Platelets contribute to the pathogenesis of experimental autoimmune encephalomyelitis

Harald F Langer1, Eun Young Choi, Hong Zhou

  • 1Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Harald.Langer@med.uni-tuebingen.de

Circulation Research
|March 30, 2012
PubMed
Abstract

Insights

Platelets contribute to central nervous system (CNS) inflammation in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS). Targeting platelets and their receptors ameliorated EAE, suggesting a new therapeutic avenue for MS.

Area of Science:

  • Neuroimmunology
  • Hematology

Background:

  • Multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE), are central nervous system (CNS) inflammatory disorders.
  • The role of platelets in autoimmune pathologies, particularly within the CNS, remains incompletely understood.

Purpose of the Study:

  • To investigate the function of platelets in mediating CNS inflammation during EAE.
  • To evaluate the therapeutic potential of targeting platelets in EAE.

Main Methods:

  • Detection of platelets in MS lesions and EAE mouse CNS.
  • Platelet depletion in EAE mice during the effector-inflammatory phase.
  • Assessment of leukocyte recruitment via intravital microscopy.
  • Targeting of platelet receptors glycoprotein Ibα (GPIbα) and glycoprotein IIb/IIIa (GPIIb/IIIa).

Main Results:

  • Platelets were found in human MS lesions and EAE mouse CNS, but not in control mice.
  • Platelet depletion significantly reduced EAE development and progression.
  • Reduced leukocyte infiltration and attenuated CNS inflammation were observed in platelet-depleted mice.
  • Targeting GPIbα and GPIIb/IIIa receptors ameliorated EAE severity.

Conclusions:

  • Platelets play a significant role in promoting CNS inflammation and pathogenesis of EAE.
  • Targeting platelet function presents a promising therapeutic strategy for treating MS.

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