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The Lesson to be Learned from CD44-Targeting by Antibody or from Knockout Mice
a The Lautenberg Center for General and Tumor Immunology, Hebrew University-Hadassah Medical School, Jerusalem, Israel b The Kennedy Institute of Rheumatology, Hammersmith, London, United Kingdom c ProChon Biotech Ltd., Kiryat Weizmann, Science Park, Rehovot, Israel d London Regional Cancer Center, University of Western Ontario, London, Ontario, Canada e Department of Rheumatology, Tel Aviv Souraski Medical Center, Ichilov Hospital, Sackler Faculty of Medicine, Tel Aviv, Israel f Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel g Department of Neurology, Laboratory of Neuroimmunology and the Agnes Ginges Center for Neurogenetics, Hadassah University Hospital, Ein Karem, Jerusalem, Israel h Diabetes Unit, Hadassah University Hospital, Jerusalem, Israel i Department of Bone Marrow Transplantation and Cancer Research Laboratory, Hadassah University Hospital, Jerusalem, Israel
Key Words: autoimmune diseases • CD44 • CD168 • hyaluronan • inflammation • molecular redundancy
Address for correspondence: Dr. David Naor, The Lautenberg Center for General and Tumor Immunology, The Hebrew University–Hadassah Medical School, Jerusalem 91120, Israel. Voice: 972-2-675-88722; fax: 972-2-642-4653. naord{at}md.huji.ac.il
CD44 is a multistructural and multifunctional glycoprotein, the diversity of which is generated by alternative splicing. In this communication we review some aspects related to CD44 structure and function in experimental autoimmune inflammation, focusing on research performed in our own laboratory. We have found that CD44 targeting by antibody, passively injected into DBA/1 mice with collagen-induced arthritis (CIA) and NOD mice with type I diabetes or actively generated by CD44 cDNA vaccination of SJL/j mice with autoimmune encephalomyelitis, markedly reduced the pathological manifestations of these diseases by attenuating cell migration of the inflammatory cells and/or by their apoptotic killing. However, genetic deletion of CD44 by knockout technology enhanced the development of CIA because of molecular redundancy mediated by RHAMM (a receptor of hyaluronan-mediated motility). The mechanisms that stand behind these findings are discussed.
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