Recombinant human TL1A protein (Active)

추가 정보

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

The protein TL1A also known as TNF-like ligand 1A is part of the tumor necrosis factor (TNF) superfamily. It is a cytokine with a molecular weight of approximately 23 kDa. Cells such as endothelial cells monocytes and fibroblasts express TL1A. TL1A predominantly acts as ligand for death receptor 3 (DR3) also called TNFRSF25 and is involved in immune response regulation. This protein can be found mainly in tissues involved in immune surveillance like lymph nodes and the gastrointestinal tract.

Biological function summary

TL1A interacts to induce T cell proliferation and cytokine production. It forms a complex with DR3 to activate downstream signaling pathways. These activities enhance adaptive immunity by stimulating T helper cells. Furthermore TL1A influences the production of inflammatory cytokines like interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-α). Through its interaction with DR3 TL1A modulates important immune responses.

Pathways

TL1A features in the TNF receptor-mediated signaling and the NF-kB signaling pathway. In these pathways it links to proteins such as RIPK1 and TRAF2. The signaling through DR3 influences cell survival differentiation and apoptosis. These pathways are important in maintaining the balance between immune activation and tolerance. By interacting with various signaling molecules TL1A orchestrates complex immune functions that ensure adequate immune responses and prevent autoimmunity.

Researchers connect TL1A with conditions like inflammatory bowel disease (IBD) and rheumatoid arthritis (RA). These conditions involve chronic inflammation and immune dysregulation where TL1A plays a role. In IBD elevated TL1A levels drive inflammation in the intestines. In RA TL1A potentially interacts with fibroblast-like synoviocytes contributing to joint inflammation and damage. Its relation to DR3 further implicates TL1A in these autoimmune disorders making it a target for therapeutic interventions aiming to mitigate immune-mediated damage.