Key result
Anti-CD4 monoclonal antibodies block IgG responses and reduce T-cell signaling in murine autoimmune cardiomyopathy.
Why the study?
T-cell immune abnormalities in dilated cardiomyopathy have been intensively studied, but the molecular mechanisms of T-cell signaling in autoimmune cardiomyopathy remain to be elucidated.
Does anti-CD4 monoclonal antibody treatment alter IgG subclass antibody response and T-cell receptor signaling molecule expression in a mouse model of autoimmune cardiomyopathy?
Does anti-CD4 monoclonal antibody treatment alter IgG subclass antibody response and T-cell receptor signaling molecule expression in a mouse model of autoimmune cardiomyopathy?
Anti-CD4 monoclonal antibody treatment inhibits T-cell proliferation and alters T-cell receptor signaling in a mouse model of autoimmune cardiomyopathy, suggesting CD4+ T-cells play a critical role in the disease.
Should not change clinical practice; leaves open CD4+ T-cell targeting in human autoimmune cardiomyopathy.
T-cell immune abnormality in patients of dilated cardiomyopathy has been intensively studied over the past 10 years. In this study, we aim to focus on the molecular mechanism of T-cells in autoimmune cardiomyopathy mouse model by detecting the expression of three T-cell signaling molecules. Balb/C mice (n = 12) were immunized with the peptides derived from human ADP/ATP carrier on the 1st, 14th, 28th, 49th and 79th days, and half of them were also injected with anti-L3T4 McAb on the - 1st, 0 and 1st days. The sham-immunized mice were taken as the controls (n = 6). The main result shows that the antibody response of IgG subclasses such as IgG1, IgG2b and IgG3 were definitely blocked except IgG2a in CD4+ cell-depleted Balb/C mice. In addition, the average mRNA expression of p56lck, p59fyn and zap-70 were all found to be dramatically higher in the mice immunized with only ADP/ATP carrier peptides than in the control-group. At meantime, reduced levels of the protein kinases p56lck, p59fyn and zap-70 were clearly observed in anti-CD4 McAb immunized group compared with DCM group. We propose that the proliferation of T-cells was significantly inhibited in anti-CD4 treated mice and CD4+ T-cells may play a critical role in ADP/ATP carrier caused mouse DCM.
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Wang et al. (2006) studied autoimmune cardiomyopathy (n=18). anti-CD4 monoclonal antibody (anti-L3T4 McAb) vs. immunized with only ADP/ATP carrier peptides (DCM group) and sham-immunized controls was evaluated on IgG subclass antibody response and mRNA expression of p56lck, p59fyn and zap-70. Anti-CD4 monoclonal antibody treatment in mice with autoimmune cardiomyopathy blocked IgG1, IgG2b, and IgG3 responses and reduced the expression of T-cell signaling molecules p56lck, p59fyn, and zap-70.
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