Magilavy D B, Foys K M, Gajewski T F
Department of Pediatrics, La Rabida-University of Chicago Institute, IL.
Eur J Immunol. 1992 Sep;22(9):2359-65. doi: 10.1002/eji.1830220927.
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.
非自身免疫品系小鼠的肝非实质细胞（NPC）仅支持Th1而非Th2辅助性T淋巴细胞（HTL）克隆的增殖。由于自身免疫性MRL/lpr小鼠品系存在多种全身性和肝脏特异性免疫缺陷，我们探究了MRL/lpr小鼠的肝辅助细胞是否能够刺激Th2 HTL增殖的可能性。我们在此报告，与MRL/++和C3H/HeN品系的肝NPC不同，8周龄以上的MRL/lpr和C3H/lpr雌性小鼠的肝NPC能够在体外支持Th1和Th2 CD4克隆的增殖。此外，与非自身免疫品系的肝淋巴细胞（HL）相比，MRL/lpr小鼠的HL能被刺激产生白细胞介素（IL）-4的程度要高得多。这些结果表明，肝NPC对Th2细胞的激活以及HL产生IL-4可能导致了MRL/lpr小鼠品系的免疫异常。
