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Updated: May 23, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
Published on: March 26, 2019
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
Rationale:
Multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE), are inflammatory disorders of the central nervous system (CNS). The function of platelets in inflammatory and autoimmune pathologies is thus far poorly defined.
Objective:
We addressed the role of platelets in mediating CNS inflammation in EAE.
Methods And Results:
We found that platelets were present in human MS lesions as well as in the CNS of mice subjected to EAE but not in the CNS from control nondiseased mice. Platelet depletion at the effector-inflammatory phase of EAE in mice resulted in significantly ameliorated disease development and progression. EAE suppression on platelet depletion was associated with reduced recruitment of leukocytes to the inflamed CNS, as assessed by intravital microscopy, and with a blunted inflammatory response. The platelet-specific receptor glycoprotein Ibα (GPIbα) promotes both platelet adhesion and inflammatory actions of platelets and targeting of GPIbα attenuated EAE in mice. Moreover, targeting another platelet adhesion receptor, glycoprotein IIb/IIIa (GPIIb/IIIa), also reduced EAE severity in mice.
Conclusions:
Platelets contribute to the pathogenesis of EAE by promoting CNS inflammation. Targeting platelets may therefore represent an important new therapeutic approach for MS treatment.
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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