T-cell survival regulator LKLF is not involved in inappropriate apoptosis of diabetes-prone BBDP rat T cells
T-cell survival regulator LKLF is not involved in inappropriate apoptosis of diabetes-prone BBDP rat T cells
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DOI：
10.1196/annals.1299.101
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发表时间：
2003-01-01
期刊：
影响因子：
--
通讯作者：
Haag, F
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文献类型：
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作者：
Diessenbacher, P;Bartels, K;Haag, F
糖尿病易感BB （dpBB）大鼠发生自身免疫性胰岛素依赖型糖尿病（IDDM）的频率很高，这是T细胞发育缺陷的结果，该缺陷是由大鼠4号染色体（lyp）上的单个基因位点突变引起的，该突变最近被鉴定为免疫相关核苷酸4 （ian4）。最近在小鼠中描述了一种类似dpBB大鼠淋巴细胞减少症的表型，这是免疫系统中转录因子LKLF（肺kkrupel样因子，KLF2）基因靶向失活的结果。我们克隆了大鼠的LKLF基因，并筛选了一组大鼠/仓鼠辐射杂交细胞系，以确定其染色体定位。我们得出结论，LKLF基因在dpBB大鼠中没有缺陷，其表达不受lyp突变的影响。
Diabetes-prone BB (dpBB) rats develop autoimmune insulin-dependent diabetes mellitus (IDDM) at high frequency as a consequence of a defect in T cell development, caused by a mutation in a single gene locus on rat chromosome 4 (lyp) which has recently been identified as immune-associated nucleotide 4 (ian4). A phenotype similar to dpBB rat lymphopenia has recently been described in the mouse as the result of the targeted inactivation of the gene for the transcription factor LKLF (Lung Kruppel-like factor, KLF2) in the immune system. We cloned the LKLF gene of the rat and screened a panel of rat/hamster radiation hybrid cell lines to determine its chromosomal localization. We conclude that the LKLF gene is not defective-in dpBB rats and that its expression is not compromised by the lyp mutation.