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Nephrol Dial Transplant (2003) 18: 1423-1426
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Angiotensin II, the immune system and renal diseases: another road for RAS?

Yusuke Suzuki1,2, Marta Ruiz-Ortega1, Carmen Gomez-Guerrero1, Yasuhiko Tomino2 and Jesus Egido1

1 Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain and 2 Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan

Correspondence and offprint requests to: J. Egido, Renal and Vascular Research Laboratory, Fundacion Jimenez Diaz, Autonoma University, Avda. Reyes Catolicos 2, 28040 Madrid, Spain. Email: jegido@fjd.es

Keywords: angiotensin II; chemokine; immune system; renal disease; renin–angiotensin system; T cell

The first 150 words of the full text of this article appear below.

Introduction

Recent findings from large clinical trials and experi-mental studies have emphasized the importance of inhibiting the renin–angiotensin system (RAS) in a wide variety of diseases. They have demonstrated that the benefits of RAS blockade may be due to the inhibition of pressor and non-pressor actions of RAS. Since elevated tissue levels of RAS components have been demonstrated in many diseases, the potential contribution of local RAS to the progression of immune and non-immune conditions has been considered in recent years. Novel components of RAS, such as a renin receptor [1] and an angiotensin-converting enzyme (ACE) 2 molecule [2], have been described in several organs, further indicating that resident and infiltrating cells possess the enzymatic machinery to perform the complete conversion to active angiotensin II (Ang II). Therefore, RAS effects may be partly dependent on the compartment in which Ang II, its major effector peptide, is generated.

. . . [Full Text of this Article]

Ang II behaves as a cytokine mediating infiltration and activation of immunocompetent cells in renal interstitium

Local RAS amplifies antigen-specific immune responses in glomerular diseases

Conclusion


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