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*
Deutsches Rheumaforschungszentrum, Berlin, Germany;
Institut für Medizinische Immunologie, Universitätsklinikum Charité, Berlin, Germany; and
Universitätsklinikum Charité, Rheumatologie/Klinische Immunologie, Berlin, Germany
Activation of autoreactive T cells is a crucial event in the
pathogenesis of autoimmune diseases. Cross-reactivity between microbial
and self Ags (molecular mimicry) is one hypothesis that could explain
the activation of autoreactive T cells. We have systematically examined
this hypothesis in experimental autoimmune encephalomyelitis using mice
bearing exclusively myelin basic protein (MBP)-specific T cells
(designated T+ 
-). A peptide substitution
analysis was performed in which each residue of the
MBPAc1–11 peptide was exchanged by all 20 naturally
occurring amino acids. This allowed the definition of the motif
(supertope) that is recognized by the MBPAc1–11-specific T
cells. The supertope was used to screen protein databases (SwissProt
and TREMBL). By the search, 832 peptides of microbial origin were
identified and synthesized. Of these, 61 peptides induced proliferation
of the MBPAc1–11-specific transgenic T cells in vitro.
Thus, the definition of a supertope by global amino acid substitution
can identify multiple microbial mimic peptides that activate an
encephalitogenic TCR. Peptides with only two native MBP-residues were
sufficient to activate MBPAc1–11-specific T cells in
vitro, and experimental autoimmune encephalomyelitis could be induced
by immunizing mice with a mimic peptide with only four native MBP
residues.
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