期刊
DIABETES
卷 54, 期 5, 页码 1423-1428出版社
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.54.5.1423
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资金
- NIAID NIH HHS [AI50059, AI053052] Funding Source: Medline
- NIDDK NIH HHS [DK065848] Funding Source: Medline
The tumor suppressor p53 regulates apoptosis, cell cycle, and oncogenesis. To explore the roles of p53 in autoimmunity, we studied type 1 diabetes and innate immune responses using C57BL/6 mice deficient in p53. We found that p53-deficient mice were more susceptible to streptozotocin-induced diabetes than control mice, and they produced higher levels of interleukin-1, -6, and 12 The innate immune response of p53(-/-) macrophages to lipolysaccharides and gamma-interferon was significantly enhanced compared with p53(+/+) cells. p53(-/-) macrophages produced more proinflammatory cytokines and higher levels of total and phosphorylated signal transducer and activator of transcription (STAT)-1. These results indicate that p53 inhibits autoimmune diabetes and innate immune responses through downregulating STAT-1 and proinflammatory cytokines.
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