Researchers at the University of Pittsburgh have successfully prevented the onset of type 1 diabetes in mice prone to developing the disease using an antibody against a receptor on the surface of immune T-cells. According to the investigators, these findings, which are being published in the journal Diabetes, have significant implications for the prevention of type 1 diabetes.
In this study, the Pitt researchers treated non-obese diabetic ( NOD ) mice with an antibody, directed against a receptor known as CD137 on the surface of T-cells. Treating NOD mice with the anti-CD137 antibodies significantly suppressed the development of diabetes, whereas most of the control mice developed diabetes by the time they were six months old.
Interestingly, the antibody therapy did not appear to cure the NOD mice because the researchers were still able to see lymphocytes in their pancreatic islets, a tell-tale sign of pancreatic inflammation and autoimmunity. In addition, when the researchers isolated cells from the spleens of the antibody-treated mice and injected these cells into immune-deficient NOD mice, seven of the nine recipient mice developed type 1 diabetes, indicating that the donor mice still harbored pathogenic T-cells. On the other hand, when the researchers transferred a certain subset of T-cells from anti-CD137-treated mice that expressed two other receptors known as CD4 and CD25 to other immune-deficient NOD mice, it prevented the onset of diabetes in the recipient mice.
According to senior author William M. Ridgway, at the University of Pittsburgh School of Medicine, this therapy, if given early enough, may offer a viable method for preventing the onset of type 1 diabetes in genetically at-risk people.
" Our studies and others suggest that CD137 plays a significant role in the development of and genetic predisposition to type 1 diabetes. In this study, for the first time, we have demonstrated that CD137 antibody therapy can suppress the development of type 1 diabetes in mice and that the effect is dependent on the induction of a certain subset of regulatory T-cells. If we can demonstrate this same genetic predisposition and therapeutic effect in human type 1 diabetes patients, then this may prove to be a significant step toward preventing this disease before it can take hold," he explained.
Source: University of Pittsburgh Medical Center, 2007
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