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可溶性CD38可显著延长记忆B细胞反应的寿命。

Soluble CD38 significantly prolongs the lifespan of memory B-cell responses.

作者信息

Liu Xue Q, Hart Derek N J, MacPherson Gordon G, Good Michael F, Wykes Michelle N

机构信息

Queensland Institute of Medical Research, The Bancroft Centre, Brisbane, Qld, Australia.

出版信息

Immunology. 2008 Sep;125(1):14-20. doi: 10.1111/j.1365-2567.2008.02914.x.

DOI:10.1111/j.1365-2567.2008.02914.x
PMID:18798916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2526255/
Abstract

The development and maintenance of memory B cells (MBC) is dependent on germinal centres (GC) with follicular dendritic cell (FDC) networks. We have previously shown that FDC networks within GC of the spleen express a novel ligand for CD38 and that the administration of soluble CD38 induces an expansion of these cellular structures. We therefore used adoptive transfer studies to investigate whether the expansion of FDC networks with soluble CD38 affected the generation and maintenance of antigen-specific MBC. These studies found that the administration of soluble CD38 significantly extended the period after which MBC could be activated and that the frequencies of these cells also were increased. In conclusion, soluble CD38 appears to significantly extend the lifespan of antibody memory by increasing the numbers of MBC.

摘要

记忆B细胞(MBC)的发育和维持依赖于具有滤泡树突状细胞(FDC)网络的生发中心(GC)。我们之前已经表明,脾脏GC内的FDC网络表达一种新型的CD38配体,并且可溶性CD38的给药会诱导这些细胞结构的扩张。因此,我们采用过继转移研究来探究可溶性CD38介导的FDC网络扩张是否会影响抗原特异性MBC的产生和维持。这些研究发现,可溶性CD38的给药显著延长了MBC能够被激活的时间,并且这些细胞的频率也增加了。总之,可溶性CD38似乎通过增加MBC的数量显著延长了抗体记忆的寿命。

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Blood. 2008 Apr 1;111(7):3644-52. doi: 10.1182/blood-2007-08-107714. Epub 2008 Jan 25.
2
Cutting edge: anti-tumor necrosis factor therapy in rheumatoid arthritis inhibits memory B lymphocytes via effects on lymphoid germinal centers and follicular dendritic cell networks.前沿:类风湿关节炎中的抗肿瘤坏死因子疗法通过对淋巴生发中心和滤泡树突状细胞网络的作用抑制记忆B淋巴细胞。
J Immunol. 2008 Jan 15;180(2):688-92. doi: 10.4049/jimmunol.180.2.688.
3
CD38 cross-linking enhances TLR-induced B cell proliferation but decreases IgM plasma cell differentiation.CD38交联增强Toll样受体诱导的B细胞增殖,但降低IgM浆细胞分化。
Eur J Immunol. 2007 Feb;37(2):358-67. doi: 10.1002/eji.200636453.
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CD38 induces apoptosis of a murine pro-B leukemic cell line by a tyrosine kinase-dependent but ADP-ribosyl cyclase- and NAD glycohydrolase-independent mechanism.CD38通过酪氨酸激酶依赖性但不依赖于ADP-核糖基环化酶和NAD糖水解酶的机制诱导小鼠前B白血病细胞系凋亡。
Int Immunol. 2006 Jul;18(7):1029-42. doi: 10.1093/intimm/dxl037. Epub 2006 May 23.
5
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Curr Opin Immunol. 2006 Jun;18(3):265-70. doi: 10.1016/j.coi.2006.03.004. Epub 2006 Apr 17.
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