Chemokines and Viral Infections of the CNS

摘要: A critical factor in the host immune response to invading pathogens, such as viral infections, is recruitment and infiltration of cells infected tissues. Although goal recruited leukocytes eliminate collateral tissue damage may be induced process, and, certain circumstances, pose a serious threat survival host. The central nervous system (CNS) unique site with limited regenerative potential therefore low threshold for inflammation-induced damage. However, CNS become target life-threatening it imperative that immunological surveillance efficient effector responses occur this organ aid pathogen clearance. traditionally characterized “immune privilege,” evidence suggests antiviral immunity does (Carson et al., 2006). Understanding how local inflammatory within regulated key understanding pathogenesis infections developing therapies promote protective limit pathogenic responses. Leukocyte any generally complex, multistep process. Under normal conditions, leukocyte migration into maintained at levels (Hickey, 2001). During virus-induced inflammation, however, extravasation increased targeted specific compartments depending on stimulus region. Chemokines chemokine receptors have been identified pivotal players regulating cell trafficking CNS. consist large family small, structurally related, chemotactic cytokines are involved lymphocytic traffic both lymphoid nonlymphoid organs emigration sites injury infection (Rossi & Zlotnik, 2000). select entry based their expression receptors, G-protein-coupled surface which characteristic seven transmembrane structure (Premack Schall, 1996). In addition targeting distinct populations during chemokines emerged crucial mediators variety biological processes including development homeostasis. With regard inflammation CNS, strategic position coordinate through regulation also final positioning activation infiltrating cells. Immune function dictate host-pathogen relationship