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Langer, H.F.* ; Choi, E.Y.* ; Zhou, H.* ; Schleicher, R.* ; Chung, K.-J.* ; Tang, Z.* ; Gobel, K.* ; Bdeir, K.* ; Chatzigeorgiou, A.* ; Wong, C.* ; Bhatia, S.* ; Kruhlak, M.J.* ; Rose, J.W.* ; Burns, J.B.* ; Hill, K.E.* ; Qu, H.* ; Zhang, Y.* ; Lehrmann, E.* ; Becker, K.G.* ; Wang, Y.* ; Simon, D.I.* ; Nieswandt, B.* ; Lambris, J.D.* ; Li, X.* ; Meuth, S.G.* ; Kubes, P.* ; Chavakis, T.*

Platelets contribute to the pathogenesis of experimental autoimmune encephalomyelitis.

Circ. Res. 110, 1202-1010 (2012)
DOI Order publishers version
Open Access Green as soon as Postprint is submitted to ZB.
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.
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Publication type Article: Journal article
Document type Scientific Article
ISSN (print) / ISBN 0009-7330
e-ISSN 1524-4571
Quellenangaben Volume: 110, Issue: 9, Pages: 1202-1010 Article Number: , Supplement: ,
Publisher Lippincott Williams & Wilkins
Reviewing status Peer reviewed
Institute(s) Institute for Pancreatic Beta Cell Research (IPI)