter-inducing IFN-beta pathwa

287 ism for the specificity of SEFIR versus Toll/IL-1R domain in their respective signaling pathways.

288 d for an immediate early phase, whereas Toll/IL-1R domain-containing adapter inducing IFN-beta is req

289 Uninjured IL-1R (-/-) or TLR4 (-/-) corneas, but not TLR2 (-/-), T

290 This mRNA is the template for a unique IL-1R protein that is identical to IL-1R1 at the C termi

291 Using IL-1R 1 knockout mice, we show that miR-135b expression

292 elicit the response were investigated using IL-1R deficient mice.

293 IL-1alpha and IL-36alpha, and signaling via IL-1R and IL-36R was required for induction of the pro-i

294 In vivo, IL-1R signaling was required for full Bhlhe40 expression

295 The points at which IL-1R signaling is required during this complex, multist

296 Importantly, blocking IL-1R with IL-1R antagonist (IL-Ra) inhibited tumor growth and meta

297 Specific blockade of IL-1R1 with IL-1R antagonist suppressed platelet stimulation by IL-1

298 was highly and specifically correlated with IL-1R antagonist (IL-1Ra).

299 ckade of IL-1beta activity by treatment with IL-1R antagonist (IL-1Ra; Anakinra) inhibited colitis ac

300 Yet, IL-1R signaling is crucial for CD4 cell accumulation and