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Publication : The role of ICAM-1 in the induction of antigen-specific T cell hyporesponsiveness.

First Author  Chung SW Year  1996
Journal  Immunol Lett Volume  50
Issue  3 Pages  155-9
PubMed ID  8803613 Mgi Jnum  J:33743
Mgi Id  MGI:81220 Doi  10.1016/0165-2478(96)02532-1
Citation  Chung SW, et al. (1996) The role of ICAM-1 in the induction of antigen-specific T cell hyporesponsiveness. Immunol Lett 50(3):155-9
abstractText  We have previously demonstrated that pre-transplant transfusion of allogeneic splenic mononuclear cells from B10.BR mice to C3H/HeJ recipient mice resulted in subsequent antigen specific skin graft prolongation and an associated predominance of IL-4-producing T lymphocytes. In this report, we examined the role of ICAM-1 in the induction of T cell hyporesponsiveness and skin graft prolongation following intrahepatic alloantigen delivery. C3H/HeJ mice receiving splenic cells from B10.BR mice intrahepatically showed antigen-specific enhanced skin graft survival. This graft survival was further prolonged following pre-treatment of infused cells with anti-ICAM-1. No such prolongation was seen following intravenous administration of cells in the presence or absence of anti-ICAM-1 pre-treatment. Anti-ICAM-1 infusion alone similarly had no effect when given intrahepatically or peripherally. T lymphocytes from the mice receiving intrahepatic splenic cells and anti-ICAM-1 produced significantly higher amounts of IL-4 compared to mice receiving intrahepatic cells alone or intravenous cells. PCR analysis of ICAM-1 mRNA transcripts demonstrated an increased expression of ICAM-1 in the spleen compared to the liver. These results suggest that ICAM-1 plays an important role in the induction of T cell hyporesponsiveness and allograft prolongation following the intrahepatic encounter of alloantigen.
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