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Role of Inflammation and Immunity in Hypertension: Recent Epidemiological, Laboratory, and Clinical Evidence

  • Pathogenesis of Hypertension (W Elliott and R Santos, Section Editors)
  • Published:
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Abstract

Inflammation has been shown to play an important role in the mechanisms involved in the pathogenesis of hypertension. Accordingly, innate and adaptive immune responses participate in blood pressure elevation. Here, we describe recent immunity studies focusing on novel inflammatory mechanisms during the hypertensive process. Different subpopulations of cells involved in innate and adaptive immune responses, such as monocyte/macrophages and dendritic cells on the one hand and B and T lymphocytes on the other hand, play roles leading to vascular injury in hypertension. Innate lymphoid cells, including natural killer cells and γ/δ T cells, have recently been demonstrated to participate in hypertensive mechanisms triggering vascular inflammation. In summary, we discuss the evidence of interaction of these different inflammatory and immune components in both experimental models and in humans during the development of hypertension.

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Acknowledgments

The work from the authors has been funded by Canadian Institutes of Health Research (CIHR) grants 82790 and 123465, a CIHR Foundation Grant, and a Canada Research Chair (CRC) on Hypertension and Vascular Research by the CRC Government of Canada/CIHR Program, and by the Canada Fund for Innovation (CFI), all to ELS.

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Correspondence to Ernesto L. Schiffrin.

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Dr. Schiffrin reports personal fees from Novartis USA and grants from Servier France. Dr. Caillon declares no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Pathogenesis of Hypertension

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Caillon, A., Schiffrin, E.L. Role of Inflammation and Immunity in Hypertension: Recent Epidemiological, Laboratory, and Clinical Evidence. Curr Hypertens Rep 18, 21 (2016). https://doi.org/10.1007/s11906-016-0628-7

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