Innate Immunity in Viral Encephalitis

摘要: Innate immune responses to pathogens are evolutionarily ancient and found in the most primitive organisms. These highly conserved not pathogen-specific, but response classes of molecular structures. Infections can be perceived both extracellularly intracellularly by Pathogen Associated Molecular Patterns (PAMPs) their host cell ligands, Recognition Receptors (PRRs), among them, Toll-Like (TLRs). The innate infection includes release soluble preformed mediators, or synthesis cytoplasmic enzymes, cytokines, chemokines, interferons (IFNs), lipid proteins complement cascade, neurotransmitters, nucleotides, components transcription factors (High Mobility Group B1, receptors for sex hormones/steroids). Directed cellular migration parenchymal astrocytes microglia, as well recruitment across blood brain barrier (BBB) circulating neutrophils, natural killer, monocytes, macrophages, dendritic cells, ultimately T lymphocytes site also hallmarks infections. responding cells contribute own secreted effector molecules activities (such phagocytosis). Distinct viruses capable infecting every type (endothelial ependymal perivascular macrophages pericytes, astrocytes, oligodendrocytes, Schwann neurons) central nervous system (CNS). CNS infections challenge with a different set problems than do peripheral viral Among complications (a) neurons that rarely express Class I II Major Histocompatibility Complex (MHC) thus suitable targets either CD4+ CD8+ MHC-restricted (b) an enclosed volume is constrained from swelling during inflammation, poorly developed lymphatic drainage, (c) immunologic privilege which leads extremely limited surveillance pathogens. Therefore, role immunity, CNS-resident products, inflammatory traverse BBB essential “buy time,” inhibiting replication dissemination, until marshal adaptive response. crucial survival infection. Consequently, successful pathogens, especially those persist, have wide variety evasive approaches limit inhibition replication. Many these pathways highlighted individual chapters precede this one. measures range neutralizing (cytokines chemokines) receptors, encoding anti-inflammatory genome, preventing signal transduction, blocking protein synthesis, degradation antiviral molecules, apoptosis, blockade nuclear pore complex. In chapter, will attempt cover breadth infection, devote more space generally under-considered aspects well-known components. There some caveats consider, experiments been performed murine model man; further, conclusions using vitro cultured (whether primary established lines) may reflect physiological conditions undisturbed CNS. Lastly, we now appreciate complexities imposed on hosts polymorphisms genes critical pathways, leading increased susceptibility resistance others.