Recombinant human CD134 / OX40L receptor protein (Fc Chimera)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

CD134 also known as OX40 or TNFRSF4 is a receptor that plays an essential role in immune response regulation. This receptor is part of the tumor necrosis factor receptor (TNFR) superfamily and has a molecular mass of approximately 50 kDa. CD134 is expressed on activated T cells particularly CD4+ T cells and is present on various other immune cells under specific conditions. The receptor binds to the OX40L its ligand which is expressed on antigen-presenting cells such as dendritic cells and B cells.

Biological function summary

CD134 influences T cell proliferation survival and memory formation being an important component of the immune system's adaptive response. OX40L engagement with CD134 enhances the activation and survival of T cells promoting long-term immunity. This interaction does not form part of a larger complex but functions as a direct signaling mechanism that augments T cell receptor (TCR) signaling leading to increased cytokine production and sustained immune responses essential for controlling infections and cancer.

Pathways

CD134 signaling intersects with the nuclear factor-kappa B (NF-κB) and phosphoinositide 3-kinase (PI3K) pathways. These pathways play significant roles in regulating immune responses and cell survival. Through the NF-κB pathway CD134 influences gene transcription related to immune activation. It also connects with other immune regulatory proteins such as CD28 which further potentiates T cell responses and enhances effector functions.

CD134 has connections to autoimmune diseases and cancers. Overactivity of the CD134-OX40L pathway can lead to exacerbated autoimmune conditions such as lupus. This receptor has also been implicated in tumor immunity where its activation enhances the anti-tumor response of T cells. CD134 interacts with CTLA-4 another immune checkpoint protein playing a role in balancing immune activation and regulation within these disease contexts.