Aggravation of murine experimental allergic encephalomyelitis by administration of T-cell receptor gammadelta-specific antibody.
Experimental allergic encephalomyelitis (EAE) is thought to be dominantly mediated by Ag-specific CD4+ MHC class II-restricted T-cells. Recent reports demonstrated accumulation of gammadelta T-cells in active multiple sclerosis (MS) plaque and infiltration into brains with EAE. However, the role of gammadelta T-cells in pathogenesis of EAE remains unknown. In the present study we have examined EAE mice administered T-cell receptor (TCR) gammadelta-specific mAb (UC7-13D5) to elucidate the potential role of gammadelta T-cells in the pathogenesis of EAE. MAb treatment led to transient depleting gammadelta T-cells in vivo. MAb-treated EAE mice showed aggravation and disease recurrence and also increased Ag-specific proliferative responses. Semiquantitative PCR analysis demonstrated an increased level of IFN-gamma mRNA expression in splenocytes from mAb-treated EAE mice during the induction and pre-relapse phase, however, aggravation and disease recurrence have not been suggested to be directly mediated by IFN-gamma in the present study. Our results imply that gammadelta T-cells play a preventing role in the recurrence of EAE.