CD3-specific monoclonal antibody was the first one used for clinical practice in field of transplantation.Recently,renewed interests have elicited in its capacity to prevent autoimmune diabetes by inducing immune tolerance.Inthis study,we tested whether this antibody can also be used to treat another kind of autoimmune diseasemyasthenia gravis(MG)and explored the possible mechanisms.MG is caused by an autoimmune damagemediated by antibody-and complement-mediated destruction of AChR at the neuromuscular junction.We foundthat administration of CD3-specific antibody(Fab)_2 to an animal model with experimental autoimmunemyasthenia gravis(EAMG)(B6 mice received 3 times of AChR/CFA immunization)could not significantly improvethe clinical signs and clinical score.When the possible mechanisms were tested,we found that CD3 antibodytreatment slightly down-regulated the T-cell response to AChR,modestly up-regulation the muscle strength.Andno significant difference in the titers of IgG2b was found between CD3 antibody treated and control groups.Thesedata indicated that CD3-specific antibody was not suitable for treating MG,an antibody-and complement-mediated autoimmune disease,after this disease has been established.The role of CD3-specific antibody in treatingthis kind of disease remains to be determined.Cellular & Molecular Immunology.2005;2(6):461-465. CD3-specific monoclonal antibody was the first one used for clinical practice in field of transplantation. Recently, renewed interests have elicited in its capacity to prevent autoimmune diabetes by inducing immune tolerance. Itis study, we tested whether this antibody can also be used to treat another kind of autoimmune disease myasthenia gravis (MG) and explored the possible mechanisms. MG is caused by an autoimmune damage mediated by antibody-and complement-mediated destruction of AChR at the neuromuscular junction. We found that administration of CD3-specific antibody (Fab) an animal model with experimental autoimmune myasthenia gravis (EAMG) (B6 mice received 3 times of AChR / CFA immunization) could not significantly improve the clinical signs and clinical score .When the possible mechanisms were tested, we found that CD3 antibody treatment slightly down-regulated the T -cell response to AChR, modestly up-regulation the muscle strength. And significant difference in the titers of IgG2b was found between CD3 antibody treated and control groups. Thesedata indicated that CD3-specific antibody was not suitable for treating MG, an antibody-and complement-mediated autoimmune disease, after this disease has been established. The role of CD3-specific antibody in treatingthis kind of disease remains to be determined. Cellular & Molecular Immunology. 2005; 2 (6): 461-465.