Unexpected autoantibody production in membrane Ig-μ-deficient/lpr mice
Unexpected autoantibody production in membrane Ig-μ-deficient/lpr mice
复制标题
DOI：
10.4049/jimmunol.165.8.4353
复制
发表时间：
2000-10-15
影响因子：
4.4
通讯作者：
Nemazee, D
中科院分区：
文献类型：
--
作者：
Melamed, D;Miri, E;Nemazee, D
在B淋巴细胞谱系中，PAS介导的细胞死亡在控制活化的成熟细胞中是重要的，但对早期发育阶段的可能功能知之甚少。在这项研究中，我们发现，在缺乏IgM跨膜尾外显子的小鼠（μ MT小鼠）中，其中B细胞发育在前B阶段被阻断，Fas或Pas配体的缺乏允许显著的B细胞发育和成熟，导致高血清IG水平。这些B细胞表现出IG重链同种型转换和自身免疫反应性，表明功能性Pas的缺乏允许缺陷和/或自身反应性B细胞在μ MT/lpr小鼠中成熟。可能允许这些B细胞成熟的机制进行了讨论。
In the B lymphocyte lineage, Pas-mediated cell death is important in controlling activated mature cells, but little is known about possible functions at earlier developmental stages. In this study we found that in mice lacking the IgM transmembrane tail exons (mu MT mice), in which B cell development is blocked at the pro-B stage, the absence of Fas or Pas ligand allows significant B cell development and maturation, resulting in high serum Ig levels. These B cells demonstrate Ig heavy chain isotype switching and autoimmune reactivity, suggesting that lack of functional Pas allows maturation of defective and/or self-reactive B cells in mu MT/lpr mice. Possible mechanisms that may allow maturation of these B cells are discussed.