Influence of interleukin-2 deficiency on the generation of autoimmune B cells.
Influence of interleukin-2 deficiency on the generation of autoimmune B cells.
复制标题
IL-2 缺乏对自身免疫 B 细胞生成的影响。
DOI：
10.1016/j.jaut.2007.06.001
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发表时间：
2007
影响因子：
12.8
通讯作者：
Miller,JohnD
中科院分区：
文献类型：
--
作者：
Wrenshall,LucileE;Smith,DeandraR;Stevens,ElliotT;Miller,JohnD
自身抗体的产生是自身免疫性疾病的主要特征之一。由于IL-2缺乏小鼠产生自身免疫，我们询问IL-2缺乏如何损害B细胞耐受的内源性机制。为此，我们将产生抗dsDNA抗体的B细胞受到适当调节的BALB B/c抗dsDNA H链敲入小鼠与IL-2缺陷小鼠交配，并评估其后代的表型。表达抗dsDNA H链敲入等位基因的IL-2缺陷小鼠产生IgM和IgG同种型的抗dsDNA抗体。这些抗体的产生是通过破坏内源性耐受的几种机制发生的，包括缺失、成熟停滞和卵泡排斥。综上所述，我们的结果表明，IL-2在调节B细胞耐受中起着重要作用。
The production of auto-antibodies is one of the predominant characteristics of autoimmune disorders. Because IL-2 deficient mice develop autoimmunity, we asked how IL-2 deficiency might impair endogenous mechanisms of B cell tolerance. To this end, we mated BALB/c anti-dsDNA H chain knock-in mice, in which B cells producing anti-dsDNA antibodies are properly regulated, with IL-2 deficient mice and assessed the phenotype of their offspring. IL-2 deficient mice expressing the anti-dsDNA H chain knock-in allele developed anti-dsDNA antibodies of both IgM and IgG isotypes. Production of these antibodies occurred through the disruption of several mechanisms of endogenous tolerance, including deletion, maturational arrest, and follicular exclusion. In summary, our results suggest that IL-2 plays an important role in regulating B cell tolerance.