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Distinct regulation of MHC molecule expression on astrocytes and microglia during viral encephalomyelitis
Author(s) -
Hamo Ludwig,
Stohlman Stephen A.,
OttoDuessel Maya,
Bergmann Cornelia C.
Publication year - 2007
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.20538
Subject(s) - microglia , biology , astrocyte , major histocompatibility complex , neuroglia , glial fibrillary acidic protein , mhc class ii , mhc class i , microbiology and biotechnology , immunology , antigen presentation , inflammation , encephalomyelitis , neuroinflammation , central nervous system , t cell , neuroscience , antigen , immune system , multiple sclerosis , immunohistochemistry
The potential interplay of glial cells with T cells during viral induced inflammation was assessed by comparing major histocompatibility complex molecule upregulation and retention on astrocytes and microglia. Transgenic mice expressing green fluorescent protein under control of the astrocyte‐specific glial fibrillary acidic protein promoter were infected with a neurotropic coronavirus to facilitate phenotypic characterization of astrocytes and microglia using flow cytometry. Astrocytes in the adult central nervous system up‐regulated class I surface expression, albeit delayed compared with microglia. Class II was barely detectable on astrocytes, in contrast to potent up‐regulation on microglia. Maximal MHC expression in both glial cell types correlated with IFN‐γ levels and lymphocyte accumulation. Despite a decline of IFN‐γ concomitant to virus clearance, MHC molecule expression on glia was sustained. These data demonstrate distinct regulation of both class I and class II expression by microglia and astrocytes in vivo following viral induced inflammation. Furthermore, prolonged MHC expression subsequent to viral clearance implies a potential for ongoing presentation. © 2007 Wiley‐Liss, Inc.