Acts as a negative regulator of innate and adaptive immunity by maintaining immune homeostasis. Negative regulator of Toll-like receptor and T-cell receptor function. Prevents hyperresponsiveness of the immune system and maintains immune homeostasis. Inhibits JUN/AP1 and NF-kappa-B activation. Promotes Fas-induced apoptosis. May interact with CASP8; however, such result is unclear. Expressed in thymus, spleen, lymph node and small intestine, but not in liver, heart, muscle, testis, spinal cord or brain. Up-regulated in the spinal cord of mice with experimental autoimmune encephalomyelitis. Constitutively expressed by macrophages, B and T-lymphocytes at various developmental stages. By TNF in fibroblasts. The central region was initially thought to constitute a DED (death effector) domain. However, 3D-structure data reveal a previously uncharacterized fold that is different from the predicted fold of a DED (death effector) domain. It consists of a large, hydrophobic central cavity that is poised for cofactor binding (By similarity). Multiorgan inflammation, splenomegaly and premature death. Mice are hypersensitive to septic shock. Belongs to the TNFAIP8 family. TNFAIP8L2 subfamily.