XXXX astrocytes are only partially competent antigen presenting cells. Possible implications for lesion development in multiple sclerosis.

@entity1 @entity2610 @entity404 @entity310 @entity3138 @entity7937 @entity1453 @entity379 @entity2071 @entity116 @entity4107
Highly purified astrocyte cultures from @entity1 embryonic brain were examined for their capacity to present antigen to human @entity4107 compatible, cytolytic @entity404 + T lymphocytes. Most astrocytes constitutively expressed HLA class I products and @entity7937 ( @entity7937 ). Constitutive expression of HLA class II, @entity1453 ( @entity1453 ) and @entity2071 ( @entity2071 ) was lower and varied among different cultures, while @entity3138 ( @entity3138 ) was absent. @entity379 alone or in combination with @entity310 strongly enhanced expression of HLA class I, HLA-DR, -DP, -DQ, @entity1453 and @entity2071 , but did not affect expression of @entity3138 ( @entity3138 ) and @entity7937 ( @entity7937 ). @entity310 alone induced only HLA class I and @entity2071 , but not HLA class II or @entity1453 . Cytokine treated, but not untreated astrocytes were able to present protein (auto-)antigens to specific T lymphocyte lines. Astrocytes expressing appropriate major histocompatibility complex class II products were lysed by @entity404 + T cells specific for @entity2610 or @entity116 toxoid. The lytic response was antigen dose dependent and HLA-DR restricted. It could be blocked by antibodies against HLA-DR determinants and against the adhesion molecules @entity1453 and @entity2071 . In remarkable contrast to their susceptibility to T cell lysis, antigen presenting astrocytes were not only completely unable to induce T cell proliferation but even inhibited proliferation. The results indicate that, although @entity1 astrocytes have the potential to present protein antigens to @entity404 + T cells, they do not induce the co-stimulatory factors required to trigger the complete T cell activation programme.
