Published online Jun 15, 2020. doi: 10.4239/wjd.v11.i6.239
Peer-review started: November 7, 2019
First decision: December 12, 2019
Revised: March 30, 2020
Accepted: April 18, 2020
Article in press: April 18, 2020
Published online: June 15, 2020
Type I diabetes (T1D) is characterized by insulin loss, accompanied by excessive inflammatory cell infiltration like macrophages and the destruction of the pancreas. Regarding the mechanochemical signaling regulation of T1D, the relationship between macrophage migration and phagocytosis is still unclear. In this study, we provided a new insight into the immune response occurring in the pancreas.
We try to provide a new insight into the mechanism of immune response occurring in the pancreas of T1D patients.
Our aim was to provide a new strategy to prevent T1D progression.
This study was performed both in vivo and in vitro. Macrophage migration and infiltration were assayed to study the mechanism of T1D immune response. The statistical analysis was performed using SPSS statistical software (version 16.0).
In this study, we found a significant decrease of CD47 in pancreatic beta islet cells stimulated with STZ and enhanced migration and infiltration of macrophages. As an integrin-associated surface factor, CD47 expression level is strongly related to the microphage immune response to inflamed pancreas beta islet.
Our study shows a new mechanistic insight into T1D from view of immune response.
This study could provide a new strategy to prevent the progression of T1D.