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J Exp Med. 2018 Jan 2;215(1):21-33. doi: 10.1084/jem.20171773. Epub 2017 Dec 15.

The immunology of hypertension.

Author information

1
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
2
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN.
3
Division of Clinical Pharmacology, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN david.g.harrison@vanderbilt.edu.

Abstract

Although systemic hypertension affects a large proportion of the population, its etiology remains poorly defined. Emerging evidence supports the concept that immune cells become activated and enter target organs, including the vasculature and the kidney, in this disease. Mediators released by these cells, including reactive oxygen species, metalloproteinases, cytokines, and antibodies promote dysfunction of the target organs and cause damage. In vessels, these factors enhance constriction, remodeling, and rarefaction. In the kidney, these mediators increase expression and activation of sodium transporters, and cause interstitial fibrosis and glomerular injury. Factors common to hypertension, including oxidative stress, increased interstitial sodium, cytokine production, and inflammasome activation promote immune activation in hypertension. Recent data suggest that isolevuglandin-modified self-proteins in antigen-presenting cells are immunogenic, promoting cytokine production by the cells in which they are formed and T cell activation. Efforts to prevent and reverse immune activation may prove beneficial in preventing the long-term sequelae of hypertension and its related cardiovascular diseases.

PMID:
29247045
PMCID:
PMC5748862
DOI:
10.1084/jem.20171773
[Indexed for MEDLINE]
Free PMC Article

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