Malkiel S, Kuan A P, Diamond B
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Mol Med Today. 1996 Aug;2(8):336-42. doi: 10.1016/1357-4310(96)81799-0.
Recent studies of heart disease suggest that immunologically mediated processes often accompany cardiac injury and can contribute to pathogenesis. Murine models of myocarditis have provided insight into the mechanisms by which autoimmune responses to cardiac antigens arise and cause tissue pathology. It is now evident that T cells, cytokines and antibodies can all contribute to cardiac injury. Furthermore, murine models have demonstrated that both the propensity to develop autoreactivity following cardiac injury and the vulnerability of the heart to these responses are under genetic control. Continued studies will help to identify susceptibility genes and might aid in the development of strategies to protect individuals at risk from immunologically mediated damage following cardiac injury.
最近关于心脏病的研究表明，免疫介导的过程常常伴随心脏损伤，并可能促进发病机制。心肌炎的小鼠模型为自身免疫反应如何针对心脏抗原产生并导致组织病理学变化的机制提供了深入见解。现在很明显，T细胞、细胞因子和抗体都可能导致心脏损伤。此外，小鼠模型已经证明，心脏损伤后产生自身反应性的倾向以及心脏对这些反应的易感性都受基因控制。持续的研究将有助于识别易感基因，并可能有助于制定策略来保护有风险的个体免受心脏损伤后免疫介导的损害。
