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首页> 外文期刊>Molecular and Cellular Biology >Redundancy in Tumor Necrosis Factor (TNF) and Lymphotoxin (LT) Signaling In Vivo: Mice with Inactivation of the Entire TNF/LT Locus versus Single-Knockout Mice
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Redundancy in Tumor Necrosis Factor (TNF) and Lymphotoxin (LT) Signaling In Vivo: Mice with Inactivation of the Entire TNF/LT Locus versus Single-Knockout Mice

机译：体内肿瘤坏死因子（TNF）和Lymphotoxin（LT）信号的冗余：灭活整个TNF / LT基因座小鼠与单基因敲除小鼠。

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摘要

Homologous genes and gene products often have redundant physiological functions. Members of the tumor necrosis factor (TNF) family of cytokines can signal activation, proliferation, differentiation, costimulation, inhibition, or cell death, depending on the type and status of the target cell. TNF, lymphotoxin α (LTα), and LTβ form a subfamily of a larger family of TNF-related ligands with their genes being linked within a compact 12-kb cluster inside the major histocompatibility complex locus. Singly TNF-, LTα-, and LTβ-deficient mice share several phenotypic features, suggesting that TNF/LT signaling pathways may regulate overlapping sets of target genes. In order to directly address the issue of redundancy of TNF/LT signaling, we used the Cre-loxP recombination system to create mice with a deletion of the entire TNF/LT locus. Mice with a triple LTβ/TNF/LTα deficiency essentially manifest a combination of LT and TNF single-knockout phenotypes, except for microarchitecture of the spleen, where the disorder of lymphoid cell positioning and functional T- and B-cell compartmentalization is severer than that found in TNF or LT single-knockout mice. Thus, our data support the notion that TNF and LT have largely nonredundant functions in vivo.
机译：同源基因和基因产物通常具有多余的生理功能。细胞因子的肿瘤坏死因子（TNF）家族的成员可以根据靶细胞的类型和状态发出信号激活，增殖，分化，协同刺激，抑制或细胞死亡。 TNF，淋巴毒素α（LTα）和LTβ形成更大的TNF相关配体家族的亚家族，它们的基因在主要组织相容性复合体位点内的紧凑12 kb簇内连接。仅有TNF-，LTα-和LTβ缺陷的小鼠具有一些表型特征，这表明TNF / LT信号传导途径可能调控靶基因的重叠集合。为了直接解决TNF / LT信号冗余的问题，我们使用Cre- loxP 重组系统来创建缺失整个TNF / LT基因座的小鼠。具有三重LTβ/ TNF /LTα缺乏症的小鼠基本上表现出LT和TNF单基因敲除表型的组合，但脾脏的微结构除外，后者的淋巴样细胞定位障碍和功能性T细胞和B细胞分隔性比脾脏更严重在TNF或LT单基因敲除小鼠中发现。因此，我们的数据支持了TNF和LT在体内具有大部分非冗余功能的观点。

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