Detects mouse OX40 Ligand/TNFSF4 in direct ELISAs and Western blots. In Western blots, approximately 5% cross-reactivity with recombinant human (rh) OX40 Ligand, rhLIGHT, recombinant mouse (rm) Fas Ligand and less than 1% cross-reactivity with rmTNF‑ alpha, rhGITR Ligand, rhTRANCE, and rhVEGI is observed.
Detection of OX40 Ligand/TNFSF4 in Activated Mouse Splenocytes by Flow Cytometry.
Mouse splenocytes were treated with LPS and recombinant mouse GM-CSF (Catalog # 415-ML), then stained with Goat Anti-Mouse OX40 Ligand/TNFSF4 PE‑conjugated Antigen Affinity-purified Polyclonal Antibody (Catalog # FAB1236P, filled histogram) or isotype control antibody (Catalog # IC108P, open histogram). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Protect from light. Do not freeze.
12 months from date of receipt, 2 to 8 °C as supplied.
Background: OX40 Ligand/TNFSF4
OX40 Ligand (OX40L), also known as gp34, is a type II transmembrane glycoprotein belonging to the TNF superfamily. Murine OX40L cDNA encodes a 198 amino acid (aa) residue protein comprised of a 28 aa N-terminal cytoplasmic domain, a 20 aa transmembrane segment, and a 150 aa C-terminal extracellular domain (1). Human and murine OX40L share 46% sequence identity at the amino acid level (1). The OX40L is expressed on activated antigen presenting cells such as B cells, macrophages, dendritic cells, and on endothelial cells at the site of inflammation. The receptor for OX40L is OX40 (CD134) that is expressed predominantly on activated CD4+ T cells. Expression of OX40 is transient following engagement of T cell receptors (2). Ligation of OX40L by OX40 stimulates proliferation and differentiation of activated B cells, and increases immunoglobulin secretion (3, 4). The expression of OX40L on B cells is up-regulated by CD40 ligation (3). Engagement of the OX40-OX40L system has co-stimulatory effects on T cells by stimulating the production of cytokines by T helper cells and increasing the survival of memory T cells (2, 5). Blocking of the OX40-OX40L interaction in vitro inhibits co-stimulation resulting in decreased T cell proliferation and adhesion of T cells to endothelial cells. Inhibition of the OX40-OX40L interaction in disease models has beneficial effects in acute graft-versus-host disease, inflammatory bowel disease, and decreases the development of collagen-induced arthritis and experimental leishmaniasis (6).
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