Abstract
In response to any danger signal, cytokines are promptly secreted to help fight back the attackers. Tumour necrosis factor (TNF) is one of the most potent inflammatory cytokines and its expression is tightly regulated to prevent uncontrolled inflammation. We have shown that three regulatory elements located in Tnf 3’untranslated region (3’UTR) cooperate post-transcriptionally to maintain low levels of Tnf expression during homeostasis. We have generated several mouse mutants lacking one or two of these regulatory elements. Consequently, these mice overexpress TNF constitutively and develop inflammatory diseases such as rheumatoid arthritis, heart valve disease or inflammatory bowel disease. These mice also present with inducible bronchus-associated lymphoid tissue (iBALT) and nodular lymphoid hyperplasia (NLH) in the bone marrow. We discuss here the role of TNF in the development of tertiary lymphoid organs.
Keywords
TNF, SLO, TLO