ライフサイエンスコーパス: IL-18R

1 IL-18R alpha alone has a weak affinity for IL-18 binding

2 IL-18R(-/-) mice display increased weight gain, ectopic

3 IL-18R/VEGF/VLA-4-expressing A375 and 1182 melanoma cell

4 ns of colony-stimulating factor 1, IL-12p40, IL-18R, oncostatin M, TNF, and vascular endothelial grow

5 ns of colony-stimulating factor 1, IL-12p40, IL-18R, oncostatin M, TNF, and vascular endothelial grow

6 e receptor (TLR) signaling, as well as IL-1R/IL-18R signals.

7 18, by other TLRs/inflammasome- and/or IL-1R/IL-18R-mediated signaling.

8 nes, and related receptors (eg, VEGFC, IL-6, IL-18R).

9 ies demonstrate that the biologically active IL-18R complex requires the membrane-proximal third Ig-l

10 mportantly, discrepancies between IL-18- and IL-18R-deficient cells suggest that IL-18Ralpha chain is

11 to B cells and was independent of IL-1R and IL-18R, cytokine receptors that also signal through MyD8

12 m of the IL-1 and Il-18 receptors (IL-1R and IL-18R, respectively).

13 was independent of signals via the IL-1R and IL-18R, suggesting a role for TLRs in MyD88-mediated T c

14 Although both IL-1R and IL-18R-deficient mice showed a reduced CHS response to D

15 ther, these data indicate that the IL-1R and IL-18R/MyD88 pathways are required in distinctly differe

16 ell as in interleukin-1 receptor (IL-1R) and IL-18R signaling.

17 y common to toll-like receptor 4, IL-1R, and IL-18R.

18 IL-12 up-regulation of both IL-18R alpha and IL-18R beta chains, although postreceptor events likely

19 rresponded to IL-12-induced IL-18R alpha and IL-18R beta chains.

20 ich comprises two subunits: IL-18R alpha and IL-18R beta.

21 steady-state mRNA levels of IL-18R alpha and IL-18R beta; the production of IFN-gamma corresponded to

22 he human NK cell line NKO, IL-18R alpha, and IL-18R beta are expressed constitutively but IL-18 did n

23 ogoR levels led to islet cell apoptosis, and IL-18R antagonised inflammatory IL-18 signalling towards

24 in SCOP2D mice and IFN-gamma, TGF-beta1, and IL-18R transcripts in SCOP5D mice.

25 IL-1 or IL-18 responses since IL-1R1 KO and IL-18R KO mice were not protected from weight loss.

26 enerated Abs to human homologues of ST2L and IL-18R and tested them against Th1/Th2, Tc1/Tc2, and NK1

27 We show for the first time that ST2L and IL-18R are stable selective cell surface markers for hum

28 Recently, we reported that ST2L and IL-18R are stably expressed on murine Th2 and Th1 cells,

29 for signaling by TLR5, as well as IL-1Rs and IL-18Rs, major downstream mediators of the Naip5/6 Nlrc4

30 Anti-IL-18R Ab also reduced in vivo IFN-gamma production by >

31 oduction was ablated in the presence of anti-IL-18R Ab.

32 l antibody (MAb) to the IL-18 receptor (anti-IL-18R MAb) prior to L. pneumophila infection inhibited

33 ntibodies (MAbs) to the IL-18 receptor (anti-IL-18R MAb), TNF-alpha (anti-TNF-alpha MAb), IL-12 (anti

34 IL-12 MAb) alone or in combination with anti-IL-18R MAb inhibited induction of intrapulmonary IFN-gam

35 in part, due to IL-12 up-regulation of both IL-18R alpha and IL-18R beta chains, although postrecept

36 This region, as examined by IL-18R binding and functional analysis, appeared to be c

37 in was compared with binding to the cellular IL-18R.

38 ice deficient in IL-18 receptor alpha chain (IL-18R) exhibited rapid graft failure (P = 0.024; IL-18-

39 In this context, IL-18R signaling increases PI3K activation and was found

40 The lack of direct IL-18R signaling in T cells, but not of IL-1R, phenocopi

41 Resting CD56+ NK cells expressed IL-18R transcript that was up-regulated by IL-12 or IL-1

42 However, there is a lack of focal IL-18R expression in their terminal field.

43 Moreover, memory T cells demonstrate high IL-18R expression and respond effectively to the combina

44 -induced conformational changes may occur in IL-18R alpha upon dimerization, leading to changes in th

45 s the receptor, only IL-9 was able to induce IL-18R via an IL-9R-JAK1/JAK3-STAT1 signaling pathway.

46 Following IL-12 pretreatment to induce IL-18R, wild-type, but not Stat4-deficient, activated T

47 n of IFN-gamma corresponded to IL-12-induced IL-18R alpha and IL-18R beta chains.

48 Our findings establish the T-cell intrinsic IL-18R/MyD88 pathway as a crucial element for induction

49 human pathogen and disclose T-cell intrinsic IL-18R/MyD88 signaling as a key pathway controlling the

50 However, limited IL-18R alpha-chain (IL-18Ralpha) expression in tissues m

51 In the human NK cell line NKO, IL-18R alpha, and IL-18R beta are expressed constitutive

52 ts suggested that the presence or absence of IL-18R signals governs the pathogenic versus protective

53 Expression by lung CD8(+) T cells of IL-18R and CD69 correlated with severity, as did mRNA tr

54 , specificity and binding characteristics of IL-18R components have only been superficially explored.

55 irus carcinogenesis or, acting downstream of IL-18R to strengthen mucosal repair, in azoxymethane (AO

56 synergistically to upregulate expression of IL-18R genes, thereby enhancing IL-18 activity.

57 Gene expression of IL-18R, which is a receptor for both IL-18 and IL-37, is

58 e domain in IL-18Ralpha for the formation of IL-18R ternary complex as well as for signal transductio

59 in of IL-18Ralpha prevented the formation of IL-18R ternary complex with IL-18R beta-chain.

60 Although lack of IL-18R decreased the magnitude of IFN-gamma producing ty

61 Finally, lack of IL-18R signal reduced dendritic cell maturation and thei

62 IL-12 increased steady-state mRNA levels of IL-18R alpha and IL-18R beta; the production of IFN-gamm

63 tly or to IL-18 when various permutations of IL-18R ectodomain chimeras were fused to their cytoplasm

64 sponses were not diminished in IL-1R(-/-) or IL-18R(-/-) mice.

65 ibition of downstream signaling in IL-1R- or IL-18R-null mice, all resulted in enhanced bacterial cle

66 s through its specific cell surface receptor IL-18R, which comprises two subunits: IL-18R alpha and I

67 of the alpha-isoform of the IL-18 receptor (IL-18R(-/-)) fed a standard chow or HFD.

68 -4, -6, -7, -9, and -11 and IL-18 receptor (IL-18R) are not essential for MSU-induced inflammation.

69 Tlr9, Tlr11 or the interleukin-18 receptor (IL-18R).

70 l lines with and without the IL-18 receptor (IL-18R)/VEGF/VLA-4-expressing phenotype were identified,

71 acking IL-18 or its ligand-binding receptor (IL-18R) should exhibit decreased cytokine and chemokine

72 express functional interleukin-18 receptors (IL-18Rs), composed of alpha and beta subunits.

73 a receptor (IFN-gammaR) but instead required IL-18R, IL-33R, and adaptor protein MyD88.

74 In related studies, IL-18R-deficient splenocytes and macrophages produced 2-

75 ceptor IL-18R, which comprises two subunits: IL-18R alpha and IL-18R beta.

76 bsence of the MyD88 pathway, indicating that IL-18R is a critical MyD88-upstream pathway involved in

77 This suggests that IL-18R beta-induced conformational changes may occur in

78 monstrate, in a murine modeling system, that IL-18R signaling plays a critical role in the pathogenes

79 The IL-18R beta cDNA was cloned from a human T-B lymphoblast

80 The IL-18R pathway, but not IL-1R, was required for early in

81 Ab against the IL-18R alpha chain, however, prevented IL-18 responsiven

82 ulation of the type 1 IL-1R (IL-1R1) and the IL-18R by their cognate ligands induces recruitment of t

83 fer experiments, we found that MyD88 and the IL-18R were required in a radioresistant cell in the sen

84 ing the majority of TLRs, the IL-1R, and the IL-18R, use a common adaptor molecule, MyD88, for transd

85 Effects of IL-18 were mediated by the IL-18R because they were absent in neurons from animals

86 tion in MEF cells from mice deficient in the IL-18R alpha-chain (IL-18Ralpha) compared with wild type

87 to IL-18, despite abundant expression of the IL-18R alpha chain.

88 nclude that functional reconstitution of the IL-18R beta chain is essential for IL-12-independent pro

89 COS-1 cells lack expression of the IL-18R beta chain.

90 l as concomitant signaling downstream of the IL-18R, suggests an IL-18-dependent mechanism in driving

91 uced, and Stat4-dependent, expression of the IL-18R.

92 To study the IL-18R complex, [(125)I]IL-18 was studied for binding to

93 binding of IL-18 to IL-18R alpha and to the IL-18R alpha/beta complex.

94 a weak affinity for IL-18 binding, while the IL-18R alpha/beta complex has a high affinity.

95 cells were transiently transfected with the IL-18R beta chain and a luciferase reporter.

96 siveness in COS-1 cells transfected with the IL-18R beta chain, suggesting that both chains be functi

97 Melanoma cells with and without the IL-18R/VEGF/VLA-4 phenotype had distinct transcript patt

98 re genes from melanomas with and without the IL-18R/VEGF/VLA-4 phenotype may serve as diagnostic biom

99 terns of melanoma cells with and without the IL-18R/VEGF/VLA-4 phenotype.

100 ed melanoma cells with, but not without, the IL-18R/VEGF/VLA-4 phenotype.

101 er cross-linking, [(125)I]IL-18 formed three IL-18R complexes with sizes of approximately 93, 160, an

102 hibitors could block the binding of IL-18 to IL-18R alpha and to the IL-18R alpha/beta complex.

103 Here we show that IL-18 binding to IL-18R alpha was inhibited by a neutralizing mAb, 125-2H

104 malous, as it exhibits little resemblance to IL-18R proteins.

105 apid graft failure (P = 0.024; IL-18- versus IL-18R-deficient grafts in WT recipients).

106 the formation of IL-18R ternary complex with IL-18R beta-chain.