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核因子-κB RelA缺陷淋巴细胞：T细胞和B细胞正常发育，IgA和IgG1产生受损，增殖反应降低。

NF-kappa B RelA-deficient lymphocytes: normal development of T cells and B cells, impaired production of IgA and IgG1 and reduced proliferative responses.

作者信息

Doi T S, Takahashi T, Taguchi O, Azuma T, Obata Y

机构信息

Laboratory of Immunology, Aichi Cancer Center Research Institute, Nagoya, Japan.

出版信息

J Exp Med. 1997 Mar 3;185(5):953-61. doi: 10.1084/jem.185.5.953.

DOI:10.1084/jem.185.5.953
PMID:9120401
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2196168/
Abstract

To investigate the function of NF-kappa B RelA (p65), we generated mice deficient in this NF-kappa B family member by homologous recombination. Mice lacking RelA showed liver degeneration and died around embryonic day 14.5. To elucidate the role of RelA in lymphocyte development and function, we transplanted fetal liver cells of 13.5-day embryos from heterozygote matings into irradiated SCID mice. Within 4 weeks, both T and B cells had developed in the SCID mice receiving relA-/- fetal liver transplants, similar to the relA+/+ and +/- cases. T cells were found to mature to Thy-1+/TCR alpha beta +/CD3+/CD4+ or CD8+, while B cells had the ability to differentiate to IgM+/B220+ and to secrete immunoglobulins. However, the secretion of IgG1 and IgA was reduced in RelA-deficient B cells. Furthermore, both T and B cells lacking RelA showed marked reduction in proliferative responses to stimulation with Con A, anti-CD3, anti-CD3 + anti-CD28, LPS, anti-IgM, and PMA + calcium ionophore. The results indicate that RelA plays a critical role in production of specific Ig isotypes and also in signal transduction pathways for lymphocyte proliferation.

摘要

为了研究核因子-κB RelA（p65）的功能，我们通过同源重组构建了该核因子-κB家族成员缺失的小鼠。缺乏RelA的小鼠出现肝脏退化，并在胚胎第14.5天左右死亡。为了阐明RelA在淋巴细胞发育和功能中的作用，我们将杂合子交配产生的13.5天胚胎的胎肝细胞移植到经辐照的严重联合免疫缺陷（SCID）小鼠体内。在4周内，接受relA - / - 胎肝移植的SCID小鼠体内T细胞和B细胞均发育，这与relA + / + 和relA + / - 情况相似。发现T细胞成熟为Thy-1 + /TCRαβ + /CD3 + /CD4 + 或CD8 + ，而B细胞有能力分化为IgM + /B220 + 并分泌免疫球蛋白。然而，RelA缺陷的B细胞中IgG1和IgA的分泌减少。此外，缺乏RelA的T细胞和B细胞对刀豆蛋白A、抗CD3、抗CD3 + 抗CD28、脂多糖、抗IgM以及佛波酯 + 钙离子载体刺激的增殖反应均显著降低。结果表明，RelA在特异性Ig同种型的产生以及淋巴细胞增殖的信号转导途径中均起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a70c9f2e5379/JEM.doi7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a8982fbd3162/JEM.doi1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/f4e1d180d1ef/JEM.doi2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/0729e7a336e8/JEM.doi3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a3599c38f19c/JEM.doi4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/70bba66a18b0/JEM.doi5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/ed589f9c5574/JEM.doi6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a70c9f2e5379/JEM.doi7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a8982fbd3162/JEM.doi1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/f4e1d180d1ef/JEM.doi2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/0729e7a336e8/JEM.doi3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a3599c38f19c/JEM.doi4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/70bba66a18b0/JEM.doi5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/ed589f9c5574/JEM.doi6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/824e/2196168/a70c9f2e5379/JEM.doi7.jpg

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