26
Views
9
CrossRef citations to date
0
Altmetric
Original Article

Fas is Expressed in Murine Pancreatic Islet Cells and an Insulinoma Cell Line but Does Not Mediate Their Apoptosis in vitro

, , , &
Pages 189-199 | Received 16 Jul 1998, Published online: 07 Jul 2009
 

Abstract

CD4+ lymphocytes are the most important effector cells in autoimmune diabetes of NOD mice, although some role of CD8+ T cells has been demonstrated. However, it is unknown how CD4+ lymphocytes are able to destroy pancreatic β-cells that do not express MHC (major histocompatibility complex) class II molecules. Apoptotic cell death mediated by an interaction of Fas with Fas ligand (FasL) could be a mechanism by which MHC class II-negative pancreatic β-celIs are destroyed by CD4+ T lymphocytes. We have examined the expression of Fas molecules in pancreatic islet cells, as well as in a NOD-derived mouse insulinoma cell line (MIN6N8). In addition, the role of Fas-mediated apoptosis in pancreatic islet cell death was explored in vitro. Although Fas expression was not detected by flow cytometric analysis, Fas transcripts were demonstrated in M1N6N8 cells and pancreatic islet cells by the sequencing analysis of the cloned reverse transcription polymerase chain reaction products using Fas-specific primers. IFN (interferon)-)γ, tumor necrosis factor-a, inter-leukin-1 and their combinations failed to enhance Fas expression. Unsorted activated splenocytes from diabetic NOD mice had cytotoxic T lymphocyte activity of a small degree against IFN-γ-treated MIN6N8 cells with FasL upregulation. However, agonistic anti-Fas antibody with or without cycloheximide did not exert cytotoxicity against MIN6N8 cells or pancreatic islets. FasL transfectant cells also did not kill MIN6N8 cells. Our data indicate that pancreatic β-islet cells express a small amount of Fas molecules but Fas molecules do not mediate apoptosis of islet cells at least in vitro.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.