Yamamura T, Namikawa T, Endoh M, Kunishita T, Tabira T
J Neurol Sci. 1986 Dec;76(2-3):269-75. doi: 10.1016/0022-510x(86)90174-7.
In an attempt to obtain insight into the pathogenesis of proteolipid apoprotein (PLP)-induced experimental allergic encephalomyelitis (EAE) in Lewis rats (Yamamura et al. 1986), PLP-sensitized lymph node cells or spleen cells were passively transferred into normal or irradiated (400 rad) recipients after incubation with concanavalin A or PLP. Clinical EAE manifested by paraparesis was successfully transferred into irradiated recipients with 2 - 2.5 X 10(8) of the primary cultured cells and histologic EAE could be transferred with as few as 5 X 10(7) cells into naive recipients. This is the first demonstration of passive EAE induced with PLP-sensitized lymphoid cells and suggests the pathogenetic importance of cell-mediated immunity to PLP.
为了深入了解脂蛋白(PLP)诱导的Lewis大鼠实验性变应性脑脊髓炎(EAE)的发病机制(Yamamura等人,1986年),将经伴刀豆球蛋白A或PLP孵育后的PLP致敏淋巴结细胞或脾细胞被动转移至正常或经照射(400拉德)的受体中。表现为轻截瘫的临床EAE可通过2 - 2.5×10⁸个原代培养细胞成功转移至经照射的受体中,而组织学EAE只需5×10⁷个细胞就能转移至未致敏受体中。这是首次证明由PLP致敏淋巴细胞诱导的被动性EAE,并提示了细胞介导的针对PLP免疫在发病机制中的重要性。