The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
Regulation of T-cell function by endogenously produced angiotensin II
Open accessAbstract
The adaptive immune response and, in particular, T cells have been shown to be important in the genesis of hypertension. In the present study, we sought to determine how the interplay between ANG II, NADPH oxidase, and reactive oxygen species modulates T cell activation and ultimately causes hypertension. We determined that T cells express angiotensinogen, the angiotensin I-converting enzyme, and renin and produce physiological levels of ANG II. AT 1 receptors were primarily expressed intracellularly, and endogenously produced ANG II increased T-cell activation, expression of tissue homing markers, and production of the cytokine TNF-α. Inhibition of T-cell ACE reduced TNF-α production, indicating endogenously produced ANG II has a regulatory role in this process. Studies with specific antagonists and T cells from AT 1 R and AT 2 R-deficient mice indicated that both receptor subtypes contribute to TNF-α production. We found that superoxide was a critical mediator of T-cell TNF-α production, as this was significantly inhibited by polyethylene glycol (PEG)-SOD, but not PEG-catalase. Thus, T cells contain an endogenous renin-angiotensin system that modulates T-cell function, NADPH oxidase activity, and production of superoxide that, in turn, modulates TNF-α production. These findings contribute to our understanding of how ANG II and T cells enhance inflammation in cardiovascular disease.
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Cites
Inflammation, Atherosclerosis, and Coronary Artery Disease
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NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
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Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.
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Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
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Self-citationThe vascular NAD(P)H oxidases as therapeutic targets in cardiovascular diseases
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Self-citationGoossens, V, Grooten, J., De Vos, K., & Fiers, W. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.18.8115 · Cited by 596
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Distinct and Nonredundant In Vivo Functions of TNF Produced by T Cells and Macrophages/Neutrophils
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Cited by
Inflammation, Immunity, and Hypertension
Harrison, D. G., Guzik, T. J., Lob, H. E., Madhur, M. S., Marvar, P. J., Thabet, S. R., Vinh, A., & Weyand, C. M. (2011) · Hypertension · doi:10.1161/hypertensionaha.110.163576 · Cited by 871
Self-citationAngiotensin II revisited: new roles in inflammation, immunology and aging
Benigni, A., Cassis, P., & Remuzzi, G. (2010) · EMBO Molecular Medicine · doi:10.1002/emmm.201000080 · Cited by 757
Counter-regulatory renin–angiotensin system in cardiovascular disease
Paz Ocaranza, M., Riquelme, J. A., García, L., Jalil, J. E., Chiong, M., Santos, R. A. S., & Lavandero, S. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0244-8 · Cited by 561
Classical Renin‐Angiotensin System in Kidney Physiology
Sparks, M. A., Crowley, S. D., Gurley, S. B., Mirotsou, M., & Coffman, T. M. (2014) · Comprehensive Physiology · doi:10.1002/cphy.c130040 · Cited by 521
T Regulatory Lymphocytes Prevent Angiotensin II–Induced Hypertension and Vascular Injury
Barhoumi, T., Kasal, D. A., Li, M. W., Shbat, L., Laurant, P., Neves, M. F., Paradis, P., & Schiffrin, E. L. (2011) · Hypertension · doi:10.1161/hypertensionaha.110.162941 · Cited by 459
Metadata
- Authors
- Hoch, N. E., Guzik, T. J., Chen, W., Deans, T., Maalouf, S. A., Gratze, P., Weyand, C., & Harrison, D. G.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2009-02
- Volume
- 296
- Issue
- 2
- Pages
- R208-R216
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W2072052992
- Cited by
- 262
- References
- 46
- FWCI
- 11.88
- Type
- journal article
- Language
- en
- Open access
- green
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