Neuronal control of the immunological microenvironment in the CNS: implications on neuronal cell death and survival

Abstract

The central nervous system (CNS) has an immunoprivileged status. In the healthy CNS, class I as well as class II major histocompatibility (MHC) molecules are virtually absent. Heterodimeric MHC molecules are essential for the initiation, propagation and effector phases of antigen-specific immune responses. Endogenous and exogenous antigenic peptides are presented via MHC molecules to T lymphocytes to enable cognate interactions. While MHC molecules are absent in the intact CNS, they are inducible on different brain cell types during inflammatory or neurodegenerative diseases. Recent evidence for the involvement of neurons in the regulation of MHC expression emerged from several studies using neuronal transection models. These models permit the analysis of cellular responses occurring locally, as well as those distant from the primary lesion, without interfering with the blood-brain barrier.