MOUSE ANTI HUMAN CD86 Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: MOUSE ANTI HUMAN CD86 Azide Free
Catalog number: genta-ABS0309
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd86

Related genes to: MOUSE ANTI HUMAN CD86 Azide Free

Symbol : cd86 NIH gene
Synonyms : CD80/86
description : CD86 molecule
type of gene : protein-coding
Other designations : CD80/86 molecule|CD86 membrane protein long isoform
Modification date : 2015-11-14

Related Pathways to: MOUSE ANTI HUMAN CD86 Azide Free

Gene about :Cd86
Pathway :Rn Toll-like receptor signaling pathway
Cd86

Related product to: MOUSE ANTI HUMAN CD86 Azide Free

Related Articles about: MOUSE ANTI HUMAN CD86 Azide Free

TLR2 affects CD86 expression and inflammatory response in burn injury mice through regulation of p38.

The aim of this study was to assess the effects of TLR2/p38/CD86 signaling pathways on inflammatory response in a mouse model of burn injury. Wild-type (TLR2+/+) and mutant-type (TLR2-/-) mice were obtained, and a mouse burn injury model was constructed. Tissue samples were detected using HE staining and Transferase Mediated Nick End Labeling (TUNEL) method. Macrophages were treated with TLR2 agonist and p38 inhibitor. The expression levels of TLR2, p38, CD86, IL-1β and TNF-α were identified by RT-qPCR, Western blot and ELISA. When compared with the sham group, the burn group had significantly higher apoptosis rate as well as higher expressions of TLR2, p38, CD86, IL-1β and TNF-α. Inhibiting TLR2 was shown to significantly reduce the expressions of p-p38, CD86, IL-1β and TNF-α. In the results of in vitro experiments, TLR2 agonist was able to increase expressions of p-p38, CD86, IL-1β and TNF-α, while p38 inhibitor was shown to reduce expressions of CD86, IL-1β and TNF-α. Our results suggested that the TLR2/p38/CD86 signaling pathway plays a vital role in burn injury inflammation. - Source :PubMed

Decreased CD1d level is associated with CD86 over-expression in B cells from systemic lupus erythematosus.

The disorder of B cells is one of the hallmarks of systemic lupus erythematosus (SLE). The activation state indicated by CD86 of B cells from SLE is well known, while the defect of regulatory B cells mediated by CD1d is also responsible for the process of SLE. In the present study, we focused on the relationship between B cell activation mediated by CD86 and B cell regulatory function mediated by CD1d. Our results showed that the level of CD1d in B cells was decreased during the early stages of B6.MRLlpr SLE mice and imiquimod-treated (IMQ-treated) mice, while the level of CD86 was significantly increased at the late stage. Moreover, the expression of CD1d showed a significantly negative correlation with CD86 level in B cells from IMQ-treated mice (r = -05741; P = 0.0022), B6.MRLlpr mice (r = -0.7091; P = 0.0268), and SLE patients (r = -0.4125; P = 0.0404). The in vivo and in vitro experiments with splenocytes demonstrated that CD1d signaling pathway could inhibit toll-like receptor 7 (TLR7)-induced CD86 expression of B cells. Further studies showed that this relationship also affected antibody production. Thus, our results confirmed the association of CD1d and CD86 levels in B cells from SLE, and demonstrated the importance to preserve the immunoregulatory function of B cells mediated by CD1d in the progression of SLE. - Source :PubMed

Pemphigus vulgaris and pemphigus foliaceus determined by CD86 and CTLA4 polymorphisms.

Pemphigus vulgaris (PV) and pemphigus foliaceus (PF) are rare autoimmune blistering diseases with presumed T-cell-dependent pathology. Activation of naïve T cells is dependent on antigen recognition, subsequent signaling through the T-cell receptor complex (signal 1), and various other interactions of T cells with antigen presenting cells that may be collectively designated as signal 2, which is unconditionally required for T-cell activation both in response to infection and to autoantigens. Among the best described interactions contributing to signal 2 are those mediated by B7 family molecules, such as CD80 and CD86 with their ligands; CD28, providing activation signals; and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), conferring inhibition. Single nucleotide polymorphisms (SNPs) within genes encoding those molecules may alter the signaling process. It is not known whether functional genetic polymorphisms within genes encoding the aforementioned proteins may increase risk for developing PV and PF and, if so, whether they might serve as biomarkers for susceptibility to these diseases. To address those questions, we examined functional single nucleotide polymorphisms within CD86 (rs1129055) and CTLA4 (rs733618 and rs5742909) genes in 61 pemphigus patients and 486 healthy controls. We found statistically significant differences in allele and genotype frequencies between PV patients and controls for rs1129055, as well as for rs5742909 among PV and PF patients. Namely, the rs1129055 A allele was significantly more common in PV patients compared with controls (35.4% versus 25.7%, respectively; P = .040), whereas the rs5742909 T allele was significantly more common in PF compared with PV patients (19.2% versus 5.2%, respectively; P = .035). The frequency of the rs5742909 T allele did not, however, differ significantly in PF or in PV compared with controls (10.5%; P = .187 and P = .100, respectively). We report a novel association of SNPs within CD86 and CTLA4 genes with pemphigus. The CD86 rs1129055 A allele appears to confer susceptibility to PV but not to PF. © 2016 Elsevier Inc. All rights reserved. - Source :PubMed

Vitamin D reduces high-fat diet induced weight gain and C-reactive protein, increases interleukin-10, and reduces CD86 and caspase-3.

Obesity can be associated with dysfunction of the immune system. An increased risk of obesity has been reported among individuals with low levels of vitamin D. However, much is still unknown about the link between vitamin D and dysfunction of the spleen and immune system in obesity. Therefore, the objectives of this study were to evaluate the effects of a high-fat diet (HFD) on the spleen and immune system and to determine the protective effects of chronic treatment with vitamin D in reversing the detrimental effects of HFD. Body weight (BW) gain, the serum levels of calcium, C-reactive protein (CRP), and interleukin-10 (IL-10), and the expression of both CD86 and caspase-3 in the spleen were investigated. Twenty-four adult male Wistar rats were divided into three equal groups: the control (C) group received a control diet for 10 weeks, the HFD-C group received a HFD for 10 weeks, and the HFD-treated group received a HFD co-administered with oral vitamin D (1μg/kg) daily for 10 weeks. Administration of vitamin D in combination with HFD significantly decreased BW gain, decreased the serum levels of both calcium and CRP, increased the serum level of IL-10, improved the general histological appearance of the spleen, and decreased the expression of both CD86 and caspase-3 in the spleen in comparison with results seen in the HFD-C group. Our data suggest that vitamin D supplementation holds promise as an adjunct treatment to alleviate the dysfunction of the spleen and immune system commonly seen in HFD-induced obesity. - Source :PubMed

Polymorphisms of RPS6KB1 and CD86 associates with susceptibility to multiple sclerosis in Iranian population.

 Multiple sclerosis (MS) is the most prevalent disorder of nervous system inflammation which involves demyelination of spinal cord; this process depends on both environmental and genetic susceptibility factors. In the present study, we examined the association between two SNPs in RPS6KB1 (rs180515) and CD86 (rs9282641) with MS in Iranian population. RPS6KB1gene encodes p70S6K1 protein which plays a key role in mTOR signaling pathway, while CD86 gene codes a membrane protein type I which belongs to immunoglobulin super family act on co-stimulation signaling pathway. - Source :PubMed

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