??博士，研究员
?联系方式: shan.jiang1975@szu.edu.cn
?通讯地址：深圳大学办公楼313室, 518060

?教育背景:
2004，重庆医科大学，获内科学博士学位
1999，重庆医科大学临床医学二系，获医学学士学位

?工作经历:
2008.9-2014.2，杜克大学，免疫学系， 博士后
2006.2-2008.8，凯斯西储大学，肿瘤和血液病系，博士后
2004.9-2006.2，上海交通大学医学院免疫研究所，博士后

?研究兴趣:
从事CD4+T细胞分化调节机制的研究。主要关注microRNA对于CD4+T细胞活化及分化的调节，发现miR-17-92家族能够促进CD4+T细胞抗小鼠黑色素瘤的免疫应答，其中miR-19b，miR-17是促进细胞活化，减少细胞凋亡，支持IFN-r分泌，抑制iTreg细胞分化的重要调控因子 (Blood. 2011; 118(20):5487-5497.）。
在寻找miR-17-92作用靶基因的过程中，甲基化DNA结合蛋白MeCP2分子引起我们的注意。在此之前，MeCP2在CD4+T细胞中的功能未知。我们的工作发现MeCP2是促进Th1，Th17分化的重要调节分子，主要通过调节miR-124的表达影响SOCS5的蛋白质水平，最终调控STAT1/STAT3的磷酸化从而达到调节Th1、Th17分化的目的。同时我们还发现，在炎症情况下MeCP2是维持foxp3在nTreg中稳定表达的重要因子（Sci Signal. 2014 Mar 11;7 (316):ra25.）。
目前在以下三个方面开展研究工作:
1.基于CAR-T细胞过继性抗肿瘤免疫治疗的研究。
2.肿瘤环境中的microRNAs介导的T细胞功能抑制机制研究。
3.寻找调控记忆性T细胞形成的重要microRNAs。

?所获奖项:
2013，美国免疫学年会, Trainee Abstract Awards
2013，杜克大学, 五年优秀服务成就奖
2012，杜克大学, Bernard Amos Annual Poster Contest，一等奖
2005，重庆市, 科技进步二等奖(结核病治疗性疫苗的实验研究)

?发表论文:
1. Li C*, Jiang S*, Liu SQ, Lykken E, Zhao LT, Sevilla J, Zhu B, Li QJ.MeCP2 enforces Foxp3 expression to promote regulatory T cells' resilience to inflammation. Proc Natl Acad Sci U S A. 2014 Jun 23. pii: . [Epub ahead of print] (* co-first authorship)
3. Liu SQ, Jiang S, Li C, Zhang B, Li QJ. miR-17-92 cluster targets Phosphatase and Tensin Homology and Ikaros Family Zinc Finger 4 to promote TH17-mediated inflammation. J Biol Chem. 2014 Mar 18. [Epub ahead of print]
4. Jiang S*, Li C*, McRae G, Lykken E, Sevilla J, Liu SQ, Wan Y, Li QJ.MeCP2 Reinforces STAT3 Signaling and the Generation of Effector CD4+ T Cells by Promoting miR-124-Mediated Suppression of SOCS5.Sci Signal. 2014 Mar 11;7 (316):ra25.(* co-first authorship)
5. Guo Q, Zhang J, Li J, Zou L, Zhang J, Xie Z, Fu X, Jiang S, Chen G, Jia Q, Li F, Wan Y, Wu Y. Forced miR-146a expression causes autoimmune lymphoproliferative syndrome in mice via downregulation of Fas in germinal center B cells. Blood. 2013 Jun 13;121(24):4875-83.
6. Yang P, Li QJ, Feng Y, Zhang Y, Markowitz GJ, Ning S, Deng Y, Zhao J, Jiang S, Yuan Y, Wang HY, Cheng SQ, Xie D, Wang XF.TGF-β-miR-34a-CCL22 signaling-induced Treg cell recruitment promotes venous metastases of HBV-positive hepatocellular carcinoma. Cancer Cell. 2012 Sep 11;22(3):291-303.
7. Shan Jiang*, Chaoran Li*, Virginie Olive, Erik Lykken, Feng Feng, Jose Sevilla, Lin He, Qi-Jing Li. Molecular dissection of the miR-17-92 cluster’s critical dual roles in promoting Th1 responses and preventing inducible Treg Differentiation. Blood. 2011 Nov 17;118(20):5487-97. (* co-first authorship)
8. Weiwen Fan, Zhe Tang, Lihong Yin, Bei Morrison, Said Hafez-Khayyata, Pingfu Fu Honglian Huang, Rakesh Bagai, Shan Jiang, Adam Kresak, Scott Howell, Amit Vasanji,Chris A. Flask, Balazs Halmos, Henry Koon, and Patrick C. Ma. MET-Independent Lung Cancer Cells Evading EGFR Kinase Inhibitors Are Therapeutically Susceptible to BH3 Mimetic Agents. Cancer Res. 2011 Jul 1;71(13):4494-505.
9. Ebert PJ, Jiang Shan, Xie J, Li QJ, Davis MM. An endogenous positively selecting peptide enhances mature T cells responses and becomes an antoantigen in the absebce of microRNA mir-181a. Nat Immunol. 2009 Nov; 10(11):1162-9.
10. Tang Z, Jiang S, Du R, Dietrich S, El Telbany AS, Chan PS, Petri ET, Boggon TJ, Halmos B, Kern JA. and Ma PC. Disruption of a conserved ion pair in EGFR differentially alters kinase inhibitor sensitivity. Oncogene. 2009 Jan 29; 28(40:518-33.
11. Tang Z, Du R, Jiang S, Wu C, Barkauskas DS, Richey J, Molter J, Lam M, Flask C, Gerson S, Dowlati A, Liu L, Lee Z, Halmos B, Wang Y, Kern JA, Ma PC. Dual MET-EGFR combinatorial inhibition against T790M-EGFR mediated erlotinib-resistant lung cancer. Br J Cancer. 2008 Sep 16; 99(6):911-22.
12. Tang Z, Jiang S, Du R and Ma PC. Mutational analysis of the lung cancer genome in novel therapy – era of high throughput sequencing. Book chapter, Tumorigenesis Research Focus.Editor, F. Columbus. Publisher, Nova Publishing, 2008.
13. Zhu DY, Jiang S, Luo XD. Therapeutic effects of Ag85B and MPT64 DNA vaccines in a murine model of Mycobacterium tuberculosis infection. Vaccine, 2005.23(37): 4619-4624.