Selection of rabbit CD4-CD8- T cell receptor-γ/δ cells by in vitro transformation with human T lymphotropic virus-I

Sansana Sawasdikosol, Bishop F. Hague, Tong Mao Zhao, Florence S. Bowers, R. Mark Simpson, Maryann Robinson, Thomas J. Kindt

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

Abstract

In vitro transformation of rabbit peripheral blood mononuclear cells (PBMC) with human T lymphotropic virus-I (HTLV)-infected human or rabbit cells resulted in CD4-CD8- cell lines, some of which caused acute leukemia when injected into rabbits. Structural analyses of the proviruses from cell lines with diverse pathogenic effects provided no clear correlation with lethality. The rabbit lines were provisionally designated T cells because they express interleukin 2R (IL-2R) and CD5 and lack surface immunoglobulin, but none express functional T cell receptor (TCR) α or β transcripts. A more detailed characterization of the HTLV-I-infected cells was required to determine cell lineage and its potential influence on pathogenic consequences. Probes for rabbit TCRγ and δ genes were derived and used to detect γ and δ TCR RNA transcripts, identifying the in vitro transformed lines as γ/δ T cells. CD4+ and CD8+ lines were derived from PBMC of HTLV-I-infected rabbits and CD4+ TCR-α/β HTLV-I lines were derived from rabbit thymus, eliminating the possibility that the HTLV-I isolates used here transform only CD4-CD8- TCR-γ/δ cells. The percentage of γ/δ cells in rabbit PBMC is relatively high (23% in adult rabbits); this with diminution of CD4+ and CD8+ cells in IL-2-supplemented PBMC or thymocyte cultures may account for selection of rabbit HTLV-I-infected γ/δ T cell lines in vitro. The availability of well-characterized T cell lines with diverse in vivo effects in the rabbit HTLV-I disease model allows evaluation of roles played by cell type in HTLV-I-mediated disease.

Original languageEnglish
Pages (from-to)1337-1345
Number of pages9
JournalJournal of Experimental Medicine
Volume178
Issue number4
StatePublished - 1 Oct 1993
Externally publishedYes

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