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Division of Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan
We have developed and described a new method of altering T
cell-mediated autoimmune diseases by immunization with the
complementary peptide against T cell epitopes. The complementary
peptide (denoted NAE 07-06) to the bovine P2 protein, residues 6070
(denoted EAN 6070), was tested in the Lewis rat model of experimental
allergic neuritis (EAN). Immunization with NAE 07-06 induced polyclonal
and monoclonal Abs that inhibited the proliferation of the P2-specific
T cell line, stimulated with EAN 6070, and recognized Vß, but not
V
, of TCRs. Proliferation of T cells treated with anti-NAE 07-06
Abs could be partially restored by treatment with rIL-2, in accordance
with an anergy model. A homologous sequence was found between NAE 07-06
and the VDJ junction of the TCR ß-chain from an EAN 6070-specific T
cell line. Rats preimmunized with NAE 07-06 in vivo before EAN
induction showed less disease severity clinically and histologically.
These data suggest a new therapeutic approach for T cell-mediated
autoimmune disorders through the induction of anti-TCR Abs with
complementary peptide Ags.
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