Background T cell immune abnormalities in patients with dilated cardiomyopathy(DCM)has been intensively studiedover the past 10 years.Our previous study has suggested that immunization of mice with the peptides derived fromhuman adenine nucleotide translocator(ANT)result in the production of autoantibodies against the ANT andhistopathological changes similar to those in human DCM.The ANT peptides can induce autoimmune cardiomyopathylike DCM in Balb/c mice.In this study we aimed to focus on the molecular mechanism of T cells in the autoimmunecardiomyopathy mouse model by detecting the expression of the two T cell signaling molecules.Methods The ANT peptides were used to cause autoimmune cardiomyopathy in Balb/c mice.Anti-L3T4 or ratanti-mouse IgG was administered to the mice(n=6 in each group)simultaneously immunized with ANT.ELISA analysiswas used to detect autoantibodies against the ANT peptides and the percentages of interferon-Y and interleukin-4producing cells among splenic CD4~+lymphocytes was determined by using flow cytometry analysis.The expression ofCD45 in spleen T cells was determined by immunohistochemistry and the mRNAs of T cell signaling molecules weredetected by real-time PCR.Results Treatment of ANT immunized Balb/c mice with anti-CD4 mAb caused a reduction in the gene expression ofP561ck and Zap-70 and a lower level of CD45 expression by spleen T cells.Also,a reverse of the Th1/Th2 ratio thatresults in the reduced production of antibodies against ANT was found in the anti-CD4 monoclonal antibodies(mAb)group.Whereas irrelevant antibody(rat anti-mouse IgG)did not suppress T cell signaling molecules nor inhibit CD45expression,and control-antibody mice did not show any significant differences compared with the DCM group.Conclusion The results show that anti-CD4 mAb is a powerful inhibitor of the early initiating events of T cell receptor(TCR)signal transduction in mouse autoimmune dilated cardiomyopathy. Background T cell immune abnormalities in patients with dilated cardiomyopathy (DCM) has been intensively studied past the past 10 years. Our previous study has suggested that immunization of mice with the peptides derived fromhuman adenine nucleotide translocator (ANT) result in the production of autoantibodies against the ANT andhistopathological changes similar to those in human DCM. These ANT peptides can induce autoimmune cardiomyopathylike DCM in Balb / c mice. In this study we aimed to focus on the molecular mechanism of T cells in the autoimmune cardiomyopathy mouse model by detecting the expression of the two T cell signaling molecules. Methods The ANT peptides were used to cause autoimmune cardiomyopathy in Balb / c mice. Anti-L3T4 or rat anti-mouse IgG were administered to the mice (n = 6 in each group) simultaneously with immunization with ANT. ELISA analysis was used to detect autoantibodies against the ANT peptides and the percent of interferon-Y and interleukin-4producing cells among splenic CD4 ~ + ly mphocytes was determined by using flow cytometry analysis. The expression of CD45 in spleen T cells was determined by immunohistochemistry and the mRNAs of T cell signaling molecules weredetected by real-time PCR. Results of treatment of ANT immunized Balb / c mice with anti-CD4 mAb caused a reduction in the gene expression of P561ck and Zap-70 and a lower level of CD45 expression by spleen T cells. Also, a reverse of the Th1 / Th2 ratio that results in the reduced production of antibodies against ANT was found in the anti-CD4 monoclonal antibodies (mAb) group. Western irrelevant antibody (rat anti-mouse IgG) did not suppress T cell signaling molecules nor inhibit CD45 expression, and control-antibody mice did not show any significant differences compared with the DCM group. Confc The results show that anti -CD4 mAb is a powerful inhibitor of the early initiating events of T cell receptor (TCR) signal transduction in mouse autoimmune dilated cardiomyopathy.