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Commentary Open Access
Volume 1 | Issue 2 | DOI: https://doi.org/10.46439/autoimmune.1.006

iBALT and nodular lymphoid hyperplasia in TNF-overexpressing mice

  • 1The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria 3052, Australia
  • 2Department of Medical Biology, The University of Melbourne, Melbourne, Victoria 3052, Australia
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Corresponding Author

Philippe Bouillet, bouillet@wehi.edu.au

Received Date: October 05, 2020

Accepted Date: November 13, 2020

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

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