Mouse 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 mice (Mus musculus). 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, molecules that regulate immune signaling, apoptosis, and inflammatory processes. In mice, 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. Mouse TNF-α has been extensively studied in genetic knockout and transgenic models, which have demonstrated its critical role in host defense against pathogens, regulation of immune responses, and control of inflammation. Murine TNF signaling is particularly important in models of autoimmune disease, infectious disease, cancer, and inflammatory disorders, including collagen-induced arthritis (a model of rheumatoid arthritis), experimental autoimmune encephalomyelitis (a model of multiple sclerosis), and tuberculosis infection models. Because mice are the most widely used experimental organisms in immunology and biomedical research, characterization of mouse TNF-α has been fundamental for understanding cytokine-mediated inflammation and the development of TNF-targeted therapies used to treat human inflammatory diseases.