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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.

Type

Journal article

Journal

Science

Publication Date

01/12/2000

Volume

290

Pages

1768 - 1771

Keywords

Animals, Antigens, CD, Antigens, Surface, Arthritis, Experimental, Cell Lineage, Central Nervous System, Denervation, Down-Regulation, Encephalomyelitis, Autoimmune, Experimental, Facial Nerve, Gene Targeting, Joints, Lymph Nodes, Macrophage Activation, Macrophages, Mice, Mice, Inbred C57BL, Microglia, Neurons, Rats, Receptors, Immunologic, Spleen