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1 n contrast to the mitogenic receptors IL-3R, IL-5R, GM-CSFR, which assemble as alphabeta heterodimers
2 ne receptor (interleukin-3 receptor [IL-3R], IL-5R, and granulocyte-macrophage colony stimulating fac
7 op a multiplex assay, in which the IL-1R and IL-5R assays were carried out in the same well with each
8 the structural interactions between IL-5 and IL-5R and the functional consequences of such interactio
10 sted of the ectodomains of the GMR-alpha and IL-5R alpha, respectively, fused to the endodomain of IL
11 or with IL-2, increased both IL-5R alpha and IL-5R beta mRNA and decreased soluble IL-5R alpha mRNA.
12 tyrosine phosphorylation of JAK2 kinase and IL-5R beta-chain and inhibited IL-5 priming of leukotrie
13 inophils, IL-5R alpha gene transcription and IL-5R alpha mRNA metabolism can be regulated by mechanis
16 th IL-5 for binding to the native alpha beta IL-5R on human cells and inhibited IL-5-mediated recepto
17 eotide technology targeting the common betac IL-5R subunit is also being used therapeutically to inhi
18 or SAC, without or with IL-2, increased both IL-5R alpha and IL-5R beta mRNA and decreased soluble IL
19 is composed of an IL-5-binding alpha-chain (IL-5R alpha) and a signal-transducing beta-chain that is
21 their degradation, ubiquitination-deficient IL-5Rs accumulated on the cell surface and displayed blu
22 experiments that in human blood eosinophils, IL-5R alpha gene transcription and IL-5R alpha mRNA meta
23 mmunoreactive major basic protein, Siglec F, IL-5R alpha-chain, and transcripts encoding mouse eosino
24 e B cells, human B cells express message for IL-5R but can respond to IL-5 only if appropriately stim
25 ligand, with the maximum effect observed for IL-5R, consistent with the clinical phenotype of eosinop
29 onstrate that cytokine-induced inhibition of IL-5R alpha mRNA accumulation occurs at the level of IL-
30 pha mRNA accumulation occurs at the level of IL-5R alpha gene transcription, whereas enhanced accumul
32 ree cytokines on eosinophils and the loss of IL-5R on airway eosinophils, it is important to take IL-
33 rization reveals that the down-regulation of IL-5R alpha mRNA is specific to IL-3, IL-5, and GM-CSF;
35 rget the eosinophilic inflammatory pathways (IL-5R and IL-5), namely mepolizumab, reslizumab, and ben
37 nd activation of the interleukin-5 receptor (IL-5R) or of the granulocyte-macrophage colony-stimulati
38 lly dependent on IL-5 and the IL-5 receptor (IL-5R), composed of a ligand binding alpha chain (IL-5Ra
39 st, benralizumab binds to the IL-5 receptor (IL-5R), preventing IL-5 from binding and leading to subs
40 tokines IL-5, IL-3, and GM-CSF down-regulate IL-5R alpha mRNA while up-regulating alpha-chain mRNAs f
41 for the IL-5R alpha, IL-5R beta, and soluble IL-5R alpha chains was detected in freshly isolated B ce
45 mab (MEDI-563), has been developed to target IL-5R and attenuate eosinophilia through antibody-depend
47 B cells with IL-4 induced expression of the IL-5R alpha-chain, while signaling through membrane Ig s
51 interaction of the dimeric peptide with two IL-5R alpha chains represents a distinctive mechanism fo