adaptor protein shc acts as an immune-regulator for the lps-stimulated maturation of bone marrow-derived dendritic cells人体自燃现象适配器蛋白质作为immune-regulator lps-stimulated成熟的骨骨髓来源树突状细胞.pdfVIP

下载本文档

5
0
约5.71万字
约 12页
2017-09-11 发布于上海
举报
版权申诉

adaptor protein shc acts as an immune-regulator for the lps-stimulated maturation of bone marrow-derived dendritic cells人体自燃现象适配器蛋白质作为immune-regulator lps-stimulated成熟的骨骨髓来源树突状细胞.pdf

1、本文档共12页，可阅读全部内容。
2、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。
3、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
4、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
5、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
6、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
7、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
8、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

adaptor protein shc acts as an immune-regulator for the lps-stimulated maturation of bone marrow-derived dendritic cells人体自燃现象适配器蛋白质作为immune-regulator lps-stimulated成熟的骨骨髓来源树突状细胞

Chen et al. BMC Immunology 2011, 12:32 /1471-2172/12/32 RESEARCH ARTICLE Open Access Adaptor protein Shc acts as an immune-regulator for the LPS-stimulated maturation of bone marrow-derived dendritic cells 1 1,2 1,3 1 1,4 1 Kuang-Den Chen , Li-Wen Hsu , Shigeru Goto , Chin-Wei Yeh , Toshiaki Nakano , Chia-Yun Lai , 1 1 1 5 6 1 Yen-Chen Chang , Chiung-Hui Hou , Chih-Chi Wang , Yu-Fan Cheng , King-Wah Chiu , Chih-Che Lin and Chao-Long Chen1* Abstract Background: The Shc isoforms is known to mediate immune responses and has been indicated as a negative regulator of autoimmunity and lymphocyte activation. We aimed to evaluate the immune-regulatory role of Shc in rat bone marrow-derived DCs in the maturation process triggered by LPS. Results: We found that, in response to LPS, expression of Shc proteins was induced and that neutralization of Shc inhibited the LPS-induced transient phosphorylation of p52Shc on pTyr239/240 in DCs of Lewis (LEW; RT1l) rats. Moreover, the significantly enhanced expression of IL-10 and the surface level of costimulatory molecule CD80, as well as suppressed expression of IL-6 and IL-12 in the Shc-silenced DCs were also observed. Similar IB phosphorylation occurred in Shc-silenced DCs primed by LPS, indicating Shc is not associated with NF-B pathway. We further demonstrate that Shc blockade on LPS-treated DCs results in significant increase of the overall STAT3 phosphorylation and the relative levels of phospho-STAT3 in the nuclear fraction. STAT3 activation by LPS with or without Shc blockade was totally abolished by SU6656