| First Author | Conti A | Year | 1996 |
| Journal | J Pineal Res | Volume | 20 |
| Issue | 3 | Pages | 164-72 |
| PubMed ID | 8797184 | Mgi Jnum | J:34277 |
| Mgi Id | MGI:81740 | Doi | 10.1111/j.1600-079x.1996.tb00253.x |
| Citation | Conti A, et al. (1996) Role of the pineal gland and melatonin in the development of autoimmune diabetes in non-obese diabetic mice. J Pineal Res 20(3):164-72 |
| abstractText | Earlier studies on the immunoregulatory role of the pineal gland and melatonin revealed that melatonin counteracts immunosuppression and thymus atrophy induced by stress or corticosteroid treatment. Moreover, melatonin protects mice injected with encephalitogenic viruses, synergizes with interleukin-2 (IL-2) in cancer immunotherapy and rescues hematopoiesis from cancer chemotherapy toxicity. In regard to the mechanism of action, melatonin seems to act directly on CD4+ lymphocytes which release opioid peptides with immunoenhancing properties along with other cytokines. Because of these findings, we investigated the role of the pineal gland and melatonin in autoimmune diabetes mellitus type I using, as an experimental model, female non-obese diabetic (NOD) mice. Mice were pinealectomized or treated chronically with melatonin (injected subcutaneously or administered via drinking water). This paper shows that neonatal pinealectomy accelerates the development of the disease in female NOD mice while exogenous melatonin protects the animals. This in spite of the fact that melatonin increased the production of insulin autoantibodies (IAA). We conclude that the pineal gland and melatonin influence the development of autoimmune diabetes although the mechanism of action that needs further investigation. |
