Abnormalities induced by the mutant gene Ipr: expansion of a unique lymphocyte subset.
Abnormalities induced by the mutant gene Ipr: expansion of a unique lymphocyte subset.
复制标题
突变基因 Ipr 引起的异常：独特淋巴细胞亚群的扩张。
作者：
H. Morse;W. Davidson;R. Yetter;E. Murphy;J. Roths;R. Coffman
携带Ipr突变的小鼠会出现大量淋巴结病和严重的自身免疫性疾病。通过使用a）单克隆抗体和FMF，以及B）IG重链基因的分子遗传学研究，评价了在淋巴组织中增殖的细胞群的特征。Ipr突变纯合子的不同品系小鼠的淋巴结细胞显示出几乎一致的Thy-1+、Ly-1+、Ly-2-、H-11+、Ly-5+、sIg-、ThB-、2C 2+、I-A-、6 B2+，因此具有T和B细胞的表面特征。对IG重链基因排列的分子遗传学研究表明，它们不像前B和B细胞那样重排。这些结果表明，在Ipr/Ipr小鼠中异常增殖的T细胞群体异常表达B细胞表面标志物。
Mice carrying the Ipr mutation develop massive lymphoadenopathy and severe autoimmune disease. The characteristics of the cell population that proliferates in lymphoid tissues were evaluated by the use of a) monoclonal antibodies and FMF, and b) molecular genetic studies of Ig heavy chain genes. The lymph node cells of different strains of mice homozygous for the Ipr mutation were shown to be almost uniformly Thy-1+, Ly-1+, Ly-2-, H-11+, Ly-5+, sIg-, ThB-, 2C2+, I-A-, 6B2+, and therefore to have surface characteristics of both T and B cells. Molecular genetic studies of the arrangements of Ig heavy chain genes showed that they were not rearranged as in pre-B and B cells. These results suggest that an abnormal proliferating population of T cells in Ipr/Ipr mice aberrantly express B cell surface markers.