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Induction of Functional Interleukin‐2 Receptor in Mouse Microglia
Author(s) -
Sawada Makoto,
Suzumura Akio,
Marunouchi Tohru
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64051973.x
Subject(s) - microglia , receptor , biology , cytokine , microbiology and biotechnology , lipopolysaccharide , immunology , inflammation , biochemistry
Interleukin (IL)‐2, initially discovered for its mitogenic activity on T cells, also acts on monocytes, resulting in the activation of cytokine production, superoxide production, and tumoricidal activity. Because severe brain damage was observed in IL‐2‐transgenic mice, this cytokine may have some influence(s) on the cells of the CNS. We investigated IL‐2 receptor‐bearing cells in the CNS and found that activated microglia expressed α‐chain mRNA and immunoreactive IL‐2 receptor β‐chain protein in culture. Although microglia did not express IL‐2 receptors under normal culture conditions, they were induced to express these receptors by lipopolysaccharide (LPS) in a time‐dependent manner. The IL‐2 receptors were found to be functional because the viability and growth activity of LPS‐treated microglia, but not untreated controls, increased in response to recombinant mouse IL‐2 as determined by a 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide colorimetric assay and bromodeoxyuridine uptake experiment, respectively. These effects of recombinant IL‐2 were blocked by pretreatment with anti‐mouse IL‐2 receptor β‐chain antibody. Our findings suggest that activated microglia in the CNS can respond to this T cell‐derived factor regulating their growth, which may be an important mechanism of communication between nervous and immune systems in physiological and pathological conditions.