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白细胞介素(IL)-7基因缺失小鼠中的淋巴细胞减少表明IL-7是一种不可或缺的细胞因子。

Lymphopenia in interleukin (IL)-7 gene-deleted mice identifies IL-7 as a nonredundant cytokine.

作者信息

von Freeden-Jeffry U, Vieira P, Lucian L A, McNeil T, Burdach S E, Murray R

机构信息

Department of Immunology, DNAX Research Institute of Cellular and Molecular Biology, Palo Alto, California 94304, USA.

出版信息

J Exp Med. 1995 Apr 1;181(4):1519-26. doi: 10.1084/jem.181.4.1519.

DOI:10.1084/jem.181.4.1519
PMID:7699333
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2191954/
Abstract

Interleukin (IL)-7 is a potent stimulus for immature T and B cells and, to a lesser extent, mature T cells. We have inactivated the IL-7 gene in the mouse germline by using gene-targeting techniques to further understand the biology of IL-7. Mutant mice were highly lymphopenic in the peripheral blood and lymphoid organs. Bone marrow B lymphopoiesis was blocked at the transition from pro-B to pre-B cells. Thymic cellularity was reduced 20-fold, but retained normal distribution of CD4 and CD8. Splenic T cellularity was reduced 10-fold. Splenic B cells, also reduced in number, showed an abnormal population of immature B cells in adult animals. The remaining splenic populations of lymphocytes showed normal responsiveness to mitogenic stimuli. These data show that proper T and B cell development is dependent on IL-7. The IL-7-deficient mice are the first example of single cytokine-deficient mice that exhibit severe lymphoid abnormalities.

摘要

白细胞介素(IL)-7 是未成熟 T 细胞和 B 细胞的强效刺激因子,对成熟 T 细胞的刺激作用相对较弱。我们通过基因靶向技术使小鼠种系中的 IL-7 基因失活,以进一步了解 IL-7 的生物学特性。突变小鼠的外周血和淋巴器官中淋巴细胞严重减少。骨髓 B 淋巴细胞生成在从 pro-B 细胞向 pre-B 细胞转变阶段受阻。胸腺细胞数量减少了 20 倍,但 CD4 和 CD8 的分布仍正常。脾脏 T 细胞数量减少了 10 倍。脾脏 B 细胞数量也减少,在成年动物中显示出未成熟 B 细胞的异常群体。脾脏中剩余的淋巴细胞群体对促有丝分裂刺激表现出正常反应。这些数据表明,T 细胞和 B 细胞的正常发育依赖于 IL-7。IL-7 缺陷小鼠是表现出严重淋巴异常的单细胞因子缺陷小鼠的首个实例。

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本文引用的文献

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Interleukin-2 receptor gamma chain mutation results in X-linked severe combined immunodeficiency in humans.白细胞介素-2受体γ链突变导致人类X连锁重症联合免疫缺陷。
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