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STATE-OF-THE-ART PAPER

The Immune System and Chronic Heart Failure

Is the Heart in Control?

James E. Fildes, PhD^_*,,_*, Steven M. Shaw, MRCP^_*, Nizar Yonan, MD^_*, and Simon G. Williams, MD^_*,

^_* Transplant Centre, University Hospital of South Manchester NHS Foundation Trust, Manchester, United Kingdom
School of Translational Medicine, Faculty of Human and Life Sciences, University of Manchester, Manchester, United Kingdom

Manuscript received August 4, 2008; revised manuscript received October 9, 2008, accepted November 2, 2008.

^_* Reprint requests and correspondence: Dr. James E. Fildes, The Transplant Centre, University Hospital of South Manchester National Health Service Foundation Trust, Manchester M23 9LT, United Kingdom (Email: james.fildes{at}manchester.ac.uk).

Despite current treatment options, the clinical course of patients with chronic heart failure is notoriously difficult to predict. Among those with similar etiologies, ejection fractions, and patient demographics, our understanding of why such variations in outcomes exist remains limited. Evidence that has been progressively gathered implicates an important role of the immune system in the propagation of heart failure. This has been derived mainly from observations that cytokines are progressively elevated in patients with poor outcomes. However, attempts at introducing various immunomodulatory therapies as a new treatment strategy have been largely unsuccessful to date. This possibly reflects a failure in recognizing the complexity of the immune system's role in chronic heart failure, which has led to an oversimplified approach to treatment. This review critically analyzes the immune treatments attempted to date and hypothesizes what is required to develop a successful future treatment strategy.

Key Words: heart failure • immune system • immunomodulation • cytokines

Abbreviations and Acronyms   APC = antigen-presenting cell   CAM = cell adhesion molecule   CHF = chronic heart failure   DC = dendritic cell   HSP = heat shock protein   IL = interleukin   LVEF = left ventricular ejection fraction   NYHA = New York Heart Association   sTNFR = soluble tumor necrosis factor receptor   TLR = toll-like receptor   TNF = tumor necrosis factor

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J. Am. Coll. Cardiol. 2009 53: A26. [Full Text] [PDF]