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- Title
Generation of allospecific cytolytic T-lymphocytes stimulated by pure pancreatic beta-cells in absence of Ia+ dendritic cells.
- Authors
Stock, Peter G.; Meloche, Mark; Ascher, Nancy L.; Chen, Sally; Bach, Fritz H.; Sutherland, David E. R.; Stock, P G; Meloche, M; Ascher, N L; Chen, S; Bach, F H; Sutherland, D E
- Abstract
A murine mixed islet-lymphocyte coculture system (MILC) was used to quantitate the immunogenicity of a pure population of pancreatic beta-cells to more clearly define whether stimulator major histocompatibility complex (MHC) class II-positive dendritic cells are a major component leading to islet immunogenicity. Pancreatic beta-cells express MHC class I antigen but not class II antigen. These experiments compared the in vitro immunogenicity of fluorescence-activated cell sorted (FACS-IV) pure beta-cells (MHC class I-positive cells only) relative to unpurified dispersed islet cells (MHC class I-positive cells and class II-positive cells). The results demonstrated the surprising finding that pure DBA/2J (H-2d) pancreatic beta-cells stimulated a strong cytotoxic T-lymphocyte (CTL) response when exposed to C57BL/6 (H-2b) allosplenocytes in the MILC, similar to DBA/2J nonpurified dispersed islet cells. Furthermore, the stimulation of CTL by both purified beta-cells and nonpurified dispersed islet cells was blocked by addition of MHC-specific anti-class I monoclonal antibody directed against stimulator MHC antigen. The data imply that the highly immunogenic MHC class II-positive passenger leukocytes present in the islets were not necessary for the generation of the immune response in the presence of MHC class I-positive beta-cells. Although most of the pretreatment regimens attempting to decrease islet immunogenicity have been directed at eliminating the MHC class II-positive passenger leukocytes from the islets, this work suggests that modulation of MHC class I antigen may be an important approach.
- Publication
Diabetes, 1989, Vol 38, p161
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diab.38.1.s161