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OX40 (CD134) and its binding partner OX40-Ligand (OX40L) represent members of the TNFR and TNF superfamilies that appear to be crucial to many types of immune reaction mediated by T cells. Emerging data have now put these molecules at the forefront of the field of what has been termed T cell costimulation.
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OX40 Promotes Effector T cell Expansion and Survival. The T cell response to any acute antigenic stimulation has three distinct phases: expansion, contraction ...
OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on ...
OX40 is a TNF-receptor family member that is expressed primarily on activated CD4+ and CD8+ T cells (16–18). Preclinical cancer models have shown that anti-OX40 ...
An agonistic monoclonal antibody against receptor OX40 (CD134), with potential immunostimulatory activity. Mimicking the natural OX4 ligand (OX40L), ...

CD134

Protein
Tumor necrosis factor receptor superfamily, member 4, also known as CD134 and OX40 receptor, is a member of the TNFR-superfamily of receptors which is not constitutively expressed on resting naïve T cells, unlike CD28. Wikipedia

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This review discusses the biology of OX40 and OX40L and summarizes the impact of the OX40–OX40L interaction on T cell subsets to provide a comprehensive understanding of anti-OX40 mAbs-based therapy.
OX40 is a type 1 transmembrane glycoprotein, reported nearly 30 years ago as a cell surface antigen expressed on activated T cells.
OX40L is the ligand for OX40 and is stably expressed on many antigen-presenting cells such as DC2s macrophages, and activated B lymphocytes.
We show that ligation of OX40 induces clonal expansion and survival of CD4 cells during primary responses, and results in the accumulation of greater numbers of memory cells with time.
We here review the immunobiology of 2 particularly promising TNFRSF target receptors, CD27 and OX40, and their respective ligands, CD70 and OX40L, focusing on their role within a tumor setting.