Scribner C L, Hansen C T, Klinman D M, Steinberg A D
J Immunol. 1987 Jun 1;138(11):3611-7.
The murine "motheaten" (me) mutation has been bred onto the NFS background and combined with the X-linked immunodeficiency (xid) mutation to investigate the effect of the xid-induced B cell maturational block on the widespread immune dysfunction, high levels of autoantibodies, and early mortality found in the motheaten mice. The xid markedly reduced spontaneous IgM secretion by spleen cells, serum IgM, anti-ssDNA antibodies, anti-bromelain-treated-erythrocyte antibodies, and T cell binding (but not thymocytotoxic) antibodies; however, neither phenotype nor mortality was affected, suggesting that other factors are responsible for early death. Marked expansion of the Ly-1+ B cell pool was prevented by xid in the motheaten mouse leaving only a very small population of sIgM-positive B cells. This failure of non-Ly-1+ B cell development in me/me X xid mice suggests that me/me leads to inhibition of non-Ly-1+ B cells and preferential expansion of Ly-1+ B cells in motheaten mice, perhaps as a result of their high levels of maturation and activation factors.
已将小鼠的“食母生”(me)突变培育到NFS背景上,并与X连锁免疫缺陷(xid)突变相结合,以研究xid诱导的B细胞成熟阻滞对食母生小鼠中广泛存在的免疫功能障碍、高水平自身抗体和早期死亡的影响。xid显著降低了脾细胞自发分泌的IgM、血清IgM、抗单链DNA抗体、抗菠萝蛋白酶处理红细胞抗体以及T细胞结合(但非胸腺细胞毒性)抗体;然而,表型和死亡率均未受影响,这表明其他因素是导致早期死亡的原因。在食母生小鼠中,xid阻止了Ly-1+B细胞池的显著扩增,仅留下极少数sIgM阳性B细胞。me/me X xid小鼠中非Ly-1+B细胞发育的这种失败表明,me/me导致食母生小鼠中非Ly-1+B细胞受到抑制,Ly-1+B细胞优先扩增,这可能是由于它们高水平的成熟和激活因子所致。