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

5 18, by other TLRs/inflammasome- and/or IL-1R/IL-18R-mediated signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 -4, -6, -7, -9, and -11 and IL-18 receptor (IL-18R) are not essential for MSU-induced inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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