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1 autoantibodies against interleukin-23 (anti-interleukin-23).
2 going chronic inflammation and production of interleukin 23.
3 nt and correlated with reduced production of interleukin 23.
4 he receptor for the proinflammatory cytokine interleukin-23.
5 0%) also had autoantibodies that neutralized interleukin-23.
6 monoclonal antibody, binds to subunit p19 of interleukin-23.
7 representative scaffolds and panned against interleukin-23.
8 hemokine genes, including the p19 subunit of interleukin-23.
9 ed levels of tumor necrosis factor alpha and interleukin-23.
10 discovery of the biological functions of the interleukin-23/-17 axis led to the identification of IL-
12 i infection, the identification of both anti-interleukin-23 and anti-interleukin-12 prompted further
15 b, an antibody that binds the p40 subunit of interleukin-23 and interleukin-12 and thereby blocks the
18 expressed high levels of interleukin-1beta, interleukin-23 and interleukin-6, and promoted T-helper
19 cts of lipopolysaccharide on interleukin-12, interleukin-23, and matrix metalloproteinase-9, suggesti
21 r modulators, interleukin 12/23 or selective interleukin 23 antagonists, and Janus kinase [JAK] inhib
22 t dominates the binding affinity for an anti-interleukin-23 (anti-IL-23) antibody by using the comple
25 ist of the p40 subunit of interleukin-12 and interleukin-23, as induction and maintenance therapy in
26 c agents, ustekinumab (an interleukin-12 and interleukin-23 blocker) and etanercept (an inhibitor of
27 ptor-induced secretion of interleukin-12 and interleukin-23 by DCs in an autocrine manner, promoted d
28 nized IgG1 monoclonal antibody that inhibits interleukin-23 by specifically targeting the p19 subunit
32 the activity of these cytokines, inhibiting interleukin-23-dependent production of interleukin-17.
36 or; 3982 (23.6%), with an interleukin 12 and interleukin 23 (IL-12/23) inhibitor; and 2711 (16.0%), w
38 atus lung infection in the presence of lower interleukin 23 (IL-23) and IL-17A production in the lung
39 cteria requires the sequential generation of interleukin 23 (IL-23) and IL-22 to induce protective mu
46 ytokine interleukin 12p70 and an increase in interleukin 23 (IL-23) production by gp120-treated mDCs.
48 egies to examine the effect that blockade of interleukin 23 (IL-23) signaling had on GVH and GVL reac
52 17 helper T cell (TH17)-associated cytokine interleukin 23 (IL-23), which was associated with positi
53 r 'imprinted' signaling via the receptor for interleukin 23 (IL-23R) in responding T cells to promote
55 ed to chronic inflammation, particularly via interleukin-23 (IL-23) and IL-17 signaling pathways.
56 Stress increased the TLO formation cytokines interleukin-23 (IL-23) and IL-22 followed by up-regulati
57 iciently low to impair cellular responses to interleukin-23 (IL-23) and partially IL-12, but not othe
60 tion of LMP7 by PR-957 blocked production of interleukin-23 (IL-23) by activated monocytes and interf
61 this study, we have identified secretion of interleukin-23 (IL-23) by donor antigen-presenting cells
63 re associated with SNPs in the IL-23R or the interleukin-23 (IL-23) cytokine itself and related downs
72 % CI, 1.10-2.63) and activating genes in the interleukin-23 (IL-23) pathway (odds ratio, 1.55; 95% CI
74 accumulated, phagocytosis was impaired, and interleukin-23 (IL-23) production was reduced in Muc5b(-
75 ed by LPS/HI have elevated expression of the interleukin-23 (IL-23) receptor, a marker of early TH17
76 is mounting evidence for a critical role of interleukin-23 (IL-23) signaling in the pathogenesis of
77 that epithelial cell-intrinsic production of interleukin-23 (IL-23) triggers an inflammatory loop in
81 ion of effector CD4(+) T cells stimulated by interleukin-23 (IL-23), but whether these cells are requ
83 Maintenance of the Th17 phenotype requires interleukin-23 (IL-23), whereas the Th1-promoting cytoki
85 for eosinophils as crucial effectors of the interleukin-23 (IL-23)-granulocyte macrophage colony-sti
88 d the influence of morphine treatment on the interleukin-23 (IL-23)/IL-17 axis and related innate imm
89 Immunity to OPC is strongly dependent on the interleukin-23 (IL-23)/IL-17R axis, as mice and humans w
91 d high affinity and selectivity to the human interleukin-23 (IL-23R) and IL-17 receptor A were used.
95 onoclonal antibody that selectively inhibits interleukin 23 (IL23), a cytokine implicated in the path
96 define a role for TLR-mediated production of interleukin-23 in immune cell homing and pathogenesis.
98 clonal antibody targeting the p19 subunit of interleukin-23, in patients with moderately-to-severely
99 This action of GM-CSF is mediated by its interleukin-23-inducing activity rather than its role as
101 gher-than-approved doses of risankizumab, an interleukin-23 inhibitor, for treatment of moderate-to-s
102 ling, and ustekinumab, an interleukin-12 and interleukin-23 inhibitor, in patients with moderate-to-s
103 n 6, interleukin 10, IL-17A, interleukin 22, interleukin 23, interferon gamma, kynurenine, and trypto
104 s initiates a cytokine cascade that includes interleukin-23, interleukin-17, and ultimately granulocy
105 D patients did not produce excess amounts of interleukin-23, interleukin-17, or tumor necrosis factor
107 The discovery of CD4+ Th17 T cells and the interleukin-23/interleukin-17 axis has challenged existi
108 olded protein response and activation of the interleukin-23/interleukin-17 axis have been observed in
110 cells and emerging data suggesting that the interleukin-23/interleukin-17 axis may be involved in th
111 -genome association studies suggest that the interleukin-23/interleukin-17 axis plays an important ro
112 beta and interleukin-6 are critical, whereas interleukin-23 is more important at later stages promoti
115 we compared guselkumab (CNTO 1959), an anti-interleukin-23 monoclonal antibody, with adalimumab in p
116 ty, humanised, IgG1 kappa antibody targeting interleukin 23 p19 that represents an evolving treatment
118 nflammatory cytokine production, depended on interleukin-23 p19 secretion, whereas interleukin-12 p35
120 nes that encode factors that function in the interleukin-23 pathway have been associated with a numbe
122 otably, genes whose products function in the interleukin-23 pathway, and transcription factors, inclu
124 NF), major histocompatibility complex (MHC), interleukin 23 receptor (IL23R) and protein tyrosine pho
126 as well as murine models have shown that the interleukin 23 receptor (IL23R) pathway plays a pivotal
127 cleotide polymorphisms (SNPs) mapping to the interleukin-23 receptor (IL-23R) and IL-12beta genes wit
129 ous European studies suggest NOD2/CARD15 and interleukin-23 receptor (IL-23R) donor or recipient vari
132 s and genetically predicted body mass index, interleukin-23 receptor, and eight circulating proteins.
133 eted oral peptide that selectively binds the interleukin-23 receptor, compared with both placebo and
134 eted oral peptide that selectively binds the interleukin-23 receptor, is under investigation for the
135 aily oral administration, treatment with the interleukin-23-receptor antagonist peptide JNJ-77242113
136 JNJ-77242113 is a novel, orally administered interleukin-23-receptor antagonist peptide that selectiv
139 Mirikizumab, a p19-directed antibody against interleukin-23, showed efficacy in the treatment of ulce
140 r antagonist peptide that selectively blocks interleukin-23 signaling and downstream cytokine product
141 targeting the p19 subunit and thus prevents interleukin-23 signaling, and ustekinumab, an interleuki
145 ophagy (eg, ATG16L1, IRGM), and genes in the interleukin-23-T helper cell 17 pathway indicate the imp
146 of pivotal mucosal cytokines, including the interleukin-23/T helper 17 cytokine, interleukin-22.
148 e is known about the effect of specific anti-interleukin-23 therapy, as compared with established ant
150 umor necrosis factor and anti-interleukin-12/interleukin-23 treatment on SB and colonic ACE2 expressi
152 patients with thymoma, the presence of anti-interleukin-23 was associated with infection status in 7
153 nfections, the presence of neutralizing anti-interleukin-23 was associated with severe, persistent op
157 l antibody and anti-p19 subunit inhibitor of interleukin-23, was demonstrated in a phase 2a trial in
158 ody to the p40 subunit of interleukin-12 and interleukin-23, was evaluated as an intravenous inductio
159 tion (MCP1, tumor necrosis factor-alpha, and interleukin-23) were significantly attenuated, whereas a
160 anism involves GM-CSF-mediated production of interleukin-23, which increases apoptosis susceptibility
162 In this phase 2 trial, selective blockade of interleukin-23 with risankizumab was associated with cli