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What is it about?
The study focused on the use of the peptide p277, derived from the human 60-kDa heat-shock protein (hsp60), as a therapeutic agent for diabetes in non-obese diabetic (NOD) mice. The effectiveness of p277 treatment was associated with the induction of peptide-specific antibodies of the IgGl isotype, suggesting a Th2-type response. The study found that the effectiveness of p277 treatment was associated with the transient activation of anti-p277 splenic T-cells that produce the Th2 cytokines interleukin-4 (IL-4) and IL-10. The Th2 response to p277 was associated with reduced Thl-type autoimmunity to hsp60 and to two other target antigens associated with diabetes: GAD and insulin. The Th2 shift appeared to be relatively specific, as spontaneous T-cell reactivity to a bacterial antigen peptide remained in the Thl mode in the p277-treated mice. Treatment with the bacterial peptide did not induce a change in cytokine profile and did not affect progression of the disease. These findings suggest that effective peptide treatment of the diabetogenic process may be explained by selective and transient activation of Th2 autoimmune reactivity.
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Why is it important?
This research is important because it identifies the potential of using peptides to treat diabetes in NOD mice. The study focuses on the peptide p277, which is derived from the human 60-kDa heat-shock protein (hsp60), and its effectiveness in arresting the autoimmune process responsible for diabetes in NOD mice. The findings suggest that the therapeutic effect of p277 treatment is associated with the induction of specific antibodies and the transient activation of Th2 cytokines, which may help reduce the progression of diabetes. Understanding the mechanisms behind the effectiveness of p277 treatment could potentially lead to the development of new therapies for diabetes in humans. Key Takeaways: 1. Peptide p277, derived from the human 60-kDa heat-shock protein (hsp60), is found to be effective in treating diabetes in NOD mice. 2. The therapeutic effect of p277 treatment is associated with the induction of specific antibodies and the transient activation of Th2 cytokines, which may help reduce the progression of diabetes. 3. The study suggests that the effectiveness of p277 treatment is relatively specific, as it does not induce a change in cytokine profile or affect the progression of the disease in mice treated with a bacterial peptide.
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This page is a summary of: Hsp60 Peptide Therapy of NOD Mouse Diabetes Induces a Th2 Cytokine Burst and Downregulates Autoimmunity to Various β-Cell Antigens, Diabetes, May 1997, American Diabetes Association,
DOI: 10.2337/diab.46.5.758.
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