Inflammation in Heart Failure
The Holy Grail?
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See related article, pp 114–122
Immuno-inflammatory mechanisms have been implicated in the initiation and progression of heart failure (HF) during the past 2 decades. Despite several investigators having postulated a pathogenic role of inflammation in HF, clinical trials of anti-inflammatory and anti-immune therapies in HF have not resulted in salutary effects.1 Absence of a beneficial effect of these therapies has led to more questions than answers. Is the presence of inflammation really bad? Is inflammation good at 1 time point and detrimental at another? Are there subsets of inflammatory cells that have a protective role and others that are detrimental? Extensive research to answer these questions has led to the identification of unique subsets of the immune cascade that might have a selective protective role in HF. One such group of cells is the CD4+ regulatory T cells (Tregs). These cells are a part of the adaptive immune response of the body and are further divided into natural and adaptive Treg cells (Figure). Natural Tregs develop in the thymus against self-antigens, whereas adaptive Tregs develop in response to an antigenic stimulation. Adaptive Tregs express a specific transcription factor called FoxP3 and are often termed as CD4+CD25+Foxp3+T cells. Tregs have been shown to have atheroprotective properties.2 Dinh et al3 showed that selective expansion of Tregs by cytokine-based interleukin-2 (IL-2)/anti–IL-2 monoclonal antibody complex therapy can attenuate atherosclerosis in mice.