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Antigenic and Immunogenic Components in Rat Liver

Antigenic and Immunogenic Components in Rat Liver We have analysed the immunogenic potential and the expression of class II major histo‐compatibility complex (MHC) antigens of the various cellular components of rat liver. A two‐step fractionation procedure was developed to isolate the following liver cellular components: hepatocytes, ‘non‐hepatocytic’ parenchymal cells, and passenger leucocytes including the Kupffer cells. A primed rejection assay with the different isolated cell populations was performed in the WF rat. The survival time of a DA cardiac allograft in a normal, non‐primed WF rat is 6.3 ± 2.1 days. DA liver hepatocytes were unable to induce accelerated rejection, reducing the survival to at most 5.5 ± 0.6 days (P= 0.374). The hepatocyte‐depleted parenchymal cell component, consisting primarily of endothelial and bile duct cells, was equally ineffective and reduced the survival to at most 5.0 ± 1.4 days (P=0.453). An accelerated rejection was obtained only with the liver passenger cell‐enriched fraction, with a reduction of survival to 3.3 ± 0.6 days (P=0.034). The expression of class II MHC antigens was analysed on frozen sections and on the disaggregated liver cells by using monoclonal mouse antisera to the common part of the class II molecule. Indirect immunofluorescence and cytological Staphylococcus aureus Cowan I rosette assays were used, respectively. The former showed that only the vascular endothelial cells and the Kupffer cells of the space of Disse expressed class II; the latter demonstrated that only the Kupffer cells had substantial amounts of class II antigens on the cell surface. The results demonstrate that the principal and perhaps only immunogenic component in rat liver is the passenger leucocytes, in particular the strongly class‐II‐expressing Kupffer cells of the passenger population. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Scandinavian Journal of Immunology Wiley

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References (18)

Publisher
Wiley
Copyright
Copyright © 1983 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0300-9475
eISSN
1365-3083
DOI
10.1111/j.1365-3083.1983.tb00766.x
Publisher site
See Article on Publisher Site

Abstract

We have analysed the immunogenic potential and the expression of class II major histo‐compatibility complex (MHC) antigens of the various cellular components of rat liver. A two‐step fractionation procedure was developed to isolate the following liver cellular components: hepatocytes, ‘non‐hepatocytic’ parenchymal cells, and passenger leucocytes including the Kupffer cells. A primed rejection assay with the different isolated cell populations was performed in the WF rat. The survival time of a DA cardiac allograft in a normal, non‐primed WF rat is 6.3 ± 2.1 days. DA liver hepatocytes were unable to induce accelerated rejection, reducing the survival to at most 5.5 ± 0.6 days (P= 0.374). The hepatocyte‐depleted parenchymal cell component, consisting primarily of endothelial and bile duct cells, was equally ineffective and reduced the survival to at most 5.0 ± 1.4 days (P=0.453). An accelerated rejection was obtained only with the liver passenger cell‐enriched fraction, with a reduction of survival to 3.3 ± 0.6 days (P=0.034). The expression of class II MHC antigens was analysed on frozen sections and on the disaggregated liver cells by using monoclonal mouse antisera to the common part of the class II molecule. Indirect immunofluorescence and cytological Staphylococcus aureus Cowan I rosette assays were used, respectively. The former showed that only the vascular endothelial cells and the Kupffer cells of the space of Disse expressed class II; the latter demonstrated that only the Kupffer cells had substantial amounts of class II antigens on the cell surface. The results demonstrate that the principal and perhaps only immunogenic component in rat liver is the passenger leucocytes, in particular the strongly class‐II‐expressing Kupffer cells of the passenger population.

Journal

Scandinavian Journal of ImmunologyWiley

Published: Jan 1, 1983

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