Using a novel approach for imaging the movement of immune cells in living animals, researchers from the Massachusetts General Hospital (MGH) Center for Immunology and Inflammatory Diseases (CIID) have identified what appear to be the initial steps leading to joint inflammation in a model of inflammatory arthritis. In their report, published online on January 19, 2017 in Science Immunology, they describe how expression of a specific molecule - complement C5a (image) - is required to cause the immune cells called neutrophils to adhere to joint surfaces and migrate into the joint, a process known to set off the inflammatory cascade. The article is titled “Complement C5a Receptor Is the Key Initiator of Neutrophil Adhesion Igniting Immune Complex–Induced Arthritis.” "Inflammatory arthritis is caused when immune cells are recruited from the blood into the joint in a highly regulated process controlled by chemoattractants and adhesion receptors," says Andrew Luster, M.D., Ph.D., Chief of the MGH Division of Rheumatology, Allergy and Immunology, Director of the CIID and senior author of the report. "But when the disease has become symptomatic, it is difficult to determine the initial steps that set off the recruitment of immune cells into the joint and the specific roles of the different chemoattractants. Our study was designed to more fully understand this process." Inflammatory arthritis includes a number of autoimmune diseases of the joints - including rheumatoid arthritis and lupus – and, in many cases, is caused by a type of inflammation called type III hypersensitivity.
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