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CD44 Involvement in Autoimmune Inflammations
Author(s) -
NAOR DAVID,
NEDVETZKI SHLOMO,
WALMSLEY MARITA,
YAYON AVNER,
TURLEY EVA A.,
GOLAN IRA,
CASPI DAN,
SEBBAN LORA ESHKAR,
ZICK YEHIEL,
GARIN TALI,
KARUSSIS DIMITRIOS,
ASSAYAGASHERIE NATHALIE,
RAZ ITAMAR,
WEISS LOLA,
SLAVIN SHIMON,
GOLAN ITSHAK
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1423.025
Subject(s) - cd44 , immunology , experimental autoimmune encephalomyelitis , nod mice , inflammation , knockout mouse , arthritis , biology , receptor , autoimmunity , medicine , cancer research , antibody , cell , genetics
: 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 .