The Central Nervous System is considered “immunologically privileged.” What does this mean? What are the features of the anatomical structures that that enable this status. What are the factors that can cause a breach into the status of this system?
How do these characteristics play a role in the efficacy of treating infections in the Nervous System, and can they contribute to the occurrence of latent infections within this system?
The central nervous system (CNS) is considered to be immune-privileged tissue in which adaptive immunity and inflammation are highly controlled. This feature serves to protect post-mitotic neural cells from potential immune response-mediated injury and death. Immune privilege is based on multiple factors, including:
1) presence of the blood-brain barrier (BBB);
2) lack of draining lymphatics;
3) a dearth of professional antigen-presenting cells (APCs), such as dendritic cells (DCs);
4) low expression levels of major histocompatibility complex (MHC) molecules; and
5) many anti-inflammatory soluble modulators.
Recently it has become clear that the immune-privileged nature of the CNS is complex and not absolute .Drainage of CNS antigens to the periphery might either contribute to tolerance to these antigens or be one of the initial steps in the pathogenesis of CNS autoimmune disease.
It has been experimentally shown that a suppressed delayed-type hypersensitivity response and ameliorated experimental autoimmune encephalomyelitis (EAE) is observed in rats three weeks after infusing myelin basic protein (MBP) into cerebrospinal fluid (CSF). However, they also found that removal of the cervical lymph nodes (CLNs) led to a substantial decrease in albumin-specific antibody titers in the serum of rats that had received albumin in the CSF, suggesting that antigen drainage from the CNS can induce an immunogenic response in the periphery. Consistent with this finding, it has been concluded that intracerebrally injected soluble and cell-bound ovalbumin (OVA) antigen can induce peripheral priming, preferential recruitment of OVA-specific CD8+ T cells to the CNSand hasten the onset of EAE. Thus, artificially increasing antigen levels in the CNS in the context of injection-induced trauma increases both afferent (antigen drainage) and efferent (leukocyte recruitment) CNS immunity, which might contribute to the initiation and/or exacerbation of CNS autoimmune disease.