A new study from the Linus Pauling Institute at Oregon State University has shown wonderful green tea health benefits. One of the compounds in green tea (EGCG) greatly increases important immune cells that help in the suppression of autoimmune disease. An estimated 4.5 million Canadians suffer from autoimmune diseases ranging from rheumatoid arthritis to lupus. The majority of conventional treatments currently available have long-term side effects due to toxicity and greatly suppress the immune system, leaving patients susceptible to a variety of viral and bacterial infections. The new study shows that 50 mg/kg of green tea derived EGCG has the ability to increase regulatory T cells in mice, which improve the function of the immune system without the negative effects.
The immune system is typically a tightly controlled process where a variety of immune cells work together to destroy unwanted invaders without damaging normal cells. This is regulated by a specific group of cells, including regulatory T cells, which turn the attacking cells on and off when an invader is present. In autoimmune disease, the process becomes dysfunctional and the attacking immune cells begin destroying healthy, normal cells. The resulting wide-spread inflammation in the body is what causes the symptoms of autoimmune disease. By affecting the expression of certain transcription factors of DNA, EGCG has been shown to greatly increase the number of regulatory T cells, thus controlling the immune response and reducing inflammation.
Conventional immune-suppressing drugs are pivotal in the short-term treatment of autoimmune disease and flare-ups and these results do not alter the need for or use of these drugs. It is the long-term toxicity effects that researchers and clinical practitioners alike are searching for. This study has given new hope for a long-term treatment for autoimmune disease that has fewer risks and side effects. In addition, the exciting new research from Oregon State University gives us more evidence that using dietary supplements and plant-based medicine can not only reduce symptoms but also act directly on DNA expression and alter the course of these debilitating diseases.
Induction of regulatory T cells by green tea polyphenol EGCG
a Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, OR, USA
b Department of Nutritional Sciences, University of Connecticut, Storrs, CT, USA
c Department of Food and Nutrition, Changwon National University, Changwon, South Korea
d Linus Pauling Institute, Oregon State University, Corvallis, OR, USA
Received 29 December 2010;
revised 7 April 2011;
accepted 21 April 2011.
Available online 20 May 2011.
Regulatory T cells (Treg) are critical in maintaining immune tolerance and suppressing autoimmunity. The transcription factor Foxp3 serves as a master switch that controls the development and function of Treg. Foxp3 expression is epigenetically regulated by DNA methylation, and DNA methyltransferase (DNMT) inhibitors can induce Foxp3 expression in naive CD4+ T cells. We showed that EGCG, a major green tea polyphenol, could act as a dietary DNMT inhibitor, and induced Foxp3 and IL-10 expression in CD4+ Jurkat T cells at physiologically relevant concentrations in vitro. We further showed that mice treated with EGCG in vivo had significantly increased Treg frequencies and numbers in spleen and lymph nodes and had inhibited T cell response. Induction of Foxp3 expression correlated with a concomitant reduction in DNMT expression and a decrease in global DNA methylation. Our data suggested that EGCG can induce Foxp3 expression and increase Treg frequency via a novel epigenetic mechanism. While the DNMT inhibitory effects of EGCG was not as potent as pharmacologic agents such as 5-aza-2′-deoxycytidine, the ability of dietary agents to target similar mechanisms offers opportunities for potentially sustained and longer-term exposures with lower toxicity. Our work provides the foundation for future studies to further examine and evaluate dietary strategies to modulate immune function.