Discovered a switch that regulates inflammation, a study published in Nature

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. –  Dr. Federica Sallusto received the degree of Doctor in Biology from the University of Rome and performed postdoctoral training at the italian Institute of Health in Rome (ISS) and at the Basel Institute for Immunology (BII). In two groundbreaking papers published in 1994 and 1995, she reported that

monocytes are precursors of DCs and showed that DC maturation could be induced by microbial stimuli. In 1995, she started her own group at the ISS focusing on allergy and after two years she moved to the BII where she started a new line of research on T cell trafficking. Her studies revealed a differential expression of chemokine receptors in human Th1 and Th2 cells leading to the characterization of “central memory” and “effector memory” T cells as memory subsets with distinct migratory capacity and function. Since 2000, she is a group leader at the IRB. Among her recent contributions are the epigenetic control of cytokine gene expression in human T cells and the characterization of Th17 and Th22 cells. To complement her work in the field of human immunology, she started a line of research to study in vivo lymphocyte migration in the mouse system. These studies have challenged current dogma by identifying new mechanisms of lymphocyte migration in inflamed lymph nodes and in the brain. She received the Pharmacia Foundation Award in 1999, the Behring Lecture Prize in 2009, and the Award of the Foundation for Study of Neurodegenerative Diseases in 2010. Since 2010 she is member of the German Academy of Science Leopoldina. News from: Institute for Research in Biomedicine

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