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A more recent version of this article appeared on July 1, 2008

Published online before print April 18, 2008
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0507312

Received for publication May 21, 2007.
Revised February 27, 2008.
Accepted for publication March 11, 2008.

Article

Mannosylated self-peptide inhibits the development of experimental autoimmune encephalomyelitis via expansion of nonencephalitogenic T cells

Junda M. Kel *{dagger}@, Bram Slutter *, Jan Wouter Drijfhout {dagger}, Frits Koning {dagger}, and Lex Nagelkerken *

*Business Unit Biosciences, TNO Quality of Life, Leiden, The Netherlands; and {dagger}Department of Immunohematology and Blood Transfusion, Leiden University Medical Centre, Leiden, The Netherlands

@ To whom correspondence should be addressed. E-mail: j.m.kel{at}amc.uva.nl.


  Abstract

Tolerance to experimental autoimmune encephalomyelitis (EAE) in SJL mice can be induced by immunization with a mannosylated form of the proteolipid protein (M-PLP139–151), despite the presence of CFA. The state of tolerance is characterized by poor delayed-type hypersensitivity responses and the absence of clinical EAE symptoms. In vivo monitoring of CFSE-labeled PLP139–151-specific TCR-transgenic (5B6) T cells revealed that immunization with M-PLP139–151 increases the clonal expansion of 5B6 T cells that do not develop full effector functions. Moreover, nonfunctional T cells obtained from M-PLP139–151-immunized mice showed poor blastogenesis and were unable to transfer EAE to naïve recipients. Nevertheless, the in vitro production of cytokines and chemokines associated with EAE was unaffected. Importantly, tolerance induced by M-PLP139–151 was abrogated by the administration of pertussis toxin, resulting in EAE development. Our results suggest that M-PLP139–151 inhibits EAE development by affecting the differentiation of T cells into encephalitogenic effector cells.

Key Words: delayed-type hypersensitivity (DTH) • tolerance • C-type lectins






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