TL1A, also known as TNFSF15, belongs to the TNF superfamily of ligands. It is expressed predominantly in endothelial cells and to a lesser extent in placenta, lung, kidney, skeletal muscle, pancreas, small intestine and colon. Expression of TL1A is inducible by TNF and IL1-alpha but not by IFN-gamma (1). TL1A can activate NF-κB and MAP kinases, and acts as an autocrine factor to induce apoptosis in endothelial cells and may function as an angiogenesis inhibitor (2). DcR-3 and DR3 are receptors for membrane-bound and soluble forms of TL1A (1). TL1A also induces secretion of IFN-gamma and GM-CSF. Treatment of T-lymphocytes with TL1A enhances expression of IL-2 receptors and increases proliferation in response to IL-2 (3). Secretion of TL1A in lymphoid organs might contribute to RA initiation by promoting autoantibody production, and TL1A secretion stimulated by inflammatory cytokines in RA joints might be a part of a vicious circle that aggravates RA pathogenesis (4). TL1A may play an important role in a Th1-mediated disease such as Crohns (5). Treatment of mice with TL1A strongly enhances graft-versus-host reactivity (1).

miteer sepspqqvys pprgkprahl tikkqtpaph lknqlsalhw ehdlgmaftk ngmkyinksl vipesgdyfi ysqitfrgtt svcgdisrgr rpnkpdsitv vitkvadsyp eparlltgsk svceisnnwf qslylgamfs leegdrlmvn vsdislvdyt kedktffgaf ll