2004年，山东师范大学生物技术专业，学士学位；
2011年，中科院上海生命科学研究院生化细胞所细胞生物学专业，博士学位；
2011-2013年，中科院上海生命科学研究院生化细胞所，研究助理；
2013-2019年，美国国立卫生研究院（NIH）过敏和感染性疾病研究所（NIAID），访问学者；
2019年起，beat365正版唯一官网“闽江学者”特聘教授，黏膜免疫课题组组长。
B.S., 2004, Shandong Normal University, Biotechnology;
Ph.D., 2011, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Cell Biology;
Research Assistant, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, 2011-2013;
Visiting Fellow, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 2013-2019;
Principal Investigator of Mucosal Immunology Group, School of Life Sciences, Xiamen University, 2019 to Present.

本课题组主要研究肠道菌群和免疫系统之间的相互作用。肠道菌群在调节个体发育、生理反应以及疾病发生和治疗中发挥了极其重要的作用。我们利用先进的成像系统和传统免疫学手段研究在生理稳态和疾病发生过程中肠道菌群对免疫系统的激活作用，以及该相互作用对于肠道菌群的发育、上皮干细胞分化、脂肪代谢和免疫炎症反应等生理功能的影响，以期为建立并维持肠道稳态和治疗肠道疾病寻求新的靶点。
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.

代表性论文(^# 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 286, 160-171
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 554, 255-259
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 359, 114-119
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 23, 201-212
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 194, 1867-1873
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 17, 169-178
7. Wang, Y., Yang, C., Mao, K., Chen, S., Meng, G.^*, and Sun, B^*. (2013) Cellular localization of NLRP3 inflammasome. Protein Cell 4, 425-431
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 185, 7699-7705
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 19, 962-972
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 9, 369-377

荣誉、奖励及参加学术团体的情况: