链脲佐菌素
糖尿病
布鲁顿酪氨酸激酶
胰岛素
B细胞
生物
内分泌学
自身免疫
内科学
细胞
免疫学
免疫系统
医学
细胞生物学
抗体
信号转导
生物化学
酪氨酸激酶
作者
Anuska Marcelino Alvares-Saraiva,Marilia Campos Tavares Novo,Vivian Cristina de Oliveira,Juliana T. Maricato,José Daniel Lopes,Ana Flavia Popi,Mário Mariano
标识
DOI:10.1002/eji.201445409
摘要
The participation of B-1 cells in a murine model of spontaneous diabetes has been recently reported. Here, we describe the role of B-1 cells in streptozotocin (STZ) induced diabetes in mice. We demonstrated that XID (B-1 cell-deficient) mice are more susceptible to STZ treatment than WT mice, as evidenced by their higher blood glucose level in response to STZ. Unexpectedly, the XID mice that were i.p. transferred with purified B-1 cells, either before or after the STZ treatment, did not develop diabetes. These cell transfers provided long-lasting protection for the XID mice against STZ-induced diabetes, suggesting that B-1 cells play an important role in the experimental diabetes pathobiology. We also showed that B-1 cell culture supernatants were able to regulate the blood glucose level of the diabetic XID mice, and we identified insulin-producing cells when B-1 cells were differentiated in B-1 cell-derived phagocyte in vitro. These findings provide a novel role for B-1 cells in metabolic processes, presenting a new mechanism to explain the pathogenesis of diabetes and a possible therapeutical target.
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