Is the concept of central nervous system immune privilege irrelevant in the setting of acute infection?

Abstract

While historically viewed as an immune-privileged area fully isolated from the immune system, the central nervous system (CNS) is now appreciated to maintain dynamic bi-directional communication with the immune system across the blood–brain barrier (BBB) (1, 2). In no setting can this communication be more urgent that acute CNS infection – a dampened or delayed host response could allow an invading virus or bacterium to gain a foothold within the brain, while over-exuberant or protracted inflammation might cause substantial collateral damage to sensitive and non-renewable cells such as neurons. In this opinion piece, we compare host immunity against one prototype virus and one prototype bacterium known to cause disease either outside or within the CNS. Allowing for some variability in disease pathogenesis, and leaving aside complex issues related to chronic intrauterine or neonatal infections, we argue that antimicrobial host responses in both CNS and non-CNS tissue compartments of adult hosts who acquire these infections exhibit many more similarities than differences. In this setting, the concept of CNS immune privilege seems antiquated.