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

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

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