CD13/Aminopeptidase N Is a Potential Therapeutic Target for Inflammatory Disorders

  • J Immunol. 2020 Jan 1;204(1):3-11. doi: 10.4049/jimmunol.1900868.
Chenyang Lu  1  2 ,  Mohammad A Amin  1 ,  David A Fox  3
Affiliations
  • 1. Division of Rheumatology, Clinical Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI 48109; and.
  • 2. Department of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China.
  • 3. Division of Rheumatology, Clinical Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI 48109; and [email protected].
PMID: 31848300 DOI: 10.4049/jimmunol.1900868
Abstract

CD13/Aminopeptidase N is a widely expressed ectoenzyme with multiple functions. As an enzyme, CD13 regulates activities of numerous cytokines by cleaving their N-terminals and is involved in Ag processing by trimming the peptides bound to MHC class II. Independent of its enzymatic activity, cell membrane CD13 functions by cross-linking-induced signal transduction, regulation of receptor recycling, enhancement of FcγR-mediated phagocytosis, and acting as a receptor for cytokines. Moreover, soluble CD13 has multiple proinflammatory roles mediated by binding to G-protein-coupled receptors. CD13 not only modulates development and activities of immune-related cells, but also regulates functions of inflammatory mediators. Therefore, CD13 is important in the pathogenesis of various inflammatory disorders. Inhibitors of CD13 have shown impressive anti-inflammatory effects, but none of them has yet been used for clinical therapy of human inflammatory diseases. We reevaluate CD13's regulatory role in inflammation and suggest that CD13 could be a potential therapeutic target for inflammatory disorders.