Transcriptional response of human microglial cells to interferon-γ

R. Bryan B Rock, S. Hu, Archana Deshpande, S. Munir, B. J. May, Cristina A Baker, Phillip K Peterson, V. Kapur

Research output: Contribution to journalArticlepeer-review

83 Scopus citations


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)-γ, which is a major mediator of macrophage activation. We describe the transcriptional profile of human fetal microglial cells at 1, 6, and 24h after IFN-γ treatment. The results show a change in the expression of 405 genes including transcriptionally induced chemokines, IFN-γ signaling factors, and major histocompatibility complex genes. Our results demonstrate that activation of microglia by IFN-γ 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-γ - a key to understanding cell-mediated immunity of the CNS.

Original languageEnglish (US)
Pages (from-to)712-719
Number of pages8
JournalGenes and Immunity
Issue number8
StatePublished - Dec 2005

Bibliographical note

Funding Information:
Special thanks to Aaron Becker and Jill Plumb-Smith at the Biomedical Genomic Center, University of Minnesota; Genya Gekker and Wen S Sheng at the Minneapolis Medical Research Foundation; and Wayne Xu at the Supercomputing Institute, University of Minnesota. The Kapur laboratory is supported, in-part, by research grants from the NIH, USDA, NSF, and DHS. BR and BM are supported by the Neurobehavior/Neuroimmune Addiction Research training program at the University of Minnesota funded by the National Institute on Drug Abuse, NIDA T32 DA07097. This work was supported in part by US Public Health Service Grant DA04381.


  • Chemokines
  • Cytokines
  • Gene expression
  • Interferon-γ
  • Microaaray analysis
  • Microglia


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