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      Increased frequency of CD4 +CD57 + senescent T cells in patients with newly diagnosed acute heart failure: exploring new pathogenic mechanisms with clinical relevance

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          Abstract

          Recent animal studies showed T cells have a direct pathogenic role in the development of heart failure (HF). However, which subsets of T cells contribute to human HF pathogenesis and progression remains unclear. We characterized immunologic properties of various subsets of T cells and their clinical implications in human HF. Thirty-eight consecutive patients with newly diagnosed acute HF (21 males, mean age 66 ± 16 years) and 38 healthy control subjects (21 males, mean age 62 ± 12 years) were enrolled. We found that pro-inflammatory mediators, including CRP, IL-6 and IP-10 and the frequencies of CD57 + T cells in the CD4 + T cell population were significantly elevated in patients with acute HF compared to control subjects. A functional analysis of T cells from patients with acute HF revealed that the CD4 +CD57 + T cell population exhibited a higher frequency of IFN-γ- and TNF-α- producing cells compared to the CD4 +CD57 T cell population. Furthermore, the frequency of CD4 +CD57 + T cells at baseline and its elevation at the six-month follow-up were significantly related with the development of cardiovascular (CV) events, which were defined as CV mortality, cardiac transplantation, or rehospitalization due to HF exacerbation. In conclusion, CD4 +CD57 + senescent T cells showed more inflammatory features and polyfunctionality and were associated with clinical outcome in patients with acute HF. More detailed study for senescent T cells might offer new opportunities for the prevention and treatment of human HF.

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          Most cited references23

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          CD4+ T cells promote the transition from hypertrophy to heart failure during chronic pressure overload.

          The mechanisms by which the heart adapts to chronic pressure overload, producing compensated hypertrophy and eventually heart failure (HF), are still not well defined. We aimed to investigate the involvement of T cells in the progression to HF using a transverse aortic constriction (TAC) model.
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            Immunosenescent CD8+ T cells and C-X-C chemokine receptor type 3 chemokines are increased in human hypertension.

            The pathogenic role of T cells in hypertension has been documented well in recent animal studies. However, the existence of T-cell-driven inflammation in human hypertension has not been confirmed. Therefore, we undertook immunologic characterization of T cells from patients with hypertension and measured circulating levels of C-X-C chemokine receptor type 3 chemokines, which are well-known tissue-homing chemokines for T cells. We analyzed immunologic markers on T cells from patients with hypertension by multicolor flow cytometry. We then measured circulating levels of the C-X-C chemokine receptor type 3 chemokines, monokine induced by γ interferon (IFN), IFN γ-induced protein 10, and IFN-inducible T-cell α chemoattractant, in patients with hypertension and in age- and sex-matched control subjects by the cytometric bead array method. In addition, we examined histological features of IFN-inducible T-cell α chemoattractant expression from renal biopsy specimens of patients with hypertensive nephrosclerosis and control subjects. The total T-cell population from patients with hypertension showed an increased fraction of immunosenescent, proinflammatory, cytotoxic CD8(+) T cells. Circulating levels of C-X-C chemokine receptor type 3 chemokines were significantly higher in patients with hypertension than in control subjects. Furthermore, immunohistochemical staining revealed increased expression of the T-cell chemokine, IFN-inducible T-cell α chemoattractant, in the proximal and distal tubules of patients with hypertensive nephrosclerosis. Immunosenescent CD8(+) T cells and C-X-C chemokine receptor type 3 chemokines are increased in human hypertension, suggesting a role for T-cell-driven inflammation in hypertension. A more detailed characterization of CD8(+) T cells may offer new opportunities for the prevention and treatment of human hypertension.
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              Activated T Lymphocytes are Essential Drivers of Pathological Remodeling in Ischemic Heart Failure.

              Inappropriately sustained inflammation is a hallmark of chronic ischemic heart failure (HF); however, the pathophysiological role of T lymphocytes is unclear.
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                Author and article information

                Contributors
                jong.chan.youn@gmail.com
                smkang@yuhs.ac
                ecshin@kaist.ac.kr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                9 September 2019
                9 September 2019
                2019
                : 9
                : 12887
                Affiliations
                [1 ]ISNI 0000 0004 0470 4224, GRID grid.411947.e, Division of Cardiology, Department of Internal Medicine, Seoul St. Mary’s Hospital, College of Medicine, , The Catholic University of Korea, ; Seoul, Republic of Korea
                [2 ]ISNI 0000 0001 2292 0500, GRID grid.37172.30, Laboratory of Immunology and Infectious Diseases, Graduate School of Medical Science and Engineering, , Korea Advanced Institute of Science and Technology (KAIST), ; Daejeon, Republic of Korea
                [3 ]ISNI 0000 0004 0470 5454, GRID grid.15444.30, Division of Cardiology, Severance Cardiovascular Hospital, , Yonsei University College of Medicine, ; Seoul, Republic of Korea
                [4 ]ISNI 0000 0001 2292 0500, GRID grid.37172.30, BioMedical Science and Engineering Interdisciplinary Program, , Korea Advanced Institute of Science and Technology (KAIST), ; Daejeon, Republic of Korea
                [5 ]ISNI 0000 0001 2292 0500, GRID grid.37172.30, Laboratory of Translational Immunology and Vaccinology, Graduate School of Medical Science and Engineering, , Korea Advanced Institute of Science and Technology (KAIST), ; Daejeon, Republic of Korea
                [6 ]ISNI 0000 0004 0647 8419, GRID grid.414067.0, Division of Cardiology, , Keimyung University Dongsan Medical Center, ; Daegu, Republic of Korea
                [7 ]ISNI 0000 0004 0470 5964, GRID grid.256753.0, Division of Cardiology, Dongtan Sacred Heart Hospital, , Hallym University College of Medicine, ; Hwaseong, Republic of Korea
                Author information
                http://orcid.org/0000-0003-0998-503X
                http://orcid.org/0000-0003-3178-0823
                http://orcid.org/0000-0001-6363-7736
                http://orcid.org/0000-0001-9856-9227
                http://orcid.org/0000-0002-6308-9503
                Article
                49332
                10.1038/s41598-019-49332-5
                6733929
                31501486
                19465b95-66d2-4e06-b83c-6d97a34a39aa
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 6 September 2018
                : 20 August 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100003725, National Research Foundation of Korea (NRF);
                Award ID: 2018R1C1B6005448
                Award Recipient :
                Funded by: the Korean Society of CardioMetabolic Syndrome, by a grant of the Korean Society for Transplantation (2016, 2017)
                Funded by: FundRef https://doi.org/10.13039/501100003621, Ministry of Science, ICT and Future Planning (MSIP);
                Award ID: KAIST Future Systems Healthcare Project
                Award Recipient :
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Uncategorized
                translational immunology,heart failure
                Uncategorized
                translational immunology, heart failure

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