Tumor necrosis factor alpha (TNFα) and Lymphotoxin alpha (LTα) (TNF (for Tumor necrosis factor alpha), LTα (for Lymphotoxin alpha))

Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine produced primarily by macrophages and other immune cells, acting as a central mediator in immune system function and inflammation. TNFα exists in both a transmembrane form and a soluble form, binding to two main receptors (TNFR1 and TNFR2) to initiate a variety of signaling pathways that can lead to inflammation, cell proliferation, apoptosis, and necroptosis. Lymphotoxin alpha (LTα), formerly called TNF-beta, is structurally and functionally related to TNFα, belonging to the same cytokine superfamily. LTα plays a distinct and essential role in the development of secondary lymphoid organs, immune regulation, and can also induce cytotoxic effects on tumor cells. Both TNFα and LTα contribute to the pathology of inflammatory, autoimmune, and malignant diseases, making them key therapeutic targets for monoclonal antibodies and receptor fusion proteins designed to block their activity[1][2][3][4][5][6].

Other names

TNFα: Tumor necrosis factor, cachectinLTα: Lymphotoxin-alpha, Tumor necrosis factor beta (TNF-β), TNF-beta

Neutralization of TNFα/LTα cytokine activity by monoclonal antibodies or receptor fusion proteins, leading to reduced inflammation and immune activation Blockade of TNF receptor interactions to prevent downstream signaling events such as activation of NF-κB and induction of apoptosis or inflammatory mediators