Willenborg D O, Sjollema P, Danta G
J Neuroimmunol. 1986 Apr;11(2):93-103. doi: 10.1016/0165-5728(86)90111-6.
Lewis rats, treated from birth with a rabbit anti-rat IgM antiserum are B-cell and immunoglobulin deficient. When sensitized with myelin basic protein (BP) and complete Freund's adjuvant (CFA), these rats do not make detectable antibodies to BP, nor do they develop clinical or histopathological evidence of allergic encephalomyelitis (EAE). We show here that transfer of anti-BP antibody containing serum to BP sensitized Ig deficient rats results in subsequent development of EAE. We also demonstrate that BP sensitized Ig deficient rats which do not develop EAE, nevertheless generate effector cells capable of transferring disease, and thus specific T-cell function is not inhibited by the anti-Ig treatment. Finally, Ig deficient rats were shown to be perfectly adequate recipients of passively induced EAE.
从出生起就用兔抗大鼠IgM抗血清处理的Lewis大鼠存在B细胞和免疫球蛋白缺陷。当用髓鞘碱性蛋白(BP)和完全弗氏佐剂(CFA)致敏时,这些大鼠不会产生可检测到的针对BP的抗体,也不会出现变应性脑脊髓炎(EAE)的临床或组织病理学证据。我们在此表明,将含抗BP抗体的血清转移至对BP致敏的Ig缺陷大鼠会导致随后EAE的发生。我们还证明,未发生EAE的对BP致敏的Ig缺陷大鼠仍能产生能够传递疾病的效应细胞,因此抗Ig处理不会抑制特异性T细胞功能。最后,Ig缺陷大鼠被证明是被动诱导EAE的理想受体。