Human TNFSF13B blocking peptide (CDBP0556)

Synthetic Human TNFSF13B blocking peptide for BL

Product Overview
BAFF ( C - term ) peptide ( human )
Species Reactivity
0.2 mg/ml
50 μg
PBS with 0.1% BSA 0.02% sodium azide pH7.2
0.02% Sodium Azide
Upon Receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This cytokine is a ligand for receptors TNFRSF13B/TACI, TNFRSF17/BCMA, and TNFRSF13C/BAFFR. This cytokine is expressed in B cell lineage cells, and acts as a potent B cell activator. It has been also shown to play an important role in the proliferation and differentiation of B cells. Alternatively spliced transcript variants encoding distinct isoforms have been identified. [provided by RefSeq, Mar 2011]
cytokine activity; protein binding; receptor binding; tumor necrosis factor receptor binding;
TNFSF13B; tumor necrosis factor (ligand) superfamily, member 13b; DTL; BAFF; BLYS; CD257; TALL1; THANK; ZTNF4; TALL-1; TNFSF20; tumor necrosis factor ligand superfamily member 13B; delta BAFF; Delta4 BAFF; B-lymphocyte stimulator; B-cell-activating factor; ApoL related ligand TALL-1; TNF homolog that activates apoptosis; dendritic cell-derived TNF-like molecule; tumor necrosis factor-like protein ZTNF4; TNF and ApoL-related leukocyte expressed ligand 1; tumor necrosis factor (ligand) superfamily, member 20;


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Differential Expression of Inflammation-Related Genes in Down Syndrome Patients with or without Periodontal Disease


Authors: Baus-Dominguez, M.; Gomez-Diaz, R.; Torres-Lagares, D.; Corcuera-Flores, J. R.; Ruiz-Villandiego, J. C.; Machuca-Portillo, G.; Gutierrez-Perez, J. L.; Serrera-Figallo, M. A.

Aim. Aware that Down Syndrome patients present among their clinical characteristics impaired immunity, the aim of this study is to identify the statistically significant differences in inflammation-related gene expression by comparing Down Syndrome patients with Periodontal Disease (DS+PD+) with Down Syndrome patients without Periodontal Disease (DS+PD-), and their relationship with periodontitis as a chronic oral inflammatory clinical feature. Materials and Methods. Case study and controls on eleven Down Syndrome patients (DS+PD+ vs. DS+PD-). RNA was extracted from peripheral blood using a Qiagen PAXgene Blood miRNA Kit when performing an oral examination. A search for candidate genes (92 selected) was undertaken on the total genes obtained using a Scientific GeneChip (R) Scanner 3000 (Thermo Fisher Scientific) and Clariom S solutions for human, mouse, and rat chips, with more than 20,000 genes annotated for measuring expression levels. Results. Of the 92 inflammation-related genes taken initially, four genes showed a differential expression across both groups with a p value of <0.05 from the data obtained using RNA processing of the patient sample. Said genes were TNFSF13B (p=0.0448), ITGB2 (p=0.0033), ANXA3 (p=0.0479), and ANXA5 (p=0.016). Conclusions. There are differences in inflammation-related gene expression in Down Syndrome patients when comparing patients who present a state of chronic oral inflammation with patients with negative rates of periodontal disease.

Upregulation of IFN-Inducible and Damage-Response Pathways in Chronic Graft-versus-Host Disease


Authors: Hakim, Frances T.; Memon, Sarfraz; Jin, Ping; Imanguli, Matin M.; Wang, Huan; Rehman, Najibah; Yan, Xiao-Yi; Rose, Jeremy; Mays, Jacqueline W.; Dhamala, Susan; Kapoor, Veena; Telford, William; Dickinson, John; Davis, Sean; Halverson, David; Naik, Haley B.; Baird, Kristin; Fowler, Daniel; Stroncek, David; Cowen, Edward W.; Pavletic, Steven Z.; Gress, Ronald E.

Although chronic graft-versus-host disease (CGVHD) is the primary nonrelapse complication of allogeneic transplantation, understanding of its pathogenesis is limited. To identify the main operant pathways across the spectrum of CGVHD, we analyzed gene expression in circulating monocytes, chosen as in situ systemic reporter cells. Microarrays identified two interrelated pathways: 1) IFN-inducible genes, and 2) innate receptors for cellular damage. Corroborating these with multiplex RNA quantitation, we found that multiple IFN-inducible genes (affecting lymphocyte trafficking, differentiation, and Ag presentation) were concurrently upregulated in CGVHD monocytes compared with normal subjects and non-CGVHD control patients. IFN-inducible chemokines were elevated in both lichenoid and sclerotic CGHVD plasma and were linked to CXCR3(+) lymphocyte trafficking. Furthermore, the levels of the IFN-inducible genes CXCL10 and TNFSF13B (BAFF) were correlated at both the gene and the plasma levels, implicating IFN induction as a factor in elevated BAFF levels in CGVHD. In the second pathway, damage-/pathogen-associated molecular pattern receptor genes capable of inducing type I IFN were upregulated. Type I IFN-inducible MxA was expressed in proportion to CGVHD activity in skin, mucosa, and glands, and expression of TLR7 and DDX58 receptor genes correlated with upregulation of type I IFN-inducible genes in monocytes. Finally, in serial analyses after transplant, IFNinducible and damage-response genes were upregulated in monocytes at CGVHD onset and declined upon therapy and resolution in both lichenoid and sclerotic CGVHD patients. This interlocking analysis of IFN-inducible genes, plasma analytes, and tissue immunohistochemistry strongly supports a unifying hypothesis of induction of IFN by innate response to cellular damage as a mechanism for initiation and persistence of CGVHD. The Journal of Immunology, 2016, 197: 3490-3503.

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