Down-Regulation of the Macrophage Lineage Through Interaction with OX2 (CD200)

Robert M. Hoek(Cellular Research (United States)), Sigrid R. Ruuls(Cellular Research (United States)), Craig A. Murphy(Cellular Research (United States)), Gavin J. Wright(University of Oxford), Ruth S. Goddard(University of Oxford), Sandra Zurawski(Cellular Research (United States)), Bianca Blom(Cellular Research (United States)), Margit Homola(Cellular Research (United States)), Wolfgang J. Streit(Allen Institute for Brain Science), Marion H. Brown(University of Oxford), A. Neil Barclay(University of Oxford), Jonathon D. Sedgwick(Cellular Research (United States))
Science
December 1, 2000
Cited by 1,020

Abstract

OX2 (CD200) is a broadly expressed membrane glycoprotein, shown here to be important for regulation of the macrophage lineage. In mice lacking CD200, macrophage lineage cells, including brain microglia, exhibited an activated phenotype and were more numerous. Upon facial nerve transection, damaged CD200-deficient neurons elicited an accelerated microglial response. Lack of CD200 resulted in a more rapid onset of experimental autoimmune encephalomyelitis (EAE). Outside the brain, disruption of CD200-CD200 receptor interaction precipitated susceptibility to collagen-induced arthritis (CIA) in mice normally resistant to this disease. Thus, in diverse tissues OX2 delivers an inhibitory signal for the macrophage lineage.


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