HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hofstetter, H. H. Articles by Lehmann, P. V. Search for Related Content PubMed PubMed Citation Articles by Hofstetter, H. H. Articles by Lehmann, P. V.

Kinetics and Organ Distribution of IL-17-Producing CD4 Cells in Proteolipid Protein 139–151 Peptide-Induced Experimental Autoimmune Encephalomyelitis of SJL Mice¹

Harald H. Hofstetter^*,, Klaus V. Toyka, Magdalena Tary-Lehmann^* and Paul V. Lehmann^2,*

^* Department of Pathology, Case Western Reserve University, Cleveland, OH 44106; and Clinical Research Group for Multiple Sclerosis, Department of Neurology, University of Würzburg, Würzburg, Germany

In experimental autoimmune encephalomyelitis (EAE), the production of proinflammatory cytokines by neuroantigen-specific T cells is thought to initiate and maintain the inflammatory autoimmune pathology. Because gene knockout strategies have shown that IFN- and TNF are not essential for EAE development, there is increasing interest in establishing the role of other proinflammatory cytokines, primarily IL-17 in EAE. We used an IL-17 ELISPOT assay to track the neuroantigen-specific IL-17-producing T cells at single-cell resolution in various organs of SJL mice undergoing PLP 139–151-induced EAE. Overall, the migration patterns and population kinetics of the PLP 139–151-specific IL-17-producing CD4 cells were reminiscent of the IFN--producing cells, with the exception of IL-17 producers far outnumbering the IFN- and IL-2 producers in the inflamed CNS. The selective enrichment of IL-17-producing CD4 cells in the CNS is suggestive of the pathogenic role of an independent (non-Th1) IL-17-producing proinflammatory effector T cell class in EAE.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by a travel scholarship of the European Neurological Society (to H.H.H.) and a nonrestricted research grant by Biogen Idec Deutschland (to H.H.H. and K.V.T.). This work was also supported by grants to P.V.L. from the National Institutes of Health (NS-39434) and to M.T.L. (AI-47756).

² Address correspondence and reprint requests to Dr. Paul V. Lehmann, Department of Pathology, Wolstein Building, Room 5129, Case Western Reserve University, Cleveland, OH 44106-4943. E-mail address: pvl2{at}po.cwru.edu

³ Abbreviations used in this paper: Th-17, CD4 memory/effector cell lineages that secretes IL-17; drLN, draining lymph node; EAE, experimental autoimmune encephalomyelitis; KO, knockout; PLP, proteolipid protein; PLPp, proteolipid protein peptide 139–151; PTX, pertussis toxin.

This article has been cited by other articles:

				R. Gold and F. Luhder Interleukin-17--Extended Features of a Key Player in Multiple Sclerosis Am. J. Pathol., January 1, 2008; 172(1): 8 - 10. [Abstract] [Full Text] [PDF]

				A. Linden A Role for the Cytoplasmic Adaptor Protein Act1 in Mediating IL-17 Signaling Sci. Signal., August 7, 2007; 2007(398): re4 - re4. [Abstract] [Full Text] [PDF]