Abstract
Many clinical and animal studies have shown that certain dietary components exert anti-inflammatory properties that aid in the amelioration of chronic inflammatory diseases. Among the various proposed channels through which dietary components affect immune responses, regulatory T-cells (Tregs) are emerging as key targets for the dietary prevention of chronic inflammatory diseases. In this review, immunoregulation by Tregs is briefly described, followed by a summary of recent advances and possible applications of techniques for the study of Tregs. In addition, this review provides an overview of the current knowledge on Treg regulation by certain dietary components, including vitamins, omega-3 polyunsaturated fatty acids, and polyphenols. The caveats of previous studies are also discussed in order to highlight the distinctions between dietary studies and immunological approaches. Consequently, this review may help to clarify the means by which nutritional components influence Tregs.
Highlights
Introduction to TCell ImmunologyHigher organisms, including humans, have immune systems developed to protect the host from potentially harmful materials originating both endogenously and exogenously
It has been reported that the orphan retinoic acid receptor (ROR) family transcription factor RORγt is essential for Th17 development and function [4], indicating that vitamin A, a precursor of retinoic acid, is a potential dietary modulator of Th17 cells and consequent inflammatory responses
More than 60% of CD4+ T-cells were converted to forkhead box P3 (Foxp3)+
Summary
Higher organisms, including humans, have immune systems developed to protect the host from potentially harmful materials originating both endogenously and exogenously. During activation by antigen encounter, naïve (previously antigen-unexposed) CD4+ T-cells (Th0) are further differentiated into effector subtypes, which have been distinguished to date as Th1, Th2, Th9, Th17, and Th22 cells, depending on the milieu of tissues, type of antigen, and corresponding co-stimulating molecules on the antigen-presenting cells. The Th1 subtype, distinguished by nuclear factors STAT1, STAT4, and T-bet, produces interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin(IL)-2, and IL-12, resulting in the activation of effector cytotoxic CD8+ T-cells and innate immune cells such as macrophages [2,3]. It has been reported that the orphan retinoic acid receptor (ROR) family transcription factor RORγt is essential for Th17 development and function [4], indicating that vitamin A, a precursor of retinoic acid, is a potential dietary modulator of Th17 cells and consequent inflammatory responses.
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