Ex vivo enzymatic treatment of aged CD4 T cells restores antigen-driven CD69 expression and proliferation in mice.
Ex vivo enzymatic treatment of aged CD4 T cells restores antigen-driven CD69 expression and proliferation in mice.
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DOI：
10.1016/j.imbio.2010.03.003
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发表时间：
2011-01
期刊：
影响因子：
2.8
通讯作者：
Miller, Richard A.
中科院分区：
文献类型：
--
作者：
Garcia, Gonzalo G.;Miller, Richard A.
免疫功能的下降与幼稚CD 4 T细胞功能的下降有关。在TCR特异性转基因AND小鼠中对幼稚CD 4 T细胞的体外研究显示，免疫突触形成、活化、增殖和细胞因子产生存在年龄相关的缺陷。先前的工作也记录了与TCR信号传导有关的表面蛋白糖基化的年龄相关的改变，并表明酶处理去除特定的表面糖蛋白可以恢复老年小鼠CD 4细胞的体外功能。在这里，过继转移系统显示，来自老年小鼠的大部分幼稚CD 4 T细胞不能表达CD 69并在抗原致敏小鼠中扩增，但这些CD 69和扩增的下降可以通过用细菌酶O-唾液酸糖蛋白内肽酶（OSGE）离体预处理T细胞来恢复。OSGE治疗还修复了体内活化后CD 69表达的年龄依赖性损失。
Declines in immune function have been associated with declines in the function of naïve CD4 T cells. In vitro studies of naïve CD4 T cells in TCR-specific transgenic AND mice have shown age-related defects in immunosynapse formation, activation, proliferation and cytokine production. Previous work has also documented age-related alteration in the glycosylation of surface proteins involved in TCR signaling, and shown that enzymatic treatments to remove specific surface glycoproteins can restore in vitro function in CD4 cells from aged mice. Here an adoptive transfer system shows that a large percentage of naïve CD4 T cells from old mice fail to express CD69 and expand in antigen primed mice, but these declines in CD69 and expansion can be restored by ex-vivo pretreatment of the T cells with the bacterial enzyme O-sialoglycoprotein endopeptidase (OSGE). OSGE treatment also repairs the age-dependent loss of CD69 expression after in vivo activation.
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影响因子：
15.3
作者：
Haynes, L;Eaton, SM;Burns, EM;Randall, TD;Swain, SL
通讯作者：
Swain, SL
影响因子：
4.3
作者：
Garcia, GG;Miller, RA
通讯作者：
Miller, RA
影响因子：
6.4
作者：
Berger, Scott B.;Akha, Amir A. Sadighi;Garcia, Gonzalo G.
通讯作者：
Garcia, Gonzalo G.
DOI：
10.1084/jem.184.5.1891
发表时间：
1996-11-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Linton PJ;Haynes L;Klinman NR;Swain SL
通讯作者：
Swain SL
影响因子：
4.4
作者：
Garcia, GG;Miller, RA
通讯作者：
Miller, RA