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CD45RC−γδ+T-cell infiltration is associated with immunologic unresponsiveness induced by prior donor-specific blood transfusion in rat hepatic allografts

Authors
Journal
Hepatology
0270-9139
Publisher
Wiley Blackwell (John Wiley & Sons)
Publication Date
Volume
33
Issue
4
Identifiers
DOI: 10.1053/jhep.2001.23503
Disciplines
  • Medicine

Abstract

Abstract Little is known regarding the role of γδ + T cells in organ transplantation. We previously reported that immunologic unresponsiveness is induced by prior donor-specific blood transfusion (DST) in rat hepatic allografts. We investigated the phenotype and distribution of γδ + T cells in the hepatic allograft, spleen, and peripheral blood of recipient rats with immunologic unresponsiveness induced by DST. γδ + T cells were enumerated in allograft livers and spleens by immunostaining and in blood by flow cytometric analysis. The phenotype of γδ + T cells was determined using CD45RC isoforms derived from alternative mRNA splicing. The cytokine profile of CD45RC + and CD45RC − γδ + T cells was analyzed by reverse transcription polymerase chain reaction. The number of γδ + T cells in hepatic infiltrates in recipient rats pretreated with DST was significantly greater than in untreated animals. This correlated with significantly higher levels of γδ T cell receptor (TCR) mRNA in hepatic allografts of DST–treated rats as compared with untreated animals. The γδ + T cell/αβ + T-cell ratio increased in hepatic infiltrates in DST–treated recipient rats but not in untreated animals. CD45RC −γδ + T cells were predominantly increased in DST–treated hepatic allografts compared with untreated allografts. Most of the intestinal intraepithelial T cells were CD45RC −γδ +. Interleukin (IL)-10 and IL-4 mRNA were detected more in CD45RC −γδ + T cells than CD45RC +γδ + T cells. CD45RC −γδ + T cells infiltrating liver allografts produce Th2-type cytokines and are associated with immunologic unresponsiveness induced by DST. (H EPATOLOGY 2001;33:877-886.)

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