Lymphocyte Subpopulations in Myocardial Infarction: a Comparison Between Peripheral and Intracoronary Blood

Overview

Journal Springerplus

Date 2015 Dec 23

PMID 26693103

Citations 4

Authors

Natalia Lluberas

Natalia Trias

Andreina Brugnini

Rafael Mila

Gustavo Vignolo

Pedro Trujillo

Ariel Duran

Sofia Grille

Ricardo Lluberas

Daniela Lens

Affiliations

Soon will be listed here.

Abstract

The frequency and profile of lymphocyte subsets within the culprit coronary artery were investigated in 33 patients with myocardial infarction and compared to their systemic circulating counterparts. T cell subsets including CD4(+)CD28null, activated and regulatory T-cells, TH1/TH2/TH17 phenotypes, NK and B-cells were studied in intracoronary (IC) and arterial peripheral blood (PB) samples. CD4(+)CD28null T-lymphocytes were significantly increased in IC compared to PB (3.7 vs. 2.9 %, p < 0.0001). Moreover, patients with more than 6 h of evolution of STEMI exhibited higher levels of CD4(+)CD28null T-cells suggesting that this subset may be associated with more intense myocardial damage. The rare NK subpopulation CD3(-)CD16(+)CD56(-) was also increased in IC samples (5.6 vs. 3.9 %, p = 0.006). CD4(+)CD28null T-cells and CD3(-)CD16(+)CD56(-) NK subpopulations were also associated with higher CK levels. Additionally, IFN-γ and IL10 were significantly higher in IC CD4(+) lymphocytes. Particular immune cell populations with a pro-inflammatory profile at the site of onset were increased relative to their circulating counterparts suggesting a pathophysiological role of these cells in plaque instability, thrombi and myocardial damage.

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References

Sondergaard S, Ullum H, Pedersen B . Proliferative and cytotoxic capabilities of CD16+CD56- and CD16+/-CD56+ natural killer cells. APMIS. 2001; 108(12):831-7. DOI: 10.1111/j.1600-0463.2000.tb00006.x. View

Gonzalez V, Falconer K, Bjorkstrom N, Blom K, Weiland O, Ljunggren H . Expansion of functionally skewed CD56-negative NK cells in chronic hepatitis C virus infection: correlation with outcome of pegylated IFN-alpha and ribavirin treatment. J Immunol. 2009; 183(10):6612-8. DOI: 10.4049/jimmunol.0901437. View

Antman E, Anbe D, Armstrong P, Bates E, Green L, Hand M . ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the.... J Am Coll Cardiol. 2004; 44(3):E1-E211. DOI: 10.1016/j.jacc.2004.07.014. View

Jonasson L, Holm J, Skalli O, Bondjers G, Hansson G . Regional accumulations of T cells, macrophages, and smooth muscle cells in the human atherosclerotic plaque. Arteriosclerosis. 1986; 6(2):131-8. DOI: 10.1161/01.atv.6.2.131. View

Zal B, Kaski J, Akiyu J, Cole D, Arno G, Poloniecki J . Differential pathways govern CD4+ CD28- T cell proinflammatory and effector responses in patients with coronary artery disease. J Immunol. 2008; 181(8):5233-41. DOI: 10.4049/jimmunol.181.8.5233. View

Liu L, Lu J, Chao P, Lin L, Zhang Z, Yang T . Lower prevalence of circulating invariant natural killer T (iNKT) cells in patients with acute myocardial infarction undergoing primary coronary stenting. Int Immunopharmacol. 2011; 11(4):480-4. DOI: 10.1016/j.intimp.2010.12.019. View

Nakajima T, Schulte S, Warrington K, Kopecky S, Frye R, Goronzy J . T-cell-mediated lysis of endothelial cells in acute coronary syndromes. Circulation. 2002; 105(5):570-5. DOI: 10.1161/hc0502.103348. View

Dumitriu I, Araguas E, Baboonian C, Kaski J . CD4+ CD28 null T cells in coronary artery disease: when helpers become killers. Cardiovasc Res. 2008; 81(1):11-9. DOI: 10.1093/cvr/cvn248. View

Martens P, Goronzy J, Schaid D, Weyand C . Expansion of unusual CD4+ T cells in severe rheumatoid arthritis. Arthritis Rheum. 1997; 40(6):1106-14. DOI: 10.1002/art.1780400615. View

10.

Libby P, Ridker P, Hansson G . Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol. 2009; 54(23):2129-38. PMC: 2834169. DOI: 10.1016/j.jacc.2009.09.009. View

11.

Sardella G, De Luca L, Francavilla V, Accapezzato D, Mancone M, Sirinian M . Frequency of naturally-occurring regulatory T cells is reduced in patients with ST-segment elevation myocardial infarction. Thromb Res. 2007; 120(4):631-4. DOI: 10.1016/j.thromres.2006.12.005. View

12.

Tedgui A, Mallat Z . Cytokines in atherosclerosis: pathogenic and regulatory pathways. Physiol Rev. 2006; 86(2):515-81. DOI: 10.1152/physrev.00024.2005. View

13.

Fuller M, Zajac A . Ablation of CD8 and CD4 T cell responses by high viral loads. J Immunol. 2002; 170(1):477-86. DOI: 10.4049/jimmunol.170.1.477. View

14.

Cooper M, Fehniger T, Turner S, Chen K, Ghaheri B, Ghayur T . Human natural killer cells: a unique innate immunoregulatory role for the CD56(bright) subset. Blood. 2001; 97(10):3146-51. DOI: 10.1182/blood.v97.10.3146. View

15.

Malarstig A, Eriksson P, Hamsten A, Lindahl B, Wallentin L, Siegbahn A . Raised interleukin-10 is an indicator of poor outcome and enhanced systemic inflammation in patients with acute coronary syndrome. Heart. 2007; 94(6):724-9. PMC: 2564840. DOI: 10.1136/hrt.2007.119271. View

16.

Grines C, Browne K, Marco J, Rothbaum D, Stone G, Okeefe J . A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group. N Engl J Med. 1993; 328(10):673-9. DOI: 10.1056/NEJM199303113281001. View

17.

Whitman S, Rateri D, Szilvassy S, Yokoyama W, Daugherty A . Depletion of natural killer cell function decreases atherosclerosis in low-density lipoprotein receptor null mice. Arterioscler Thromb Vasc Biol. 2004; 24(6):1049-54. DOI: 10.1161/01.ATV.0000124923.95545.2c. View

18.

Nakai Y, Iwabuchi K, Fujii S, Ishimori N, Dashtsoodol N, Watano K . Natural killer T cells accelerate atherogenesis in mice. Blood. 2004; 104(7):2051-9. DOI: 10.1182/blood-2003-10-3485. View

19.

Sardella G, Mancone M, Canali E, Di Roma A, Benedetti G, Stio R . Impact of thrombectomy with EXPort Catheter in Infarct-Related Artery during Primary Percutaneous Coronary Intervention (EXPIRA Trial) on cardiac death. Am J Cardiol. 2010; 106(5):624-9. DOI: 10.1016/j.amjcard.2010.04.014. View

20.

Zal B, Kaski J, Arno G, Akiyu J, Xu Q, Cole D . Heat-shock protein 60-reactive CD4+CD28null T cells in patients with acute coronary syndromes. Circulation. 2004; 109(10):1230-5. DOI: 10.1161/01.CIR.0000118476.29352.2A. View