The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published 19 September 2005. doi:10.1084/jem.20050660
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 6, 853-863
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 2530K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kihara, Y.
Right arrow Articles by Shimizu, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kihara, Y.
Right arrow Articles by Shimizu, T.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

ARTICLE

 Dual phase regulation of experimental allergic encephalomyelitis by platelet-activating factor

Yasuyuki Kihara1, Satoshi Ishii1, Yoshihiro Kita1, Akiko Toda1, Atsuyoshi Shimada2, and Takao Shimizu1

1 Department of Biochemistry and Molecular Biology, Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan
2 Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, Aichi 480-0392, Japan

CORRESPONDENCE Takao Shimizu: tshimizu{at}m.u-tokyo.ac.jp

Experimental allergic encephalomyelitis (EAE) serves as a model for multiple sclerosis and is considered to be a CD4+ Th1 cell–mediated autoimmune disease. To investigate the role of platelet-activating factor (PAF) in this disease, PAF receptor (PAFR) KO (PAFR-KO) and wild-type (WT) mice, on a C57BL/6 genetic background, were immunized with myelin oligodendrocyte glycoprotein 35–55. The levels of PAF production and PAFR mRNA expression in the spinal cord (SC) correlated with the EAE symptoms. PAFR-KO mice showed lower incidence and less severe symptoms in the chronic phase of EAE than WT mice. However, no difference was observed in T cell proliferation, Th1-cytokine production, or titer of IgG2a between both genotypes. Before onset, as revealed by microarray analysis, mRNAs of inflammatory mediators and their receptors—including IL-6 and CC chemokine receptor 2—were down-regulated in the SC of PAFR-KO mice compared with WT mice. Moreover, in the chronic phase, the severity of inflammation and demyelination in the SC was substantially reduced in PAFR-KO mice. PAFR-KO macrophages reduced phagocytic activity and subsequent production of TNF-{alpha}. These results suggest that PAF plays a dual role in EAE pathology in the induction and chronic phases through the T cell–independent pathways.

Abbreviations used: cPLA2, cytosolic phospholipase A2; CNS, central nervous system; EAE, experimental allergic encephalomyelitis; ESI, electrospray ionization; H&E, hematoxylin-eosin; LFB, luxol fast blue; lyso-PAF AT; lyso-PAF acetyltransferase; MCP, monocyte chemoattractant protein; MOG, myelin oligodendrocyte glycoprotein; MS, multiple sclerosis; MS/MS, tandem mass spectrometry; PAF, platelet-activating factor; PAFR, PAF receptor; SC, spinal cord.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS