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AnonTechie writes:

Ars Technica recently published a story: Immune cells tweak the body’s metabolism to help control obesity.

Obesity has reached epic proportions in the United States and is rising in other developed and developing countries as they adopt our diet and lifestyle. Autoimmune diseases, like celiac disease and multiple sclerosis, and allergies, also immune-mediated, have blossomed recently, too.

These conditions have exploded within too short of a time period to be attributable to genetic changes, so environmental factors, from synthetic pesticides to plastics to antibiotics, have been blamed for their increased prevalence. While it's probably simplistic to search for one cause to explain away both these types of modern ills, some studies are indicating that immune cells and molecules are important for regulating metabolism—and are dysregulated in obesity.

A specific type of immune cell, called Group 2 innate lymphoid cells (ILC2s), were found in white adipose tissue in mice last year. Now, they have been found in the same tissue in humans. Obese people, along with obese mice, have fewer of these cells in their fat than lean individuals do.

These cells respond to an immune signaling molecule called interleukin 33 (IL-33); that same molecule diminishes obesity by increasing caloric expenditure. This increased caloric expenditure is not due to increased physical activity or to burning more calories as more food is consumed. Instead, IL-33 just enhances the number of calories burned by normal physiological processes. Researchers figured all of this out by playing with mice deficient in IL-33 as well as those deficient in ILC2s—feeding them high fat versus regular chow, treating them with injections of IL-33, and comparing them to normal mice.

[Abstract]: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14115.html