on April 2, 2012
The cells of the immune system possess powerful weapons that are able to fight off the invasion of microorganisms, yet at the same time can cause collateral damage. In particular, the Th17 lymphocytes, which carry this name because they produce interleukin-17, are important for the protection against fungi and bacteria but can also cause chronic inflammation and autoimmunity. In a paper published in the April 1st issue of the journal Nature, a team of researchers from the Institute for Research in Biomedicine in Bellinzona, led by Dr. Federica Sallusto, describes for the first time in humans, two types of Th17 cells. The first type of Th17 cell is very inflammatory because, in addition to interleukin-17, it produces another cytokine, interferon-gamma. The other type of Th17 cell produces interleukin-17 and another cytokine, interleukin-10, that inhibits inflammation. Using a new approach that combines in vitro experiments with the study of memory cells, the team has been able to identify the switch that regulates the production of these two different types of cells. The researchers have shown that interleukin-1, produced by monocytes (the cells that stimulate the immune response) is able to both stop the production of interleukin-10 and stimulate the production of interferon-gamma. These results have been confirmed by a study of patients with excessive production of interleukin-1, in cooperation with the Gaslini Institute of Genoa. This research therefore reveals that interleukin-1 plays a fundamental role in determining the inflammatory or anti-inflammatory activity of T lymphocytes, thus allowing adequate inflammatory responses but at the same time limiting collateral damage.
