Type 1 Diabetes Worsens Heart Attacks (IMAGE)
Caption
This image shows the proposed pathogenesis of post-infarction autoimmunity (PIA) in type 1 diabetes. (1) Absence of α-myosin expression in thymus leads to the escape of high-avidity cardiac myosin-specific naïve CD4+ T cells into the peripheral blood. (2) Myocardial infarction triggers the release of large amounts of cardiac myosin, followed by (3) influx of innate immune cells including macrophages and dendritic cells (DCs) into the infarct zone, with engulfment of necrotic myocytes and activation ("maturation") of DCs. (4) Mature DCs then migrate to cardiac-draining lymph node and present cardiac myosin peptides to naïve CD4+ T cells. In autoimmune-prone hosts -- such as NOD mice or type 1 diabetes patients -- due to defective immunoregulation, cardiac myosin-specific CD4+ T cells become persistently activated, and migrate from the cardiac lymph node back into the injured heart, causing further injury. (5) This secondary injury forms a "positive feedback loop" for the activation and expansion of cardiac myosin-specific CD4+ T cells, leading to chronic cardiac autoimmunity with impaired infarct healing (‘PIA’). This image relates to a paper that appeared in the June 13, 2012, issue of Science Translational Medicine, published by AAAS. The paper, by Dr. R.V. Gottumukkala at Harvard Medical School in Boston, Mass., and colleagues, was titled, "Myocardial Infarction Triggers Chronic Cardiac Autoimmunity in Type 1 Diabetes."
Credit
Image courtesy of Myra A. Lipes
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