Hunger-Spiking Neurons May Control Multiple Sclerosis And Other Autoimmune Diseases

If appetite-promoting AgRP neurons are chronically suppressed, resulting in less appetite and a lighter body weight, T-cells tend to promote inflammation-like processes resulting in autoimmune responses that may lead to multiple sclerosis and other autoimmune diseases, scientists at Yale School of Medicine discovered.In the peer-reviewed journal, Proceedings of the National Academy of Sciences (PNAS), the authors explained that neurons that regulate hunger in the CNS (central nervous system) also control the functions of immune cells, suggesting that eating behavior is a defense mechanism against infections and the development of autoimmune disease.Over the last few years, there has been a steady increase in the number of Americans with autoimmune diseases. These illnesses occur when the person’s own immune system attacks healthy tissue and cells is if they were harmful pathogens.How different types of T-cells interact are at the heart of fighting off infections as well as the development of autoimmune disorders.Lead author Tamas Horvath, the Jean and David W. Wallace Professor of Biomedical Research and chair of comparative medicine at Yale School of Medicine, said:

“We’ve found that if appetite-promoting AgRP neurons are chronically suppressed, leading to decreased appetite and a leaner body weight, T cells are more likely to promote inflammation-like processes enabling autoimmune responses that could lead to diseases like 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 and team carried out an animal experiment in which mice had Sirt1 – a signaling molecule that controls the hunger-promoting neuron AgRP in the hypothalamus – knocked out. These mice, referred to as “Sirt1-deficient mice”, had reduced regulatory T-cell function and greater effector T-cell activity, making them more vulnerable to developing an animal-equivalent of multiple sclerosis.Horvath said:   — click here to read more

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