Researchers at the University of Calgary have just published work on the regulation of immune response in Inflammatory Bowel Disease (IBD) which pinpoints the effect of a specific protein released by bacteria of genus bacteroides. Among the undeniably "real" diseases resulting from dysregulation is diabetes. Here's a link to the actual paper in Cell. There has been a known association between type 1 diabetes and autoantibodies to GAD65 for some time, but the trigger for excessive production of this was unknown. Note that this is a distinct part of immune response associated with B-cells and plasma cells. We now learn that CD8+ (cytotoxic) T-cells, which kill cells in the pancreas to cause diabetes, are more usefully active in suppressing inflammatory response in the gut. This does not take place due to T-cells in isolation, but via dendritic immune cells lining the gut. Dendritic cells also play significant roles in pancreatic function in a number of diseases. I'm now wondering if the antibodies to GAD65 appear after cells are damaged by cytotoxic T-cells. This result should most definitely be followed up, if only because preventing the life-long problems of diabetes would be of considerable benefit to public health. It is unlikely to be a trivial problem of too much something, but rather a matter of regulating immune response to balance inflammation in the gut against damage to pancreatic cells. The exciting thing is that we now have very specific targets for interventions.