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Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury
Author(s) -
Lehnardt Seija
Publication year - 2010
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20928
Subject(s) - microglia , neuroinflammation , innate immune system , biology , immune system , proinflammatory cytokine , acquired immune system , pattern recognition receptor , immunology , neuroscience , toll like receptor , neurodegeneration , immunity , ccl18 , inflammation , medicine , disease , pathology
Microglia are key players of the immune response in the central nervous system (CNS) and, being the resident innate immune cells, they are responsible for the early control of infections and for the recruitment of cells of the adaptive immune system required for pathogen clearance. The innate and adaptive immune responses triggered by microglia include the release of proinflammatory mediators. Although an efficient immune response is required for the defense against invading pathogens, an inflammatory response in the CNS may also lead to tissue injury and neurodegeneration. Engagement of Toll‐like receptors (TLRs), a major family of pattern recognition receptors that mediate innate immunity but also link with the adaptive immune response, provides an important mechanism by which microglia are able to sense both pathogen‐ and host‐derived ligands within the CNS. Although there is an increasing body of evidence that TLR signaling mediates beneficial effects in the CNS, it has become clear that TLR‐induced activation of microglia and the release of proinflammatory molecules are responsible for neurotoxic processes in the course of various CNS diseases. Thus, the functional outcome of TLR‐induced activation of microglia in the CNS depends on a subtle balance between protective and harmful effects. This review focuses on the neurodegenerative effects of TLR signaling in the CNS. © 2009 Wiley‐Liss, Inc.