Liver of MRL/lpr mice contain interleukin-4-producing lymphocytes and accessory cells that support the proliferation of Th2 helper T lymphocyte clones.

Hepatic nonparenchymal cells (NPC) from mice of nonautoimmune strains support the proliferation of only Th1 and not Th2 helper T lymphocyte (HTL) clones. Because of the multiple systemic and liver-specific immune defects in the autoimmune MRL/lpr mouse strain, we have explored the possibility that hepatic accessory cells from MRL/lpr mice are capable of stimulating the proliferation of Th2 HTL. We report here that hepatic NPC from MRL/lpr and C3H/lpr female mice older than 8 weeks, in contrast to hepatic NPC from MRL/++ and C3H/HeN strains, are able to support in vitro the proliferation of both Th1 and Th2 CD4 clones. Additionally, hepatic lymphocytes (HL) from MRL/lpr mice can be stimulated to produce interleukin (IL)-4 to a much higher degree than HL from the nonautoimmune strains. These results suggest that the activation of Th2 cells by hepatic NPC and production of IL-4 by HL may contribute to the immunologic aberrations in the MRL/lpr mouse strain.