1. ¹Department of Medicine, Division of Infectious Diseases and International Medicine, University of Minnesota Medical School, University of Minnesota, Minneapolis, MN, USA
2. ²Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, University of Minnesota, Minneapolis, MN, USA
3. ³Biomedical Genomic Center, University of Minnesota, Minneapolis, MN, USA
4. ⁴Department of Microbiology, University of Minnesota, Minneapolis, MN, USA

Correspondence: Dr V Kapur, Department of Microbiology and Biomedical Genomics Center, 1500 Gortner Avenue, University of Minnesota, St Paul, MN 55108, USA. E-mail: vkapur@umn.edu

Received 25 February 2005; Revised 27 May 2005; Accepted 27 May 2005; Published online 15 September 2005.

Abstract

Microglia, the resident macrophages in the central nervous system (CNS), play a pivotal role in innate and adaptive immune responses in the brain. The immune functions of microglia are regulated by cytokines, including interferon (IFN)-, which is a major mediator of macrophage activation. We describe the transcriptional profile of human fetal microglial cells at 1, 6, and 24 h after IFN- treatment. The results show a change in the expression of 405 genes including transcriptionally induced chemokines, IFN- signaling factors, and major histocompatibility complex genes. Our results demonstrate that activation of microglia by IFN- induces proinflammatory T-lymphocyte-related chemokine genes as well as genes involved in antigen presentation. As a result, signals for T-cell infiltration and antigen presentation are produced to allow for microglia–T-cell interactions that likely contribute to defense against invading pathogens. In sum, our results provide a foundation for the molecular mechanisms of the microglial response to IFN-—a key to understanding cell-mediated immunity of the CNS.