Mitosis and apoptosis of microglia in vivo induced by an anti-CR3 antibody which crosses the blood-brain barrier

Reid, D.M., Perry, V.H, Andersson, P.-B. and Gordon, S. (1993) Mitosis and apoptosis of microglia in vivo induced by an anti-CR3 antibody which crosses the blood-brain barrier. Neuroscience, 56 (3), 529-533. (doi:10.1016/0306-4522(93)90353-H).

Abstract

Microglia, the resident tissue macrophages of the central nervous system¹³, have a highly differentiated morphology and do not express many of the antigens typically associated with other tissue macrophages.^13,18. Activation of microglia is associated with a change in morphology and an increase in their repertoire of antigen expression. Microglia become activated in many neuropathological conditions including chronic neurodegenerative diseases and human immunodeficiency virus neuropathology,^5,17 yet little is known of the mechanisms involved. Here we demonstrate for the first time that microglia can be activated and induced to divide and/or undergo apoptosis via a β₂integrin (complement receptor type 3, CR3, Mac-1 or CD11b CD18) using an anti-CR3 monoclonal antibody (McAb5C6).¹⁵ This antibody, which has been shown to block myelomonocytic recruitment during central nervous system inflammation,¹ is unique in that it can cross the intact blood-brain barrier to activate microglia. Since CR3 not only binds the iC3b component of the alternative complement cascade but also denatured proteins⁴ this suggests a potential route for microglia activation in neuropathological conditions.

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