AGGRAVATION OF MURINE EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS BY ADMINISTRATION OF T-CELL RECEPTOR GAMMA-DELTA-SPECIFIC ANTIBODY

Experimental allergic encephalomyelitis (EAE) is thought to be dominan tly mediated by Ag-specific CD4(+) MHC class II-restricted T-cells. Re cent reports demonstrated accumulation of gamma delta T-cells in activ e multiple sclerosis (MS) plaque and infiltration into brains with EAE . However, the role of ya T-cells in pathogenesis of EAE remains unkno wn. In the present study we have examined EAE mice administered T-cell receptor (TCR) gamma delta-specific mAb (UC7-13D5) to elucidate the p otential role of gamma delta T-cells in the pathogenesis of EAE. MAb t reatment led to transient depleting gamma delta T-cells in vivo. MAb-t reated EAE mice showed aggravation and disease recurrence and also inc reased Ag-specific proliferative responses. Semiquantitative PCR analy sis demonstrated an increased level of IFN-gamma mRNA expression in sp lenocytes from mAb-treated EAE mice during the induction and pre-relap se phase, however, aggravation and disease recurrence have not been su ggested to be directly mediated by IFN-gamma in the present study. Our results imply that gamma delta T-cells play a preventing role in the recurrence of EAE.