Astrocytes and central nervous system endothelial cells do not express B7-1 (CD80) or B7-2 (CD86) immunoreactivity during experimental autoimmune encephalomyelitis

The identity of cell types within the central nervous system (CNS) capable of activating T lymphocytes is a fundamental issue in the understanding of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). To become fully activated, a T cell must recognize its antigen and receive co-stimulation, the latter being optimally delivered via B7-1 and/or B7-2 molecules expressed by the antigen presenting cell (APC). There are conflicting reports regarding whether astrocytes or CNS endothelial cells (EC) can act as fully competent APCs. The present studies were performed to determine whether astrocytes or CNS EC express B7-1 or B7-2 immunoreactivity during EAE. No expression of B7-1 or B7-2 by either astrocytes or EC was detected during acute, remitting, relapsing or chronic EAE, whether EAE was induced by active immunization or cell transfer using five different myelin antigens. These results suggest that neither astrocytes nor CNS EC can deliver co-stimulatory signals via B7 molecules in the setting of murine EAE, rendering them incapable of acting as fully competent APCs.(C) 2000 Elsevier Science B.V.