The A-1 antigen: a novel marker in experimental peripheral nerve injury.

Expression of the Schwann cell phenotype is regulated by signals from the adjoining axon. After axotomy, the Schwann cell ceases the production and maintenance of the myelin sheath and assumes phagocytic properties necessary to digest its own myelin. The molecular mechanisms responsible for this behavior remain unclear. A monoclonal antibody termed BIKS was produced after the immunization of mice with guinea pig lymphoid tissue. This antibody recognizes a cytoplasmic vesicle-associated molecule (A-1 antigen) which is abundant in all tissue macrophages but is also expressed in small amounts in normal Schwann cells. Following axotomy, the A-1 antigen appears to be translocated from a perinuclear site to accumulate in large quantities around myelin ovoids in Schwann cells, as well at the nodes of Ranvier-sites where Wallerian degeneration is known to commence. The level of the antigen remains high when axons are prevented from regeneration. During repair of crush injury, however, the level of antigen drops concomitant with the ingrowth of regenerating axons, suggesting axonal control of A-1 antigen expression.