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Natural killer (NK) cell deficit in coronary artery disease: no aberrations in phenotype but sustained reduction of NK cells is associated with low‐grade inflammation

Summary Although reduced natural killer (NK) cell levels have been reported consistently in patients with coronary artery disease (CAD), the clinical significance and persistence of this immune perturbation is not clarified. In this study we characterized the NK cell deficit further by determining (...

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Published in:Clinical and experimental immunology 2014-01, Vol.175 (1), p.104-112
Main Authors: Backteman, K., Ernerudh, J., Jonasson, L.
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description Summary Although reduced natural killer (NK) cell levels have been reported consistently in patients with coronary artery disease (CAD), the clinical significance and persistence of this immune perturbation is not clarified. In this study we characterized the NK cell deficit further by determining (i) differentiation surface markers and cytokine profile of NK cell subsets and (ii) ability to reconstitute NK cell levels over time. Flow cytometry was used to analyse NK cell subsets and the intracellular cytokine profile in 31 patients with non‐ST elevation myocardial infarction (non‐STEMI), 34 patients with stable angina (SA) and 37 healthy controls. In blood collected prior to coronary angiography, the proportions of NK cells were reduced significantly in non‐STEMI and SA patients compared with controls, whereas NK cell subset analyses or cytokine profile measurements did not reveal any differences across groups. During a 12‐month follow‐up, the proportions of NK cells increased, although not in all patients. Failure to reconstitute NK cell levels was associated with several components of metabolic syndrome. Moreover, interleukin (IL)‐6 levels remained high in patients with sustained NK cell deficit, whereas a decline in IL‐6 (P 
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In this study we characterized the NK cell deficit further by determining (i) differentiation surface markers and cytokine profile of NK cell subsets and (ii) ability to reconstitute NK cell levels over time. Flow cytometry was used to analyse NK cell subsets and the intracellular cytokine profile in 31 patients with non‐ST elevation myocardial infarction (non‐STEMI), 34 patients with stable angina (SA) and 37 healthy controls. In blood collected prior to coronary angiography, the proportions of NK cells were reduced significantly in non‐STEMI and SA patients compared with controls, whereas NK cell subset analyses or cytokine profile measurements did not reveal any differences across groups. During a 12‐month follow‐up, the proportions of NK cells increased, although not in all patients. Failure to reconstitute NK cell levels was associated with several components of metabolic syndrome. Moreover, interleukin (IL)‐6 levels remained high in patients with sustained NK cell deficit, whereas a decline in IL‐6 (P &lt; 0·001) was seen in patients with a pronounced increase in NK cells. In conclusion, we found no evidence that reduction of NK cells in CAD patients was associated with aberrations in NK cell phenotype at any clinical stage of the disease. 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Moreover, interleukin (IL)‐6 levels remained high in patients with sustained NK cell deficit, whereas a decline in IL‐6 (P &lt; 0·001) was seen in patients with a pronounced increase in NK cells. In conclusion, we found no evidence that reduction of NK cells in CAD patients was associated with aberrations in NK cell phenotype at any clinical stage of the disease. Conversely, failure to reconstitute NK cell levels was associated with a persistent low‐grade inflammation, suggesting a protective role of NK cells in CAD.</description><subject>Adult</subject><subject>coronary artery disease</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - immunology</subject><subject>Coronary Artery Disease - pathology</subject><subject>cytokines</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - immunology</subject><subject>Inflammation - pathology</subject><subject>Interleukin-6 - blood</subject><subject>Interleukin-6 - immunology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Killer Cells, Natural - pathology</subject><subject>leukocytes</subject><subject>Lymphocyte Count</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - immunology</subject><subject>Myocardial Infarction - pathology</subject><subject>natural killer cell</subject><subject>Original</subject><issn>0009-9104</issn><issn>1365-2249</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><recordid>eNqNks1uEzEUhUcIRENgwQsgS2zaxbT-nzELpCoUqFqFDbC1HM-dxGUyTm0PUXZ9hD4Gz8WT4CSlokhIeHNl-bvH9x6donhJ8DHJ58SCOyaUEvyoGBEmRUkpV4-LEcZYlYpgflA8i_EqX6WU9GlxQDlVteLVqPgxNWkIpkPfXNdBQIfTiyNkoetQA62zLiHXI-uD703YIBMS5NK4CCbCG9R7ZGYQgknO93GLrhbQ-7RZAZoNCcUhJuN6aFCAZrBbCvkWTS92X-SGiEyM3jqTMrN2aYE6v_55czsPpoGs13ZmudypPy-etKaL8OKujosv788-Tz6Wl58-nE9OL0srCMeltDXmXIGRVglOKgFYcQAys0JSRtqWVRWW0DI8o9awWjaCMs4Yk03NWyvYuCj3unENq2GmV8Et8-raG6ffua-n2oe57tygCc5NLPNv93yGl9BY6FO280Hbw5feLfTcf9esVrUQKgsc3gkEfz1ATHrp4tYe04MfoiZcUYmlkOQ_UClIxWmFM_r6L_TKD6HPzmkiqBKCyjz9uDjaUzb4GAO093MTrLfR0jlaehetzL76c9F78neWMnCyB9aug82_lfTk7Hwv-QuoB9sd</recordid><startdate>201401</startdate><enddate>201401</enddate><creator>Backteman, K.</creator><creator>Ernerudh, J.</creator><creator>Jonasson, L.</creator><general>Oxford University Press</general><general>British Society for Immunology</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>DG8</scope></search><sort><creationdate>201401</creationdate><title>Natural killer (NK) cell deficit in coronary artery disease: no aberrations in phenotype but sustained reduction of NK cells is associated with low‐grade inflammation</title><author>Backteman, K. ; Ernerudh, J. ; Jonasson, L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5140-6c80449ea6c954175e094ee1bc56231ff37706ef30b2ca386d52343336d84fc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Adult</topic><topic>coronary artery disease</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - immunology</topic><topic>Coronary Artery Disease - pathology</topic><topic>cytokines</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - immunology</topic><topic>Inflammation - pathology</topic><topic>Interleukin-6 - blood</topic><topic>Interleukin-6 - immunology</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Killer Cells, Natural - pathology</topic><topic>leukocytes</topic><topic>Lymphocyte Count</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - immunology</topic><topic>Myocardial Infarction - pathology</topic><topic>natural killer cell</topic><topic>Original</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Backteman, K.</creatorcontrib><creatorcontrib>Ernerudh, J.</creatorcontrib><creatorcontrib>Jonasson, L.</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Free Archive</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Linköpings universitet</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Backteman, K.</au><au>Ernerudh, J.</au><au>Jonasson, L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Natural killer (NK) cell deficit in coronary artery disease: no aberrations in phenotype but sustained reduction of NK cells is associated with low‐grade inflammation</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2014-01</date><risdate>2014</risdate><volume>175</volume><issue>1</issue><spage>104</spage><epage>112</epage><pages>104-112</pages><issn>0009-9104</issn><issn>1365-2249</issn><eissn>1365-2249</eissn><abstract>Summary Although reduced natural killer (NK) cell levels have been reported consistently in patients with coronary artery disease (CAD), the clinical significance and persistence of this immune perturbation is not clarified. In this study we characterized the NK cell deficit further by determining (i) differentiation surface markers and cytokine profile of NK cell subsets and (ii) ability to reconstitute NK cell levels over time. Flow cytometry was used to analyse NK cell subsets and the intracellular cytokine profile in 31 patients with non‐ST elevation myocardial infarction (non‐STEMI), 34 patients with stable angina (SA) and 37 healthy controls. In blood collected prior to coronary angiography, the proportions of NK cells were reduced significantly in non‐STEMI and SA patients compared with controls, whereas NK cell subset analyses or cytokine profile measurements did not reveal any differences across groups. During a 12‐month follow‐up, the proportions of NK cells increased, although not in all patients. Failure to reconstitute NK cell levels was associated with several components of metabolic syndrome. Moreover, interleukin (IL)‐6 levels remained high in patients with sustained NK cell deficit, whereas a decline in IL‐6 (P &lt; 0·001) was seen in patients with a pronounced increase in NK cells. In conclusion, we found no evidence that reduction of NK cells in CAD patients was associated with aberrations in NK cell phenotype at any clinical stage of the disease. Conversely, failure to reconstitute NK cell levels was associated with a persistent low‐grade inflammation, suggesting a protective role of NK cells in CAD.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>24298947</pmid><doi>10.1111/cei.12210</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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ispartof Clinical and experimental immunology, 2014-01, Vol.175 (1), p.104-112
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1365-2249
language eng
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source PubMed Central
subjects Adult
coronary artery disease
Coronary Artery Disease - blood
Coronary Artery Disease - immunology
Coronary Artery Disease - pathology
cytokines
Female
Flow Cytometry
Follow-Up Studies
Humans
inflammation
Inflammation - blood
Inflammation - immunology
Inflammation - pathology
Interleukin-6 - blood
Interleukin-6 - immunology
Killer Cells, Natural - immunology
Killer Cells, Natural - metabolism
Killer Cells, Natural - pathology
leukocytes
Lymphocyte Count
Male
Middle Aged
Myocardial Infarction - blood
Myocardial Infarction - immunology
Myocardial Infarction - pathology
natural killer cell
Original
title Natural killer (NK) cell deficit in coronary artery disease: no aberrations in phenotype but sustained reduction of NK cells is associated with low‐grade inflammation
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