anciendaze
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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.
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.
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