The relationship between metabolism and the immune system has received increasing attention over the past few years.

Previous studies have found that certain immune cells help to control fat tissue's release or storage of energy. Moreover, fat cells produce various inflammatory molecules that can disrupt the balance established by a normal immune system. Because of this, some experts consider obesity to be an autoimmune, inflammatory disorder.

Scientists discovered that mice that lacked certain dendritic immune cells that release a toxic molecule called perforin progressively gained weight and exhibited features of the metabolic syndrome.

The animals also had an altered collection of T immune cells residing in their fat tissue. Depleting these T cells prevented the mice that lacked the perforin-expressing dendritic cells from gaining weight or developing metabolic abnormalities.

Notably, mice lacking these regulatory dendritic cells were also found to be more prone to develop another form of autoimmunity with symptoms similar to those found in multiple sclerosis.

These combined observations suggest that one function of these perforin-expressing dendritic cells is to remove potentially autoimmune T cells, and in so doing, decrease inflammation. While the connection between fat cells and inflammation has already been shown in mice fed a high-fat diet, this is the first time that researchers have demonstrated the connection in animals on a regular diet, simply by eliminating perforin-expressing dendritic cells.

The findings indicate that perforin-expressing dendritic cells are critical for protecting against metabolic syndrome and autoimmunity, and shifting the abundance of these cells in relation to other immune cell populations may help prevent or treat such conditions.

http://www.cell.com/immunity/abstract/S1074-7613(15)00347-7