We all know that the immune system is designed to ward off foreign agents that may harm our body. We also know that a healthy lifestyle and certain genetic traits help prevent obesity.
Recent research now indicates that some aspects of our immune system might also be involved in preventing obesity. Scientists have shown that mice lacking a specific immune cell gained excessive weight and developed metabolic anomalies despite being on a standard diet.
This has prompted researchers to believe that obesity could, in fact, be an autoimmune, inflammatory disorder.
How Immune System Might Be Involved
A possible association between the immune system and metabolism has been highlighted frequently in the past years. Previous studies have shown that certain types of immune cells play a role in controlling the release and storage of energy from fat tissues. Moreover, fat cells produce many inflammatory molecules that are capable of disrupting the balance of a normal immune system.
Yair Reisner, of the Weizmann Institute of Science in Israel, along with colleagues sought out to study the underlying immunological mechanisms that control the metabolic fate of fat tissue. They observed that mice lacking certain dendritic immune cells, which release a toxin (perforin), gradually gained excessive weight and presented features similar to those of the metabolic syndrome.
Furthermore, these mice also had an altered group of T immune cells inhabiting their fat tissue. Depleting these cells prevented mice that lacked perforin-producing dendritic cells from gaining weight and any associated metabolic anomalies.
“We also observed that mice lacking these regulatory dendritic cells were more likely to develop another form of autoimmunity with similar symptoms found in multiple sclerosis”, added Reisner.
Explaining The Connection
These results imply that one function of the perforin-secreting dendritic cells is to eradicate potentially autoimmune T-cells, and as a result, reduce inflammation. This is the first study that indicates a connection between animals on a standard diet and the protective role of perforin-producing dendritic cells against autoimmunity and metabolic abnormalities.
Reisner stated that the research highlights how increasing the amount of these cells, in relation to other immune cells, could possibly help prevent, manage or treat obesity and other conditions. Though it is hard to predict how these findings could assist with patient care, further research should be pursued to see whether the absence of these rare subpopulation of cells is linked to obesity, metabolic syndromes, or any autoimmune diseases.
The research was published in Immunity.