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1 going chronic inflammation and production of interleukin 23.
2 nt and correlated with reduced production of interleukin 23.
3 he receptor for the proinflammatory cytokine interleukin-23.
4 representative scaffolds and panned against interleukin-23.
5 hemokine genes, including the p19 subunit of interleukin-23.
6 ed levels of tumor necrosis factor alpha and interleukin-23.
7 discovery of the biological functions of the interleukin-23/-17 axis led to the identification of IL-
10 b, an antibody that binds the p40 subunit of interleukin-23 and interleukin-12 and thereby blocks the
12 expressed high levels of interleukin-1beta, interleukin-23 and interleukin-6, and promoted T-helper
13 cts of lipopolysaccharide on interleukin-12, interleukin-23, and matrix metalloproteinase-9, suggesti
15 t dominates the binding affinity for an anti-interleukin-23 (anti-IL-23) antibody by using the comple
17 c agents, ustekinumab (an interleukin-12 and interleukin-23 blocker) and etanercept (an inhibitor of
18 ptor-induced secretion of interleukin-12 and interleukin-23 by DCs in an autocrine manner, promoted d
19 nized IgG1 monoclonal antibody that inhibits interleukin-23 by specifically targeting the p19 subunit
22 the activity of these cytokines, inhibiting interleukin-23-dependent production of interleukin-17.
26 atus lung infection in the presence of lower interleukin 23 (IL-23) and IL-17A production in the lung
27 cteria requires the sequential generation of interleukin 23 (IL-23) and IL-22 to induce protective mu
32 ytokine interleukin 12p70 and an increase in interleukin 23 (IL-23) production by gp120-treated mDCs.
34 egies to examine the effect that blockade of interleukin 23 (IL-23) signaling had on GVH and GVL reac
38 17 helper T cell (TH17)-associated cytokine interleukin 23 (IL-23), which was associated with positi
39 r 'imprinted' signaling via the receptor for interleukin 23 (IL-23R) in responding T cells to promote
41 ed to chronic inflammation, particularly via interleukin-23 (IL-23) and IL-17 signaling pathways.
44 tion of LMP7 by PR-957 blocked production of interleukin-23 (IL-23) by activated monocytes and interf
45 this study, we have identified secretion of interleukin-23 (IL-23) by donor antigen-presenting cells
55 accumulated, phagocytosis was impaired, and interleukin-23 (IL-23) production was reduced in Muc5b(-
56 ed by LPS/HI have elevated expression of the interleukin-23 (IL-23) receptor, a marker of early TH17
59 ion of effector CD4(+) T cells stimulated by interleukin-23 (IL-23), but whether these cells are requ
61 Maintenance of the Th17 phenotype requires interleukin-23 (IL-23), whereas the Th1-promoting cytoki
63 for eosinophils as crucial effectors of the interleukin-23 (IL-23)-granulocyte macrophage colony-sti
65 d the influence of morphine treatment on the interleukin-23 (IL-23)/IL-17 axis and related innate imm
66 Immunity to OPC is strongly dependent on the interleukin-23 (IL-23)/IL-17R axis, as mice and humans w
69 onoclonal antibody that selectively inhibits interleukin 23 (IL23), a cytokine implicated in the path
70 define a role for TLR-mediated production of interleukin-23 in immune cell homing and pathogenesis.
71 clonal antibody targeting the p19 subunit of interleukin-23, in patients with moderately-to-severely
72 This action of GM-CSF is mediated by its interleukin-23-inducing activity rather than its role as
73 ling, and ustekinumab, an interleukin-12 and interleukin-23 inhibitor, in patients with moderate-to-s
74 n 6, interleukin 10, IL-17A, interleukin 22, interleukin 23, interferon gamma, kynurenine, and trypto
75 s initiates a cytokine cascade that includes interleukin-23, interleukin-17, and ultimately granulocy
76 D patients did not produce excess amounts of interleukin-23, interleukin-17, or tumor necrosis factor
78 The discovery of CD4+ Th17 T cells and the interleukin-23/interleukin-17 axis has challenged existi
79 olded protein response and activation of the interleukin-23/interleukin-17 axis have been observed in
81 cells and emerging data suggesting that the interleukin-23/interleukin-17 axis may be involved in th
82 -genome association studies suggest that the interleukin-23/interleukin-17 axis plays an important ro
83 beta and interleukin-6 are critical, whereas interleukin-23 is more important at later stages promoti
86 we compared guselkumab (CNTO 1959), an anti-interleukin-23 monoclonal antibody, with adalimumab in p
87 ty, humanised, IgG1 kappa antibody targeting interleukin 23 p19 that represents an evolving treatment
89 nflammatory cytokine production, depended on interleukin-23 p19 secretion, whereas interleukin-12 p35
91 nes that encode factors that function in the interleukin-23 pathway have been associated with a numbe
93 otably, genes whose products function in the interleukin-23 pathway, and transcription factors, inclu
95 NF), major histocompatibility complex (MHC), interleukin 23 receptor (IL23R) and protein tyrosine pho
96 as well as murine models have shown that the interleukin 23 receptor (IL23R) pathway plays a pivotal
97 cleotide polymorphisms (SNPs) mapping to the interleukin-23 receptor (IL-23R) and IL-12beta genes wit
98 ous European studies suggest NOD2/CARD15 and interleukin-23 receptor (IL-23R) donor or recipient vari
100 targeting the p19 subunit and thus prevents interleukin-23 signaling, and ustekinumab, an interleuki
103 ophagy (eg, ATG16L1, IRGM), and genes in the interleukin-23-T helper cell 17 pathway indicate the imp
104 of pivotal mucosal cytokines, including the interleukin-23/T helper 17 cytokine, interleukin-22.
106 e is known about the effect of specific anti-interleukin-23 therapy, as compared with established ant
109 ody to the p40 subunit of interleukin-12 and interleukin-23, was evaluated as an intravenous inductio
110 tion (MCP1, tumor necrosis factor-alpha, and interleukin-23) were significantly attenuated, whereas a
111 anism involves GM-CSF-mediated production of interleukin-23, which increases apoptosis susceptibility
112 In this phase 2 trial, selective blockade of interleukin-23 with risankizumab was associated with cli
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