There may be a connection between metabolic defects and arthritis. Autoimmunity is a biological betrayal. Your immune system is there to defend you against outsiders like viral, bacterial, fungal or protozoan pathogens and to weed out cancer cells before they become tumors. Yet in rheumatoid arthritis, type-1 diabetes and multiple sclerosis, to name a few of the most well known autoimmune diseases, immune soldiers called T cells turn on one or another of your own tissues and launch increasingly vicious aberrant assaults on it.
Nobody’s sure exactly what causes any of these disparate disorders, although combinations of inherited susceptibility and environmental triggers surely loom large as contributors.
In a new study in the Journal of Experimental Medicine, Stanford rheumatologists Connie Weyand, MD, and Jorg Goronzy, MD, and their colleagues have fingered a particular metabolic defect that appears to be specific to rheumatoid arthritis. T cells have an odd job description, which calls for them to mostly sit around and spend their lives loafing but, as soon as they recognize – or get a bit trigger-happy and think they recognize – a foreign intruder, to spring into action, multiplying and morphing as they do.