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Soluble CD84 ELISA

CD84 is a survival receptor for CLL cells

Chronic lymphocytic leukemia (CLL) is characterized by the accumulation of CD5+ B lymphocytes in peripheral blood, lymphoid organs and bone marrow. The main feature of the disease is accumulation of the malignant cells due to decreased apoptosis. CD84 belongs to the signaling lymphocyte activating molecule family of immunoreceptors, and has an unknown function in CLL cells. Here, we show that the expression of CD84 is significantly elevated from the early stages of the disease, and is regulated by macrophage migration inhibitory factor and its receptor, CD74. Activation of cell surface CD84 initiates a signaling cascade that enhances CLL cell survival. Both downmodulation of CD84 expression and its immune-mediated blockade induce cell death in vitro and in vivo. In addition, analysis of samples derived from an on-going clinical trial, in which human subjects were treated with humanized anti-CD74 (milatuzumab), shows a decrease in CD84 messenger RNA and protein levels in milatuzumab-treated cells. This downregulation was correlated with reduction of Bcl-2 and Mcl-1 expression. Thus, our data show that overexpression of CD84 in CLL is an important survival mechanism that appears to be an early event in the pathogenesis of the disease. These findings suggest novel therapeutic strategies based on the blockade of this CD84-dependent survival pathway.

Binsky-Ehrenreich I et al. Oncogene. 2014 Feb 20;33(8):1006-16

Genome-wide association study and gene expression analysis identifies CD84 as a predictor of response to etanercept therapy in rheumatoid arthritis

Anti-tumor necrosis factor alpha (anti-TNF) biologic therapy is a widely used treatment for rheumatoid arthritis (RA). It is unknown why some RA patients fail to respond adequately to anti-TNF therapy, which limits the development of clinical biomarkers to predict response or new drugs to target refractory cases. To understand the biological basis of response to anti-TNF therapy, we conducted a genome-wide association study (GWAS) meta-analysis of more than 2 million common variants in 2,706 RA patients from 13 different collections. Patients were treated with one of three anti-TNF medications: etanercept (n = 733), infliximab (n = 894), or adalimumab (n = 1,071). We identified a SNP (rs6427528) at the 1q23 locus that was associated with change in disease activity score (ΔDAS) in the etanercept subset of patients (P = 8 × 10(-8)), but not in the infliximab or adalimumab subsets (P>0.05). The SNP is predicted to disrupt transcription factor binding site motifs in the 3' UTR of an immune-related gene, CD84, and the allele associated with better response to etanercept was associated with higher CD84 gene expression in peripheral blood mononuclear cells (P = 1 × 10(-11) in 228 non-RA patients and P = 0.004 in 132 RA patients). Consistent with the genetic findings, higher CD84 gene expression correlated with lower cross-sectional DAS (P = 0.02, n = 210) and showed a non-significant trend for better ΔDAS in a subset of RA patients with gene expression data (n = 31, etanercept-treated). A small, multi-ethnic replication showed a non-significant trend towards an association among etanercept-treated RA patients of Portuguese ancestry (n = 139, P = 0.4), but no association among patients of Japanese ancestry (n = 151, P = 0.8). Our study demonstrates that an allele associated with response to etanercept therapy is also associated with CD84 gene expression, and further that CD84expression correlates with disease activity. These findings support a model in which CD84 genotypes and/or expression may serve as a useful biomarker for response to etanercept treatment in RA patients of European ancestry.
Cui J. et al. PLoS Genet. 2013 Mar;9(3):e1003394. 

CD84 is Markedly Upregulated in Kawasaki Disease Arteriopathy

BACKGROUND: The major goals of Kawasaki Disease (KD) therapy are to reduce inflammation and prevent thrombosis in the coronary arteries (CA), but some children do not respond to currently available non-specific therapies. New treatments have been difficult to develop because the molecular pathogenesis is unknown.
METHODS:To identify dysregulated gene expression in KD CA, we performed high-throughput RNA sequencing on KD and control CA, validated potentially dysregulated genes by real-time RT-PCR, and localized protein expression by immunohistochemistry.
RESULTS: Signaling lymphocyte activation molecule CD84 was upregulated 16-fold (p<0.01) in acute KD CA (within 2 months of onset) and 32-fold (p<0.01) in chronic CA (5 months to years after onset). CD84 was localized to inflammatory cells in KD tissues. Genes associated with cellular proliferation, motility and survival were also upregulated in KD CA, and immune activation molecules MX2 and SP140 were upregulated in chronic KD.
CONCLUSIONS: CD84, which facilitates immune responses and stabilizes platelet aggregates, is markedly upregulated in KD CA in patients with acute and chronic arterial disease. We provide the first molecular evidence of dysregulated inflammatory responses persisting for months to years in CA significantly damaged by KD.
Reindel R et al. Clin Exp Immunol. 2014 Mar 17. doi: 10.1111/cei.12327. [Epub ahead of print]
  Human Soluble CD84 ELISA Kit
Code No.: SK00632-01
Size: 96 T
Price: $420.00 USD
Standard range156-10000 pg/ml
Sensitivity: 70 pg/ml
Sample Type: serum, plasma
sample require:100 uL per well
Intra-CV: 4-6%
Inter-CV: 8-10%
Data Sheet: PDF


Human Soluble CD84 Recombinant
Code No.: 00632-01-10
Size: 10 ug
Price: $220.00 USD
Protein ID:Q9UIB8
Gene ID: 8832
MW:45 KD
Tag: His Tag on C-Terminus
Expressed: 293 cells derived
Purity: 95%
Data Sheet: PDF
Anti Human Soluble CD84 IgG
Code No.: A00632-01-100
Size: 100 ug
Price: $290.00 USD
Host: Rabbit
Antigen: human CD84 ECD
Ab Type: Polyclonal IgG
Purification: Protein A
Applications: WB, E
Working Dilution: 1-2ug/ml
Data Sheet: PDF



Code No.
Price ($)
Soluble CD84 (Human) ELISA Kit SK00632-01 96 T 420.00
Soluble CD84 (Human) standard
10 ug
Mouse Anti Soluble CD84(Human) IgG
100 ug