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Production of interferon- by microglia

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan

T Mizuno

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan

H Takeuchi

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan

H Kato

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan

J Wang

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan

N Mitsuma

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan

A Suzumura

Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusaku, Nagoya 464-8601, Japan, suzumura{at}riem.nagoya-u.ac.jp

Neural cells do not usually interact with immune cells because of the lack of major histocompatibility complex (MHC) antigen expression. Interferon- (IFN-) enables this interaction via induction of MHC antigen expression in neural cells. Thus, IFN- is a critical cytokine for the development of central nervous system (CNS) pathologies. IFN-, however, is considered to be produced exclusively by lymphoid cells. Here, we show for the first time that murine microglia produce IFN- in response to IL-12 and/or IL-18, using RT-PCR detection of IFN- mRNA and Western blotting and immunohistochemical analysis for cytoplasmic expression of IFN-. Stimulation of microglia with IL-12 and IL-18 resulted in MHC class II mRNA expression in microglia. Since IL-12 and IL-18 are produced in the CNS by glial cells, these cytokines may play a critical role in the initiation of neural immune cell interaction and the induction of autoimmune processes in the CNS via induction of IFN- and MHC antigens.

Key Words: cytokine • EAE/MS • INF- • MHC • microglia

Multiple Sclerosis, Vol. 12, No. 5, 558-564 (2006)
DOI: 10.1177/1352458506070763


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