TY  - JOUR
A1  - Ulrichs, Karin
A1  - Müller-Buchholtz, W.
T1  - MHC class II antigen expression on the various cells of normal and activated isolated pancreatic islets
N2  - It is the aim of this study to characterize and quantify the cells within isolated rat islets that express MHC class 11 antigens. A set of five monoelonal antibodies and two polyclonal antisera of defined specificlty were used in combination with a newly devised procedure for three·dimensional immunofluorescence evaluation of intact islets. It is shown that in addition to passen· ger cells, such as Iymphocytes, macro· phages, and dendrlticlike cells, vascular endothelial and endocrine cells are also capable of expressing class 11 antigens. This expression Is strongly influenced by in vitro culture. pregnancy, streptozotocin- induced diabetes, transplantation trauma, and alloantigenic stimuli. The pos· sible role of the above cells in antigen presentation related to islet transplantation is discussed.
KW  - pancreas Islets
KW  - beta cells
KW  - islet transplantation
KW  - la antigens
Y1  - 1985
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-44722
ER  - 
TY  - JOUR
A1  - Chen, Chunguang
A1  - Rawat, Divya
A1  - Samikannu, Balaji
A1  - Bender, Markus
A1  - Preissner, Klaus T.
A1  - Linn, Thomas
T1  - Platelet glycoprotein VI‐dependent thrombus stabilization is essential for the intraportal engraftment of pancreatic islets
JF  - American Journal of Transplantation
N2  - Platelet activation and thrombus formation have been implicated to be detrimental for intraportal pancreatic islet transplants. The platelet‐specific collagen receptor glycoprotein VI (GPVI) plays a key role in thrombosis through cellular activation and the subsequent release of secondary mediators. In aggregometry and in a microfluidic dynamic assay system modeling flow in the portal vein, pancreatic islets promoted platelet aggregation and triggered thrombus formation, respectively. While platelet GPVI deficiency did not affect the initiation of these events, it was found to destabilize platelet aggregates and thrombi in this process. Interestingly, while no major difference was detected in early thrombus formation after intraportal islet transplantation, genetic GPVI deficiency or acute anti‐GPVI treatment led to an inferior graft survival and function in both syngeneic mouse islet transplantation and xenogeneic human islet transplantation models. These results demonstrate that platelet GPVI signaling is indispensable in stable thrombus formation induced by pancreatic islets. GPVI deficiency resulted in thrombus destabilization and inferior islet engraftment indicating that thrombus formation is necessary for a successful intraportal islet transplantation in which platelets are active modulators.
KW  - basic (laboratory) research / science
KW  - coagulation and hemostasis
KW  - graft survival
KW  - islet transplantation
KW  - molecular biology
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-224471
VL  - 21
SP  - 2079
EP  - 2089
ER  -