Pisetsky D S, Caster S A, Piper M, Scott D W, Steinberg A D
Cell Immunol. 1984 Mar;84(1):32-40. doi: 10.1016/0008-8749(84)90074-1.
The relationship between colony formation (cloning) of B cells and their activation in murine autoimmunity was investigated in MRL-lpr/lpr and MRL.xid mice. Cells from MRL-lpr/lpr mice showed similar requirements for in vitro growth as normal CBA/J and BALB/c cells, with maximal colony formation in the presence of the supporting factors lipopolysaccharide and sheep red blood cells. The frequency of colony-forming cells from MRL-lpr/lpr spleens or hapten-specific B-cell preparations was slightly greater than the two normal control strains, with this difference significant only for a comparison of BALB/c and MRL-lpr/lpr spleens. In contrast, MRL-lpr/lpr mice bearing the xid gene for B-cell immunodeficiency (MRL.xid) had markedly reduced B-cell colony formation. These mice nevertheless expressed anti-DNA antibodies, although at levels reduced from that of MRL-lpr/lpr controls. These results indicate that enhanced in vitro colony formation need not accompany B-cell hyperactivity in murine autoimmune disease and that autoantibody production can occur in mice with impairment in this growth property.
在MRL-lpr/lpr和MRL.xid小鼠中研究了B细胞集落形成（克隆）与其在小鼠自身免疫中的激活之间的关系。来自MRL-lpr/lpr小鼠的细胞对体外生长的需求与正常CBA/J和BALB/c细胞相似，在存在支持因子脂多糖和绵羊红细胞的情况下集落形成达到最大值。来自MRL-lpr/lpr脾脏或半抗原特异性B细胞制剂的集落形成细胞频率略高于两个正常对照品系，仅在比较BALB/c和MRL-lpr/lpr脾脏时，这种差异才具有显著性。相比之下，携带B细胞免疫缺陷xid基因的MRL-lpr/lpr小鼠（MRL.xid）的B细胞集落形成明显减少。然而，这些小鼠表达抗DNA抗体，尽管其水平低于MRL-lpr/lpr对照。这些结果表明，在小鼠自身免疫性疾病中，体外集落形成增强不一定伴随着B细胞的过度活跃，并且在这种生长特性受损的小鼠中也可以产生自身抗体。
