Yale School of Medicine researchers have found that neurons (central nervous system cells) that control hunger also regulate immune cell functions, implicating eating behavior as a defense against infections and autoimmune disease development.

The researchers concluded that eating behavior is a defense mechanism against infections. When appetite-promoting AgRP neurons are chronically suppressed (leading to decreased appetite and body weight, which may be due to medications or dieting), T cells are more likely to promote inflammation-like processes enabling autoimmune responses that could lead to autoimmune disease.

Lead author Tamas Horvath and his research team conducted their study in two sets of transgenic mice. In one set, they knocked out Sirt1, a signaling molecule that controls the hunger-promoting neuron AgRP in the hypothalamus. These Sirt1-deficient mice had decreased regulatory T cell function and enhanced effector T cell activity, leading to their increased vulnerability in an animal model of multiple sclerosis.

“If we can control this mechanism by adjusting eating behavior and the kinds of food consumed, it could lead to new avenues for treating autoimmune diseases,” Horvath added.

Source:

Peart, Karen, Yale News, March 25, 2013.

"Hunger-Spiking Neurons May Control Multiple Sclerosis and Other Autoimmune Diseases," Medical News Today, March 29, 2013.