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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.
8 sted using in vivo and in vitro IEC-specific IL-10 receptor 1 (IL-10R1) depletion under homeostatic c
10 ithin the YXXQ-STAT3-docking site within the IL-10 receptor 1 and that no other signals appeared to b
11 STAT protein phosphorylation is identical to IL-10 receptor activation on normal cells and similar to
13 ed more IL-10 and expressed higher levels of IL-10 receptor after CD40 engagement compared to other B
14 ated IL-10) is a first-in-class, long-acting IL-10 receptor agonist that induces oligoclonal T-cell e
16 pe, IL-10 reporter, and conditional IL-10 or IL-10 receptor alpha (IL-10Ralpha) knockout mice by mean
17 that Treg cells possess higher expression of IL-10 receptor alpha and that Treg cell IL-10 receptor a
18 analysis of the intracellular domain of the IL-10 receptor alpha chain showed that whereas two redun
19 n of IL-10 receptor alpha and that Treg cell IL-10 receptor alpha expression directly correlates with
21 vealed that the epithelial anti-inflammatory IL-10 receptor alpha subunit (IL-10RA) is also important
22 protein 3 (FOXP3), CD40 ligand (CD40L), and IL-10 receptor alpha(IL10RA), as well as patients with t
23 ore rapidly in the presence of an anti-human IL-10 receptor-alpha antibody, and efferocytosis by IL-1
25 e IL-2 receptor gamma(IL2RG) gene as well as IL-10 receptor and CD40 ligand deficiencies had normal o
26 , designated cmvIL-10, binds to the cellular IL-10 receptor and effects potent immune suppression.
27 xtracellular domain of the recombinant human IL-10 receptor and IL-10 is consistent with two IL-10 ho
28 IL-10 provides neuroprotection by acting via IL-10 receptor and PI3K/AKT and STAT-3 signal transducti
32 (+) T cells expressed elevated levels of the IL-10 receptor and were directly activated by IL-10, res
33 fects were specifically mediated through the IL-10 receptor and were not observed when DCs were treat
36 ignificant upregulation of HLA-C, HLA-G, the IL-10 receptor, and other markers involved in innate imm
37 he overexpression of interleukin-10 (IL-10), IL-10 receptor, and suppressor of cytokine signaling (SO
38 ansiently during the chronic phase with anti-IL-10 receptor antibodies achieved sterile cure, suggest
40 nositide 3-kinase (PI3K) inhibitor, and anti-IL-10 receptor antibody revealed that the PI3K pathway i
42 e anti-inflammatory effects of IL-37 because IL-10-receptor antibody blockade did not reverse IL-37-m
44 class II cytokine receptor that consisted of IL-10 receptor beta (IL-10Rbeta) and an orphan class II
45 lymorphism (A/G) at cDNA position 238 of the IL-10 receptor beta gene (IL10RB/c238) was genotyped in
46 present study, we examined variation in the IL-10 receptor beta gene as a further test of the hypoth
47 increased 6.5-fold and minimal responses to IL-10 receptor blockade suggested downregulated IL-10.
48 ice, migration assays, and antibody-mediated IL-10 receptor blockade to study plasmacytosis-associate
51 cytokine-inhibited mice were treated with an IL-10 receptor blocking antibody and a TLR-9 agonist, an
54 sponses are enhanced in the presence of anti-IL-10 receptor-blocking Abs or on the removal of CD14+ c
55 esistance because its neutralization with an IL-10 receptor-blocking monoclonal antibody allowed accu
56 s directly recruited to the ligand-activated IL-10 receptor by binding to specific but redundant rece
59 an accessory chain essential for the active IL-10 receptor complex and to initiate IL-10-induced sig
60 re, we explored whether the stability of the IL-10 receptor complex contributes to the immunomodulato
67 lysaccharide (LPS)-challenged mice harboring IL-10 receptor-deficient microglia displayed neuronal im
68 r mice (VertX), cell-type-specific IL-10 and IL-10 receptor deletion mice, and bone marrow chimeric m
69 , we demonstrated that transient blockade of IL-10 receptor during the T cell priming phase early in
73 f inhibition involved decreased cell surface IL-10 receptor expression and Jak1 activation and was de
74 We propose that CD8(+) T cells increase DRG IL-10 receptor expression and that IL-10 suppresses the
76 est that to optimize TR1 cell-based therapy, IL-10 receptor expression has to be taken into considera
78 tudy, we undertook a biochemical analysis of IL-10 receptor expression on freshly isolated B-CLL cell
79 es compared with control monocytes, although IL-10 receptor expression was similar in SLE and control
83 infection in normal mice, anti-interleukin (IL)-10 receptor (IL-10R) monoclonal antibody (MAb) treat
84 oblot analysis was preformed to identify the IL-10 receptor (IL-10R) and phosphorylated or nonphospho
85 eiotropy by determining the structure of the IL-10 receptor (IL-10R) complex by cryo-electron microsc
90 ulated with Helicobacter hepaticus plus anti-IL-10 receptor (IL-10R) monoclonal antibody was exacerba
91 0 within tumors, and therapeutic blockade of IL-10 receptor (IL-10R) was equivalent to CSF-1 neutrali
94 ection upregulated IL-10R1, a subunit of the IL-10 receptor (IL-10R), and also SOCS3, a negative regu
97 e cells, we previously demonstrated that the IL-10 receptor (IL-10R1) is expressed in dorsal root gan
98 ically, we generated mice harboring IL-10 or IL-10 receptor (IL-10Ralpha) mutations in intestinal lam
101 Genetic ablation of Axl and Mertk in M s or IL-10 receptor in DCs or Timp1 substantially reduced MPE
103 4(+) T cells differentially express IL-6 and IL-10 receptors in an activation state-dependent manner,
104 4 and IL-10, promoted clustering of IL-4 and IL-10 receptors in sensory neurons, leading to unique si
105 In contrast, an antagonistic antibody to the IL-10 receptor increased LPS-induced hepatomegaly by as
106 duction requires two distinct regions of the IL-10 receptor intracellular domain and thereby establis
110 , IL-10R1, the ligand-binding subunit of the IL-10 receptor, is predominantly expressed by TNF-produc
112 These results suggest complex regulation of IL-10 receptor-ligand interactions and subsequent biolog
113 Last, mice with muscle-specific ablation of IL-10 receptor (M-IL10R(-/-)) were generated to determin
114 it to evade host immune reactions through an IL-10 receptor mediated immune-suppression pathway.
118 presence on the intracellular domain of the IL-10 receptor of a carboxyl-terminal sequence containin
119 interleukin-10 (IL-10), which activated the IL-10 receptor on HSCs to dampen their profibrotic activ
120 reases macrophage-derived IL-10 signaling to IL-10 receptors on Advillin+ sensory neurons to resolve
124 oduction in lesions, and blocking the murine IL-10 receptor prevented antibody-mediated disease exace
125 -339) peptide antigen, together with an anti-IL-10 receptor (R) mAb led to the enhancement of a Th1 r
126 t with a functional blocking antibody to the IL-10 receptor reduced both Stat-3 and AKT phosphorylati
127 dministration of an antibody that blocks the IL-10 receptor restored T-cell function and eliminated v
130 ese events were prevented by either blocking IL-10 receptor signaling or inhibiting proteasome degrad
132 mice and transgenic mice with impairment in IL-10 receptor signaling were used to test the activity
135 t specificity and express between 47 and 127 IL-10 receptor sites per cell, with a dissociation const
136 ansgenic mice expressing a dominant-negative IL-10 receptor specifically in T cells (CD4dnIL-10Ralpha
137 domization analysis ahowed that the APOE and IL-10 receptor subunit B genes were causally linked to i
138 hat muscle cells in mdx muscle expressed the IL-10 receptor, suggesting that IL-10 could have direct
139 od dendritic cells were found to express the IL-10 receptor, suggesting that IL-10 may directly act o
140 in binding of one or more components of the IL-10 receptor system, and thus the structural differenc
141 different molecular mechanisms to engage the IL-10 receptors that ultimately enhance the respective a
142 ) protein recruitment to the interleukin 10 (IL-10) receptor, the STAT proteins activated by IL-10 in
143 ertheless, the signaling pathway used by the IL-10 receptor to generate the anti-inflammatory respons
145 7) in the intracellular domain of the murine IL-10 receptor were found to be redundantly required for