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

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

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

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

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

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

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

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

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

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

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

14 Thus, the IL-1beta-IL-1R signaling pathway may contribute to skin inflammat

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

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

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

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

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

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

21 of recipients lacking mature IL-1beta, IL-6, IL-1R, MyD88, or IL-6R impair CD4(+) and CD8(+) T cell r

22 In addition, IL-1R signaling appears to correlate with psoriasis dise

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

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

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

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

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

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

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

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

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

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

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

34 equired interleukin-23 receptor (IL-23R) and IL-1R but not IL-6R signaling for their maintenance and

35 Cytokines IL-4 and IL-1R antagonist were also detected in association with

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 Food and Drug Administration (FDA)-approved IL-1R antagonist; or parthenolide, a caspase-1 and nucle

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

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

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

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

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

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

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

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

69 effects of IL-1alpha/beta are controlled by IL-1R antagonist (IL-1Ra).

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 tic, suggesting a mechanism by which chronic IL-1R signaling could be leading to cachexia-associated

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

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

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

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

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

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

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

80 Together, our data indicate a role for IL-1R as a regulator of host homeostasis and point to ca

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

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

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

84 In this study, we sought to determine how IL-1R-associated kinase-M (IRAK-M), a negative regulator

85 Signaling through the type I IL-1R has recently been shown to control disease toleran

86 ndent on intact signaling through the type I IL-1R receptor.

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

88 e network at different levels, we identified IL-1R-associated kinase 1 (IRAK1) as the dose-sensing no

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

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

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

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

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

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

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

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

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

98 1, and inhibition of downstream signaling in IL-1R- or IL-18R-null mice, all resulted in enhanced bac

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

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

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

102 ernative activation marker, can drive innate IL-1R-dependent neutrophil recruitment during infection

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

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

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

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

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

108 y response, interleukin-1 receptor knockout (IL-1R(-/-)) and caspase-1(-/-) mice had 350 and 30 copie

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

110 Compared with wild-type mice, IL-1R(-/-) mice have more severe liver and adipose tissu

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

112 genital infection using Chlamydia muridarum, IL-1R signaling plays a critical role in oviduct tissue

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

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

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

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

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

118 -1 is essential downstream from TLRs but not IL-1Rs in fibroblasts, whereas it plays a redundant role

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

120 This was due to the ability of IL-1R(-/-) mice to recover from cachexia, an immune-meta

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

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

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

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

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

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

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

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

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

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

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

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

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

134 cells protected against aGVHD independent of IL-1R and TLR4 signaling in two murine HCT models.

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

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

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

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

139 olonic spray increased circulating levels of IL-1R antagonist (IL-1Ra).

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

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

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

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

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

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

146 ination of microglia or selective removal of IL-1R in microglia or endothelia.

147 To investigate the role of IL-1R signaling pathways during IRI, we treated syngenei

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 -1beta (IL-1beta knockout) or IL-1 receptor (IL-1R knockout; n=10 each).

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

164 us far implicated in interleukin-1 receptor (IL-1R) and Toll-like receptor (TLR) immune responses.

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

166 adaptor protein Toll/interleukin-1 receptor (IL-1R) domain-containing adaptor-inducing beta interfero

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

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

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

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

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

172 ective expression of IL-1 and IL-1 receptor (IL-1R) in either microglia or endothelia reveal that IL-

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

174 ing cytokine signaling by the IL-1 receptor (IL-1R) pathway and inflammasome activation.

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

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

177 e receptor (TLR) and interleukin-1 receptor (IL-1R) signaling dynamics relied on a dose-dependent, au

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

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

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

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

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

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

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

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

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

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

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

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

190 regulatory roles of interleukin-1 receptor (IL-1R)-associated kinase 4 (IRAK4) and Bruton's tyrosine

191 Transcriptome profiling of IL-1 receptor (IL-1R)-depleted senescent cells indicates that IL-1 cont

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

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

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

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

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

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

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

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

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

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

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

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

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

205 Surprisingly, IL-1R(-/-) mice had better long-term survival than wild-

206 We hypothesized that IL-1R-associated kinase 1 (IRAK1), a key signaling media

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

208 In this study we show that IL-1R(-/-) mice can control T. gondii burden throughout

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

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

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

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

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

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

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

216 ring alloreactivity uses the ST2 but not the IL-1R or TLR4 pathways, and ST2 represents a potential a

217 athway involving IRAK4 and TRAF6 but not the IL-1R/TLR-IRAK adaptor MyD88.

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

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

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

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

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

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

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

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

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

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

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

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

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

231 t both IL-1alpha and IL-1beta signal through IL-1R to upregulate the SASP in a cooperative manner.

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

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

234 Other miRNAs like miR-155-5p modulate TLR-, IL-1R-, TNFR-, and IFNAR-mediated signaling pathways ups

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

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

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

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

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

240 0 expression was primarily dependent on TLR2/IL-1R.

241 10(-/-) DCs expressed larger numbers of TLR4/IL-1R molecules and had enhanced IL-1beta production.

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

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

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

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

246 e two proinflammatory cytokines that bind to IL-1R.

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

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

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

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

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

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

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

254 Here, we show that removal of the Toll-IL-1R protein SARM from macrophages uncouples inflammaso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Here, we report an unconventional IL-1R-MyD88-IRAK2-PHB/OPA1 signaling axis that reprogram

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

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

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

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