       Document 0661
 DOCN  M9610661
 TI    Microglia: intrinsic immuneffector cell of the brain.
 DT    9601
 AU    Gehrmann J; Matsumoto Y; Kreutzberg GW; Department of Pathology,
       University Hospital, Zurich,; Switzerland.
 SO    Brain Res Brain Res Rev. 1995 Mar;20(3):269-87. Unique Identifier :
       AIDSLINE MED/96031752
 AB    Microglia form a regularly spaced network of resident glial cells
       throughout the central nervous system (CNS). They are morphologically,
       immunophenotypically and functionally related to cells of the
       monocyte/macrophage lineage. In the ultimate vicinity of the blood-brain
       barrier two specialized subsets of macrophages/microglia can be
       distinguished: firstly, perivascular cells which are enclosed within the
       basal lamina and secondly juxtavascular microglia which make direct
       contact with the parenchymal side of the CNS vascular basal lamina but
       represent true intraparenchymal resident microglia. Bone marrow chimera
       experiments indicates that a high percentage of the perivascular cells
       undergoes replacement with bone marrow-derived cells. In contrast,
       juxtavascular microglia like other resident microglia form a highly
       stable pool of CNS cells with extremely little turnover with the bone
       marrow compartment. Both the perivascular cells and the juxtavascular
       microglia play an important role in initiating and maintaining CNS
       autoimmune injury due to their strategic localization at a site close to
       the blood-brain barrier, their rapid inducibility for MHC class II
       antigens and their potential scavenger role as phagocytic cells. The
       constantly replaced pool of perivascular cells probably represents an
       entry route by which HIV gets access to the brain. Microglia are the
       first cell type to respond to several types of CNS injury. Microglial
       activation involves a stereotypic pattern of cellular responses, such as
       proliferation, increased or de-novo expression of immunomolecules,
       recruitment to the site of injury and functional changes, e.g., the
       release of cytotoxic and/or inflammatory mediators. In addition,
       microglia have a strong antigen presenting function and a pronounced
       cytotoxic function. Microglial activation is a graded response, i.e.,
       microglia only transform into intrinsic brain phagocytes under
       conditions of neuronal and or synaptic/terminal degeneration. In
       T-cell-mediated autoimmune injury of the nervous system, microglial
       activation follows these lines and occurs at an early stage of disease
       development. In experimental autoimmune encephalomyelitis (EAE),
       microglia proliferate vigorously, show a strong expression of MHC class
       I and II antigens, cell adhesion molecules, release of reactive oxygen
       intermediates and inflammatory cytokines and transform into phagocytic
       cells. Due to their pronounced antigen presenting function in vitro,
       activated microglia rather than astrocytes or endothelial cells are the
       candidates as intrinsic antigen presenting cel of the brain. In contrast
       to microglia, astrocytes react with a delay, appear to encase
       morphologically the inflammatory lesion and may be instrumental in
       downregulating the T-cell-mediated immune injury by inducing T-cell
       apoptosis.(ABSTRACT TRUNCATED AT 400 WORDS)
 DE    Brain/*CYTOLOGY/*IMMUNOLOGY  Microglia/*IMMUNOLOGY  Support, Non-U.S.
       Gov't  JOURNAL ARTICLE  REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

