Pober Jordan S
J Clin Invest. 2014 Oct;124(10):4234-6. doi: 10.1172/JCI77766. Epub 2014 Sep 17.
T cells are required for significant blood pressure elevation in mouse models of hypertension. Recent evidence suggests that the treatments that raise blood pressure in these animal models also cause oxidation within DCs, resulting in formation of isoketal adducts of self-proteins, which activate antigen-presenting functions of these cells and serve as a source of modified self-antigens. T cells specific for these modified self-antigens then produce cytokines that promote blood pressure elevation, consistent with the idea that hypertension is an autoimmune response to altered self. Here, I will review the new evidence for this idea put forth by Kirabo and colleagues in this issue of the JCI, identify a number of as yet unanswered questions, and discuss some of the therapeutic implications.
在高血压小鼠模型中，T细胞是显著血压升高所必需的。最近的证据表明，在这些动物模型中升高血压的治疗方法也会导致树突状细胞（DCs）内发生氧化，从而形成自身蛋白质的异酮加合物，这些加合物激活这些细胞的抗原呈递功能，并作为修饰自身抗原的来源。针对这些修饰自身抗原的T细胞随后产生促进血压升高的细胞因子，这与高血压是对改变的自身的自身免疫反应这一观点一致。在此，我将回顾基拉博及其同事在本期《临床研究杂志》（JCI）中提出的这一观点的新证据，指出一些尚未得到解答的问题，并讨论一些治疗意义。
