毛開睿

毛開睿

毛開睿,男,博士廈門大學生命科學學院教授、博士生導師。

基本介紹

  • 中文名:毛開睿
  • 畢業院校:中科院上海生命科學研究院生化細胞所
  • 學位/學歷:博士
  • 職業:教師
  • 專業方向:腸道菌群和免疫系統之間的相互作用
  • 任職院校:廈門大學
個人經歷,研究領域,學術成果,

個人經歷

2004年,山東師範大學生物技術專業,獲理學學士學位;
2011年,中科院上海生命科學研究院生化細胞所,獲理學博士學位;
2011-2013年,中科院上海生命科學研究院生化細胞所,研究助理;
2013-2019年,美國國立衛生研究院(NIH)過敏和感染性疾病研究所(NIAID),訪問學者;
2019年起,廈門大學生命科學學院“閩江學者”特聘教授,黏膜免疫課題組組長。
2004, B.Sc., Shandong Normal University;
2011, Ph.D., Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences;
2011-2013, Research Assistant, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences;
2013-2019, Visiting Fellow, National Institute of Allergy and Infectious Diseases, National Institutes of Health;
2019-, Principal Investigator of Mucosal Immunology Group, School of Life Sciences, Xiamen University.

研究領域

本課題組主要研究腸道菌群免疫系統之間的相互作用。腸道菌群在調節個體發育、生理反應以及疾病發生和治療中發揮了極其重要的作用。我們利用先進的成像系統和傳統免疫學手段研究在生理穩態和疾病發生過程中腸道菌群對免疫系統的激活作用,以及該相互作用對於腸道菌群的發育、上皮幹細胞分化、脂肪代謝和免疫炎症反應等生理功能的影響,以期為建立並維持腸道穩態和治療腸道疾病尋求新的靶點。
The mammalian gut is colonized with trillions of micro-organisms termed the “microbiota”, which not only help their host with nutrient absorption, but also are intimately involved in various aspects of host physiology and pathology, including nervous system development, immune function and diseases, as well as tumorigenesis and the response to cancer therapy. Given the complexity and diversity of the microbiota, mammalian hosts have evolved a complex immune system that continuously interact with microbiota to maintain the physiological stability and local tissue homeostasis. We will combine traditional immune measurement such as flow cytometry with modern genomic technologies and especially highly multiplexes, quantitative immunohistochemistry to advance our understanding of the interaction between gut microbiota and host immune system and to discover new targets for establishment of gut homeostasis and treatment of bowel diseases.

學術成果

代表性論文(Selected Publications, # co-first author, * corresponding author)
1. Huang, Y.*, Mao, K.*, and Germain, R. N. (2018) Thinking differently about ILCs-Not just tissue resident and not just the same as CD4(+) T-cell effectors.Immunol Rev
2. Mao, K.*, Baptista, A. P., Tamoutounour, S., Zhuang, L., Bouladoux, N., Martins, A. J., Huang, Y., Gerner, M. Y., Belkaid, Y., and Germain, R. N.* (2018) Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism.Nature
3. Huang, Y.*, Mao, K., Chen, X., Sun, M. A., Kawabe, T., Li, W., Usher, N., Zhu, J., Urban, J. F., Jr., Paul, W. E., and Germain, R. N.* (2018) S1P-dependent interorgan trafficking of group 2 innate lymphoid cells supports host defense.Science
4. Mao, K., Chen, S., Chen, M., Ma, Y., Wang, Y., Huang, B., He, Z., Zeng, Y., Hu, Y., Sun, S., Li, J., Wu, X., Wang, X., Strober, W., Chen, C.*, Meng, G.*, and Sun, B*. (2013) Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS-induced septic shock.Cell Res
5. Mao, K., Chen, S., Wang, Y., Zeng, Y., Ma, Y., Hu, Y., Zhang, H., Sun, S., Wu, X., Meng, G., Pei, G.*, and Sun, B*. (2015) beta-arrestin1 is critical for the full activation of NLRP3 and NLRC4 inflammasomes.J Immunol
6. Zhong, C., Cui, K., Wilhelm, C., Hu, G., Mao, K., Belkaid, Y., Zhao, K., and Zhu, J*. (2016) Group 3 innate lymphoid cells continuously require the transcription factor GATA-3 after commitment.Nat Immunol
7. Wang, Y., Yang, C., Mao, K., Chen, S., Meng, G.*, and Sun, B*. (2013) Cellular localization of NLRP3 inflammasome.Protein Cell
8. Hu, Y., Mao, K., Zeng, Y., Chen, S., Tao, Z., Yang, C., Sun, S., Wu, X., Meng, G., and Sun, B*. (2010) Tripartite-motif protein 30 negatively regulates NLRP3 inflammasome activation by modulating reactive oxygen species production.J Immunol
9. Wang, Y., Mao, K., Sun, S., Lin, G., Wu, X., Yao, G., and Sun, B*. (2009) Trichosanthin functions as Th2-type adjuvant in induction of allergic airway inflammation.Cell Res
10. Shi, M., Deng, W., Bi, E., Mao, K., Ji, Y., Lin, G., Wu, X., Tao, Z., Li, Z., Cai, X., Sun, S., Xiang, C.*, and Sun, B*. (2008) TRIM30 alpha negatively regulates TLR-mediated NF-kappa B activation by targeting TAB2 and TAB3 for degradation.Nat Immunol

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