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FLT-3 expression and function on microglia in multiple sclerosis.

Cynthia A DeBoy1, Horea Rus, Cosmin Tegla

  • 1Neurology, Johns Hopkins University, Pathology 627, 600 N. Wolfe Street, Baltimore, MD 21287,USA.

Experimental and Molecular Pathology
|June 23, 2010
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FMS-like tyrosine-3 (FLT-3) is present in multiple sclerosis (MS) brain cells, including microglia. Inhibiting FLT-3 in mice reduced inflammation and may offer a new therapeutic target for MS.

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Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Neuroscience

Background:

  • Microglial activation and inflammatory cell infiltration are key pathological features of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE).
  • Current MS therapies primarily target the peripheral immune system, leaving microglia, the resident immune cells of the central nervous system (CNS), untargeted.
  • FMS-like tyrosine-3 (FLT-3) is known to be expressed on hematopoietic and dendritic cells, and its inhibition was previously shown to ameliorate EAE by modulating dendritic cell function.

Purpose of the Study:

  • To investigate the expression and role of FLT-3 in the CNS, particularly in the context of MS.
  • To determine if FLT-3 is expressed on microglia within the MS brain and if it influences microglial function.
  • To explore the potential of FLT-3 as a therapeutic target for mitigating CNS inflammation in MS.

Main Methods:

  • Immunohistochemical analysis of FLT-3 expression in MS brain tissue compared to control brain.
  • Characterization of FLT-3 expressing cells in MS brain using markers like CD209 (dendritic cell marker).
  • In vitro studies involving inhibition of FLT-3 in murine microglia to assess its impact on inflammatory responses (MHC class II, CD86 expression, IL-6 secretion).

Main Results:

  • FLT-3 expression was detected in perivascular cuffs, brain parenchyma, and non-lesioned areas of MS brains, but not in control brains.
  • FLT-3 was found on two cell populations in MS brain: CD209-positive (dendritic cells) and CD209-negative cells (potentially microglia).
  • FLT-3 inhibition in murine microglia dose-dependently blocked IFN-γ-induced MHC class II and CD86 expression and LPS-induced IL-6 secretion.

Conclusions:

  • FLT-3 is expressed in the MS brain on both infiltrating dendritic cells and resident microglia.
  • FLT-3 plays a role in microglial activation and their function as antigen-presenting cells, contributing to CNS inflammation.
  • FLT-3 inhibition presents a potential therapeutic strategy for modulating microglial activity and mitigating neuroinflammation in MS.