Immunological function in mice lacking the Rac-related GTPase RhoG
Immunological function in mice lacking the Rac-related GTPase RhoG
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DOI：
10.1128/mcb.24.2.719-729.2004
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发表时间：
2004-01-01
影响因子：
5.3
通讯作者：
Turner, M
中科院分区：
文献类型：
--
作者：
Vigorito, E;Bell, S;Turner, M
RhoG是一种在淋巴细胞中高度表达的低分子量GTP酶，其在体外激活基因转录并促进细胞骨架重组。为了研究RhoG的体内功能，我们产生了RhoG基因靶向破坏的纯合小鼠。尽管没有RhoG，但B和T淋巴细胞的发育不受影响。然而，血清免疫球蛋白G1（IgG 1）和IgG 2b水平增加，以及对胸腺依赖性抗原的体液免疫应答轻度增加。此外，响应于抗原受体交联的B-和T-细胞增殖略有增加。虽然RhoG缺陷产生一个温和的表型，我们的实验表明，RhoG可能有助于免疫反应的负调节。缺乏强表型可能表明RhoG与淋巴细胞中的其他Rac蛋白的功能冗余。
RhoG is a low-molecular-weight GTPase highly expressed in lymphocytes that activates gene transcription and promotes cytoskeletal reorganization in vitro. To study the in vivo function of RhoG, we generated mice homozygous for a targeted disruption of the RhoG gene. Despite the absence of RhoG, the development of B and T lymphocytes was unaffected. However, there was an increase in the level of serum immunoglobulin G1 (IgG1) and IgG2b as well as a mild increase of the humoral immune response to thymus-dependent antigens. In addition, B- and T-cell proliferation in response to antigen receptor cross-linking was slightly increased. Although RhoG deficiency produces a mild phenotype, our experiments suggest that RhoG may contribute to the negative regulation of immune responses. The lack of a strong phenotype could indicate a functional redundancy of RhoG with other Rac proteins in lymphocytes.