Lymphotoxin  beta R (LT beta R; also called TNFRSF3, TNF RIII,or TNF Rrp) is a type I transmembrane glycoprotein within the TNF receptor superfamily (1-3). The rat LT beta R cDNA encodes a 415 amino acid (aa) protein that includes a 30 aa signal peptide, a 191 aa extracellular domain (ECD), a 23 aa transmembrane domain, and a 171 aa cytoplasmic domain. The ECD contains four cysteine-rich motifs characteristic of the TNF receptor superfamily (2). Within the ECD, rat LT beta R shares 90% and 66% aa sequence identity with the ECD of mouse and human LT beta R, respectively. Soluble LT beta R, which can be formed by proteolytic cleavage of the ECD, functions as a decoy receptor for LT beta R ligands and is involved in the suppression of autoimmunity (4, 5). LT beta R is constitutively expressed in cells of myeloid lineage and is upregulated during tissue regeneration (6). It is expressed on mesenchymal stromal organizing cells that give rise to primary, secondary, and tertiary lymphoid structures (7-9). Mice deficient in LT beta R fail to form secondary lymphoid structures (4). LT beta R ligands include homotrimers of LIGHT/TNFSF14 and the heterotrimeric Lymphotoxin alpha 1/ beta 2 (2). Ligand engagement of LT beta R has been shown to induce NF kappa B activation through canonical (IKK) or alternative (NIK/RelB) signaling pathways (5, 10). LT beta R signaling induces production of cytokines (TRANCE/RANK Ligand/TNFSF11, IL-7), chemokines (CXCL8/IL-8, CXCL13/BCL/BCA-1, CCL19/MIP-3 beta, CCL21/6Ckine, CCL2/MCP-1), and adhesion molecules (VCAM-1/CD106, ICAM-1/CD54, MAdCAM) (8, 11). LT beta R is involved in lipid metabolism, atherosclerosis, and intestinal epithelial homeostasis (4, 12, 13). It also regulates cell growth and can initiate inflammation-related carcinogenesis (5, 14).