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these findings provide a novel mechanism by which microbial-derived butyrate promotes barrier through IL-10RA-dependent repression of claudin-2 (show CLDN2 ELISA Kits)
Expression of IL10R subunits within the leukocyte population (CD45 (show PTPRC ELISA Kits)(+) cells) was significantly higher in primary brain tumors than in metastases.
This study showed that lack of association with schizophrenia was detected for IL10 (show IL10 ELISA Kits) and IL10RA single polymorphisms and haplotypes.
The IL-10RA rs9610 A allele was increased in rheumatoid arthritis (RA) patient group compared with control subjects. Interestingly, significant differences were detected both in the allele and genotype frequencies of rs9610 between anti-CCP (show CRYGD ELISA Kits) (anti-cyclic citrullinated peptide) positive patients and anti-CCP (show CRYGD ELISA Kits) negative patients. The findings suggest that IL-10RA rs9610 polymorphism might contribute to RA susceptibility.
The quantitative methods used in this study have shown non-altered expression levels of different microglial markers (Iba-1 (show AIF1 ELISA Kits), Cd11b (show ITGAM ELISA Kits) and CD68 (show CD68 ELISA Kits)), together with increased expression of IL6 (show IL6 ELISA Kits), IL10RA, colony stimulating factor (show CSF2 ELISA Kits) 3 receptor and toll-like receptor 7 (show TLR7 ELISA Kits) in the thalamus in FFI, which explains the seemingly contradictory results of the previous studies.
These results suggest that S138G loss-of-function polymorphism of the IL-10R1 may be important risk factor in increasing susceptibility to multiple sclerosis.
Results reveal the structure of box1 from class II cytokine receptors IFNLR1 (show IL28RA ELISA Kits) and IL10RA bound to the FERM-SH2 domain of human JAK1 (show JAK1 ELISA Kits), identifying a consensus motif for JAK1 (show JAK1 ELISA Kits) interaction.
Interleukin 10 (show IL10 ELISA Kits) and interleukin 10 receptor (show IL10RB ELISA Kits) expression was also enriched in interferon gamma (show IFNG ELISA Kits)-expressing activated CD8 (show CD8A ELISA Kits)(+) T cells. Treatment of anti-CD3 (show CD3 ELISA Kits)/CD28 (show CD28 ELISA Kits)-stimulated, purified CD8 (show CD8A ELISA Kits)(+) T cells with interleukin 10 (show IL10 ELISA Kits) alone could significantly enhance CD8 (show CD8A ELISA Kits)(+) T cell survival, an effect dependent on interleukin 10 receptor (show IL10RB ELISA Kits) expression
a JAK2 (show JAK2 ELISA Kits) Inhibitor Suppresses a BCL6 (show BCL6 ELISA Kits)-dependent IL10RA/JAK2 (show JAK2 ELISA Kits)/STAT3 (show STAT3 ELISA Kits) Pathway in High Grade B-cell Lymphoma.
results suggest that IL10 (show IL10 ELISA Kits)-mediated inhibition of autophagy is facilitated by the cross talk between STAT3 (show STAT3 ELISA Kits), AKT (show AKT1 ELISA Kits), and mTOR (show FRAP1 ELISA Kits); in other words, the IL10 (show IL10 ELISA Kits)-IL10R-STAT3 (show STAT3 ELISA Kits) and IL10 (show IL10 ELISA Kits)-AKT (show AKT1 ELISA Kits)-mTOR (show FRAP1 ELISA Kits) pathways.
this study shows that the upregulation of IL-10Ra by STAT3 (show STAT3 ELISA Kits) contributed to the suppressive function of dendritic cellss following histone deacetylase (show HDAC1 ELISA Kits) inhibition
The investigation of the IL-10R complex revealed that both the extracellular and intracellular domains of IL-10R2 (show IL10RB ELISA Kits) influence the conformation of IL-10R1 and that both domains were required for transducing IL-10 (show IL10 ELISA Kits) signals.
ablation of IL-10 (show IL10 ELISA Kits) signaling in Th2 cells led to enhanced Th2 cell survival and exacerbated pulmonary inflammation in a murine model of house dust mite allergy
TR1 (show TXNRD1 ELISA Kits) cell regulatory activity is dependent on IL-10 (show IL10 ELISA Kits) receptor signaling.
loss of IL-10R signaling impaired the generation and function of anti-inflammatory intestinal and bone-marrow-derived macrophages and their ability to secrete IL-10 (show IL10 ELISA Kits).
loss of IL-10 (show IL10 ELISA Kits) receptor expression impaired the critical conditioning of monocyte-derived macrophages and resulted in spontaneous development of severe colitis.
Recent findings review how IL10 (show IL10 ELISA Kits)- and IL10R-dependent signaling modulates innate and adaptive immune responses in the murine intestine.
Treatment of mice with rIFN-gamma was sufficient to drive expression of IL-10R1 in the colonic epithelium. Intestinal epithelial-specific IL-10R1-null mice were more susceptible to DSS (show PMP22 ELISA Kits) colitis associated with increased intestinal permeability.
Inhibition of IL-10R signaling during bacillus Calmette-Guerin (BCG (show SLC11A1 ELISA Kits)) vaccination increases and balances IFN-gamma (show IFNG ELISA Kits) and IL-17A (show IL17A ELISA Kits) responses in favor of the host.
IL-10R subunit-alpha signaling plays a key role in the development as well as B-cell help function of T (follicular helper) cells in vitro and in vivo.
The protein encoded by this gene is a receptor for interleukin 10. This protein is structurally related to interferon receptors. It has been shown to mediate the immunosuppressive signal of interleukin 10, and thus inhibits the synthesis of proinflammatory cytokines. This receptor is reported to promote survival of progenitor myeloid cells through the insulin receptor substrate-2/PI 3-kinase/AKT pathway. Activation of this receptor leads to tyrosine phosphorylation of JAK1 and TYK2 kinases. Two transcript variants, one protein-coding and the other not protein-coding, have been found for this gene.
interleukin 10 receptor 1
, interleukin-10 receptor subunit alpha
, interleukin 10 receptor, alpha
, interleukin-10 receptor subunit alpha-like
, IL-10 receptor subunit alpha
, IL-10R subunit 1
, IL-10R subunit alpha
, interleukin-10 receptor alpha chain
, interleukin-10 receptor subunit 1