Adoptive transfer of experimental allergic encephalomyelitis after in vitro treatment with recombinant murine interleukin-12. Preferential expansion of interferon-gamma-producing cells and increased expression of macrophage-associated inducible nitric oxide synthase as immunomodulatory mechanisms.

摘要: In an adoptive transfer model of experimental allergic encephalomyelitis, stimulation lymph node cells with proteolipid protein and recombinant murine interleukin (rmIL)-12 before cell accelerated the onset exacerbates clinical disease. vitro in presence rmIL-12 was associated increase interferon-gamma-producing a decrease IL-4-producing cells, indicating preferential expansion Th1 effector cells. This supported by finding that severe disease rapid could be transferred as few 10 x 10(6) rmIL-12-stimulated Immunohistochemical analysis confirmed after coincided acute inflammatory response central nervous system. At peak disease, both control treatment groups exhibited extensive cellular infiltration characteristic perivascular cuffing. No notable differences either composition or cytokine expression within lesions were seen between groups. However, frequency macrophages stained positively for inducible nitric oxide synthase increased animals challenged rmIL-12-treated The results suggest that, addition to promoting vitro, secondary vivo effects leading macrophage activation may contribute protracted course system inflammation this model.