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Human T and Natural Killer Cells Possess a Functional Renin-Angiotensin System: Further Mechanisms of Angiotensin II–Induced Inflammation

Mollie Jurewicz^*, David H. McDermott, Joan M. Sechler, Kathryn Tinckam^*, Ayumi Takakura^*, Charles B. Carpenter^*, Edgar Milford^* and Reza Abdi^*

^* Transplantation Research Center, Renal Division, Brigham and Women's Hospital, Boston, Massachusetts; and Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland

Address correspondence to: Dr. Reza Abdi, Transplantation Research Center, Renal Division, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, MA 02115. Phone: 617-732-5259; Fax: 617-732-5254; E-mail: rabdi{at}rics.bwh.harvard.edu

Received for publication July 6, 2006. Accepted for publication January 18, 2007.

The renin-angiotensin system (RAS) plays an important role in the regulation of inflammation and in the progression of chronic kidney disease. Accumulation of inflammatory cells into the renal parenchyma has been a hallmark of chronic kidney disease; however, little is known concerning the presence and the function of RAS elements in T and natural killer (NK) cells. Here is reported a co-stimulatory effect of angiotensin II (AngII) by showing an augmentation of mitogen and anti–CD3-stimulated T and NK cell proliferation with AngII treatment. Angiotensinogen and AngI also generated the same effect, suggesting that NK and T cells have functional renin and angiotensin-converting enzyme activity. Indeed, they express renin, the renin receptor, angiotensinogen, and angiotensin-converting enzyme by mRNA analysis. Flow cytometric analysis and Western blot revealed angiotensin receptor 2 (AT₂) expression in T and NK cells, whereas AT₁ expression was found in T and NK cells and monocytes by Western blot. These receptors were shown to be functional in calcium signaling, chemotaxis, and proliferation. However, AT₁ and AT₂ antagonists alone or in combination were unable to abrogate completely the effects of AngII, suggesting that another AngII receptor may also be functional in leukocytes. This is the first study to show that T and NK cells are fully equipped with RAS elements and are potentially capable of producing and delivering AngII to sites of inflammation. Because their chemotaxis is enhanced by AngII, this creates a potential inflammatory amplification system.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673