We have previously reported that a fetal liver-derived hepatocyte clone, FHC-4D2, can support hematopoiesis in vitro. Here, we show that fetal thymocytes (FT) or adult thymocytes (AT) proliferate on the monolayer of FHC- 4D2 cells in the presence of rIL-2. Fresh thymocytes contained few TCR- γδ+ cells (<4% for FT and <1% for AT); significant numbers of TCR-γδ+ cells were detected (2-11% for FT and 15-33% for AT) after the coculture with FHC-4D2 and rIL-2. Although FT-derived TCR-γδ+ cells predominantly used the Vγ5 chain, the major population in AT-derived TCR-γδ+ cells used Vγ1, Vγ4, or Vγ7 chains. Both FT- and AT-derived TCR-γδ+ cells killed FcR-bearing target cells when incubated with anti-TCR-γδ Ab. Half of FT- derived TCR-γδ+ cells were CD4-CD8α+8β-; the rest were CD4- CD8α- 8β- . AT-derived TCR-γδ+ cells expressed neither CD4 nor CD8 molecules. Separation of thymocytes from FHC-4D2 cells with a membrane filter reduced the proliferative response by two- to threefold. Taken together, these results demonstrate that a fetal hepatocyte clone supports thymocytes to develop preferentially into TCR-γδ+ cells in cooperation with rIL-2 through cell-cell contact, that the repertoire and the phenotype of induced TCR-γδ+ cells are determined by the age of the mice, and that hepatocytes might thus play an active role in T lymphopoiesis in the fetal liver.
|Number of pages||10|
|Journal||Journal of Immunology|
|Publication status||Published - 1995|
ASJC Scopus subject areas
- Immunology and Allergy