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1 sis of the interaction between IL-10 and the IL-10 receptor.
2 -10-mediated effects and is a subunit of the IL-10 receptor.
3 Ba/F3 cells that stably expressed the murine IL-10 receptor.
4 histochemistry that cortical neurons express IL-10 receptor.
5 odies specific for interleukin-10 (IL-10) or IL-10 receptor.
6 production from microglial cells through the IL-10 receptor.
7 n of KC, even though the cells expressed the IL-10 receptor.
9 ithin the YXXQ-STAT3-docking site within the IL-10 receptor 1 and that no other signals appeared to b
10 STAT protein phosphorylation is identical to IL-10 receptor activation on normal cells and similar to
12 ed more IL-10 and expressed higher levels of IL-10 receptor after CD40 engagement compared to other B
13 that Treg cells possess higher expression of IL-10 receptor alpha and that Treg cell IL-10 receptor a
14 analysis of the intracellular domain of the IL-10 receptor alpha chain showed that whereas two redun
15 n of IL-10 receptor alpha and that Treg cell IL-10 receptor alpha expression directly correlates with
17 vealed that the epithelial anti-inflammatory IL-10 receptor alpha subunit (IL-10RA) is also important
18 protein 3 (FOXP3), CD40 ligand (CD40L), and IL-10 receptor alpha(IL10RA), as well as patients with t
19 ore rapidly in the presence of an anti-human IL-10 receptor-alpha antibody, and efferocytosis by IL-1
21 e IL-2 receptor gamma(IL2RG) gene as well as IL-10 receptor and CD40 ligand deficiencies had normal o
22 , designated cmvIL-10, binds to the cellular IL-10 receptor and effects potent immune suppression.
23 xtracellular domain of the recombinant human IL-10 receptor and IL-10 is consistent with two IL-10 ho
24 IL-10 provides neuroprotection by acting via IL-10 receptor and PI3K/AKT and STAT-3 signal transducti
28 (+) T cells expressed elevated levels of the IL-10 receptor and were directly activated by IL-10, res
29 fects were specifically mediated through the IL-10 receptor and were not observed when DCs were treat
32 he overexpression of interleukin-10 (IL-10), IL-10 receptor, and suppressor of cytokine signaling (SO
33 ansiently during the chronic phase with anti-IL-10 receptor antibodies achieved sterile cure, suggest
35 nositide 3-kinase (PI3K) inhibitor, and anti-IL-10 receptor antibody revealed that the PI3K pathway i
37 e anti-inflammatory effects of IL-37 because IL-10-receptor antibody blockade did not reverse IL-37-m
38 class II cytokine receptor that consisted of IL-10 receptor beta (IL-10Rbeta) and an orphan class II
39 lymorphism (A/G) at cDNA position 238 of the IL-10 receptor beta gene (IL10RB/c238) was genotyped in
40 present study, we examined variation in the IL-10 receptor beta gene as a further test of the hypoth
41 increased 6.5-fold and minimal responses to IL-10 receptor blockade suggested downregulated IL-10.
42 ice, migration assays, and antibody-mediated IL-10 receptor blockade to study plasmacytosis-associate
45 cytokine-inhibited mice were treated with an IL-10 receptor blocking antibody and a TLR-9 agonist, an
48 sponses are enhanced in the presence of anti-IL-10 receptor-blocking Abs or on the removal of CD14+ c
49 esistance because its neutralization with an IL-10 receptor-blocking monoclonal antibody allowed accu
50 s directly recruited to the ligand-activated IL-10 receptor by binding to specific but redundant rece
52 an accessory chain essential for the active IL-10 receptor complex and to initiate IL-10-induced sig
57 r mice (VertX), cell-type-specific IL-10 and IL-10 receptor deletion mice, and bone marrow chimeric m
58 , we demonstrated that transient blockade of IL-10 receptor during the T cell priming phase early in
61 f inhibition involved decreased cell surface IL-10 receptor expression and Jak1 activation and was de
62 We propose that CD8(+) T cells increase DRG IL-10 receptor expression and that IL-10 suppresses the
64 est that to optimize TR1 cell-based therapy, IL-10 receptor expression has to be taken into considera
66 tudy, we undertook a biochemical analysis of IL-10 receptor expression on freshly isolated B-CLL cell
67 es compared with control monocytes, although IL-10 receptor expression was similar in SLE and control
69 infection in normal mice, anti-interleukin (IL)-10 receptor (IL-10R) monoclonal antibody (MAb) treat
70 oblot analysis was preformed to identify the IL-10 receptor (IL-10R) and phosphorylated or nonphospho
75 ulated with Helicobacter hepaticus plus anti-IL-10 receptor (IL-10R) monoclonal antibody was exacerba
76 0 within tumors, and therapeutic blockade of IL-10 receptor (IL-10R) was equivalent to CSF-1 neutrali
79 ection upregulated IL-10R1, a subunit of the IL-10 receptor (IL-10R), and also SOCS3, a negative regu
82 ically, we generated mice harboring IL-10 or IL-10 receptor (IL-10Ralpha) mutations in intestinal lam
85 4(+) T cells differentially express IL-6 and IL-10 receptors in an activation state-dependent manner,
86 In contrast, an antagonistic antibody to the IL-10 receptor increased LPS-induced hepatomegaly by as
87 duction requires two distinct regions of the IL-10 receptor intracellular domain and thereby establis
91 , IL-10R1, the ligand-binding subunit of the IL-10 receptor, is predominantly expressed by TNF-produc
92 These results suggest complex regulation of IL-10 receptor-ligand interactions and subsequent biolog
93 Last, mice with muscle-specific ablation of IL-10 receptor (M-IL10R(-/-)) were generated to determin
98 presence on the intracellular domain of the IL-10 receptor of a carboxyl-terminal sequence containin
101 oduction in lesions, and blocking the murine IL-10 receptor prevented antibody-mediated disease exace
102 -339) peptide antigen, together with an anti-IL-10 receptor (R) mAb led to the enhancement of a Th1 r
103 t with a functional blocking antibody to the IL-10 receptor reduced both Stat-3 and AKT phosphorylati
104 dministration of an antibody that blocks the IL-10 receptor restored T-cell function and eliminated v
107 ese events were prevented by either blocking IL-10 receptor signaling or inhibiting proteasome degrad
109 mice and transgenic mice with impairment in IL-10 receptor signaling were used to test the activity
111 t specificity and express between 47 and 127 IL-10 receptor sites per cell, with a dissociation const
112 ansgenic mice expressing a dominant-negative IL-10 receptor specifically in T cells (CD4dnIL-10Ralpha
113 hat muscle cells in mdx muscle expressed the IL-10 receptor, suggesting that IL-10 could have direct
114 od dendritic cells were found to express the IL-10 receptor, suggesting that IL-10 may directly act o
115 in binding of one or more components of the IL-10 receptor system, and thus the structural differenc
116 different molecular mechanisms to engage the IL-10 receptors that ultimately enhance the respective a
117 ) protein recruitment to the interleukin 10 (IL-10) receptor, the STAT proteins activated by IL-10 in
118 ertheless, the signaling pathway used by the IL-10 receptor to generate the anti-inflammatory respons
119 7) in the intracellular domain of the murine IL-10 receptor were found to be redundantly required for
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