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Direct activation of innate and antigen-presenting functions of microglia following infection with Theiler's virus

J K Olson1, A M Girvin, S D Miller

  • 1Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Northwestern University Medical School, Chicago, Ilinois 60611, USA.

Journal of Virology
|September 18, 2001
PubMed

Insights

Theiler

Area of Science:

  • Neuroimmunology
  • Virology
  • Immunology

Background:

  • Microglia are the primary immune cells of the central nervous system (CNS).
  • Theiler's murine encephalomyelitis virus (TMEV) infection in mice leads to persistent CNS microglia infection and chronic autoimmune demyelination.
  • The role of microglia activation in initiating adaptive immune responses during TMEV infection is not fully understood.

Purpose of the Study:

  • To investigate whether TMEV infection activates microglial innate immune functions.
  • To determine if TMEV-infected microglia can act as antigen-presenting cells (APCs) for T-cell activation.
  • To explore the potential of microglia in initiating autoimmune responses against myelin antigens.

Main Methods:

  • Persistent infection of microglia cell lines with TMEV.
  • Analysis of cytokine and costimulatory molecule expression in infected microglia.
  • Assessment of antigen processing and presentation capabilities of TMEV-infected microglia using CD4(+) Th1 cells.

Main Results:

  • TMEV infection persistently infected microglia and upregulated innate immune cytokines (TNF-α, IL-6, IL-18, type I interferons).
  • Infected microglia showed increased expression of MHC class II, IL-12, and costimulatory molecules (B7-1, B7-2, CD40, ICAM-1).
  • TMEV-infected microglia efficiently presented viral and myelin epitopes to CD4(+) Th1 cells.

Conclusions:

  • TMEV infection activates microglia's innate immune functions and APC capabilities.
  • Activated microglia can present viral and self-antigens, potentially initiating autoimmune responses.
  • Microglia play a crucial role in bridging innate and adaptive immunity during persistent viral CNS infections.

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