T cells of mice treated with mPEG-myasthenogenic peptide conjugate are involved in protection against EAMG by stimulating lower pathogenic antibody responses

Experimental autoimmune myasthenia gravis (EAMG) can be induced in C57BL/6 (B6) mice by immunization with Torpedo californica acetylcholine receptor ( tAChR), We had previously shown that pretreatment with a monomethoxypolyeth ylene glycol (mPEG) conjugate of myasthenogenic tAChR alpha-chain peptide a lpha 125-148 (mPEG-peptide) suppressed EAMG, In order to understand the mec hanism involving T cells in the induction of this suppression, we have stud ied, in the present work, the in vitro responses of T cells from mPEG-pepti de treated B6 mice after an initial tAChR injection to determine the early effect of mPEG-peptide treatment on these responses. Treatment with mPEG-pe ptide reduced the T cell responses to tAChR and several tAChR alpha-chain p eptides, To further investigate the T cell helper function in vivo, we tran sferred T cells from B6 mice that received either mPEG-peptide or control P BS followed by two tAChR injections to non-immune B6 mice. T fell transfer from mPEG-peptide pretreated mice down regulated, in recipient mice, Ab ind uction (after cell transfer) and Ab production (after two tAChR injections) toward alpha-chain peptides, Treatment of B6 mice with mPEG-peptide did no t alter the ability of their APC to present peptide alpha 146-162 to peptid e-specific B6 T cells. The results indicate that suppression of EAMG by tre atment with mPEG-peptide is due to T cell involvement and not to a defect i n APC function.