Equine Tumor Necrosis Factor Alpha (TNF-α) (also known as TNF or cachectin) is a proinflammatory cytokine that plays a central role in innate immune responses, inflammation, and host defense against pathogens in horses (Equus caballus). TNF-α is a member of the tumor necrosis factor (TNF) superfamily, which includes related cytokines such as TNF-β (lymphotoxin-α), Fas ligand (FasL), CD40 ligand (CD40L), and TRAIL, proteins that regulate immune signaling, apoptosis, and inflammatory pathways. In horses, TNF-α is primarily produced by activated macrophages, monocytes, dendritic cells, and T lymphocytes in response to infection, endotoxin exposure, or tissue injury. TNF-α exerts its biological effects by binding to TNF receptors TNFR1 (p55) and TNFR2 (p75), activating intracellular signaling pathways including NF-κB, MAPK, and caspase-mediated pathways, which regulate cytokine production, immune cell activation, apoptosis, and inflammatory responses. In equine health, TNF-α is an important mediator of inflammatory responses associated with bacterial infections, endotoxemia, and systemic inflammatory conditions, including colic-associated endotoxemia, septicemia, and equine laminitis, where elevated TNF-α levels contribute to vascular inflammation and tissue damage. TNF-α also participates in immune responses to respiratory infections and inflammatory airway diseases. Because TNF-α is a key regulator of inflammation and immune defense, equine TNF-α is widely studied in veterinary immunology, inflammatory disease research, and endotoxemia models, contributing to improved understanding of immune responses and inflammatory regulation in horses.