Synaptic rearrangement following axonal injury: Old and new players.
Previous work indicates that the weak expression in neural tissues of beta 2-microglobulin (beta 2-m) and major histocompatibility complex (MHC) class I gene products can be increased experimentally. Physiologic conditions in which greater neural MHC expression occurs are not well defined. Here we have asked whether protection from blood-borne antigens afforded by the blood-brain barrier is related to the lack of MHC expression. A rabbit antiserum raised against purified mouse beta 2-m was used in an immunocytochemical assay. The serum reacted strongly with lymphoid tissues and was inhibited by purified beta 2-m. No beta 2-m was detected in neurons or glia in any brain area examined. A barrier-free region, the area postrema, showed the same lack of neural cell staining. Blood vessel walls in the same sections were beta 2-m+. It is unlikely that these staining patterns are due to cell type-specific beta 2-m degradation, since frozen and formaldehyde-perfused, paraffin-embedded preparations gave similar results. Failure to detect beta 2-m in the area postrema suggests that passive exposure to environmental antigens, immunomodulators, or immunocompetent cells is not sufficient to induce neural class I expression. Rather, if increased expression of beta 2-m and class I occurs in vivo, additional stimulus is required.