Riggs J E, Stowers R S, Mosier D E
Division of Immunology, Medical Biology Institute, La Jolla, California 92037.
J Exp Med. 1991 Jan 1;173(1):265-8. doi: 10.1084/jem.173.1.265.
Mice with the autosomal recessive severe combined immune deficiency (scid) mutation lack mature lymphocytes because of defective joining of T cell receptor and immunoglobulin (Ig) gene segments. Penetrance of this mutation is incomplete since 10-25% of SCID mice produce some T or B lymphocytes. This "leaky" phenotype could be due to a reversion of the mutation in some mice or to a constant, low frequency of functional lymphocytes generated in all SCID mice with variable survival of such cells. We report here that all SCID mice can be stimulated to produce functional B cells by the transfer of normal neonatal, but not adult, T cells. T cell-induced rescue of C.B-17scid B cells results in high levels of Ig expressing the Ighb allotype of the SCID recipient. These results show that all SCID mice generate some functional B cells, the majority of which do not survive in the absence of a subset of T cells present in high frequency in the neonate.
具有常染色体隐性严重联合免疫缺陷(scid)突变的小鼠由于T细胞受体和免疫球蛋白(Ig)基因片段连接缺陷而缺乏成熟淋巴细胞。该突变的外显率不完全,因为10%-25%的SCID小鼠会产生一些T或B淋巴细胞。这种“渗漏”表型可能是由于某些小鼠的突变回复,或者是由于所有SCID小鼠中持续产生的低频率功能性淋巴细胞以及此类细胞的不同存活率。我们在此报告,通过转移正常新生而非成年T细胞,所有SCID小鼠均可被刺激产生功能性B细胞。T细胞诱导的C.B-17scid B细胞挽救导致表达SCID受体Ighb同种异型的Ig水平升高。这些结果表明,所有SCID小鼠都会产生一些功能性B细胞,其中大多数在缺乏新生小鼠中高频存在的T细胞亚群时无法存活。