个人简介

M.D., Medicine, Tsingtao University School of Medicine, Qingdao, China, 1983 Ph.D., Biomedical Sciences, University of California, San Francisco, CA, 1997 Jian-Dong Li, professor and director of the Center for Inflammation, Immunity and Infection, specializes in research on inflammation, innate immunity and respiratory infections. His current research focuses on inducible negative feedback regulation of inflammation, which provides novel insights into the tight regulation of inflammation and may lead to the identification of novel therapeutic targets. He is also studying the regulation of host survival in Streptococcus pneumoniae and influenza infections and developing novel therapeutic agents for inflammatory and infectious diseases. Li earned his M.D. from Tsingtao University School of Medicine in China and his Ph.D. in Biomedical Sciences from the University of California.

研究领域

Inflammation is a hallmark of many serious human inflammatory diseases, including infectious diseases, chronic obstructive pulmonary diseases, otitis media, asthma, arthritis, inflammatory bowel disease, atherosclerosis and cancer. We primarily focus on understanding the molecular basis of inflammatory diseases and further developing novel anti-inflammatory therapeutic agents.

Appropriate inflammation is a protective host defense response to remove the injurious stimuli as well as initiate tissue healing and repair process. However, overactive inflammation is detrimental to the host, leading to inflammatory diseases. Thus, inflammation must be tightly regulated. In contrast to the positive regulation, inducible negative feedback regulation plays an important role in preventing overactive inflammation. Understanding the molecular mechanisms underlying tight regulation of inflammation will lead to development of novel anti-inflammatory strategies. Moreover, because inflammation is a complex biological response of the body to harmful stimuli, interdisciplinary collaborative efforts would be critical for fully understanding the molecular pathogenesis and thus accelerating the successful development of novel therapeutics.

近期论文

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Komatsu K, Lee JY, Miyata M, Hyang Lim J, Jono H, Koga T, Xu H, Yan C, Kai H, Li JD. Inhibition of PDE4B suppresses inflammation by increasing expression of the deubiquitinase CYLD. Nature Communications. 9;4:1684. doi: 10.1038/ncomms2674, 2013 Lim JH, Jono H, Komatsu K, Woo CH, Lee J, Huang Y, Zhang W, Park SH, Kim YI, Choi YD, Shen H, Heo KS, Xu H, Bourne P, Koga T, Xu H, Yan C, Chen LF, Feng XH, Li JD. CYLD negatively regulates Transforming Growth Factor-b signaling via deubiquitinating Akt. Nature Communications. 3:771. doi: 10.1038/ncomms1776, 2012. Xu, X, Woo CH, Steere RR, Lee BC, Huang YX, Wu J, Pang J, Lim JH, Xu H, Zhang W, Konduru AS, Yan C, Cheeseman MT, Brown SD, Li JD. EVI1 acts as an inducible negative feedback regulator of NF-kB by inhibiting p65 acetylation. J. Immunol. 188:6371-80, 2012 Lee J, Komatsu K, Lee BC, Lim JH, Jono H, Xu H, Kai H, Zhang ZJ, Yan C, Li JD. Phosphodiesterase 4B mediates extracellular signal-regulated kinase-dependent up-regulation of mucin MUC5AC protein by Streptococcus pneumoniae by inhibiting cAMP-protein kinase A-dependent MKP-1 phosphatase pathway. J Biol Chem. 287:22799-811, 2012 Jeon KI, Xu X, Aizawa T, Lim JH, Jono H, Kwon DS, Abe JI, Berk BC, Li JD*, Yan C*. Vinpocetine inhibits NF-kappa B-dependent inflammation via an IKK-dependent but PDE-independent mechanism. Proc Natl Acad Sci U S A. 107:9795-800, 2010. *Corresponding authors. Ishinaga H, Jono H, Lim JH, Komatsu K, Xu X, Lee J, Woo CH, Xu H, Feng XH, Chen LF, Yan C, Li JD. Synergistic induction of NF-kB by TGF-b and TNF-a is mediated by PKA-dependent RelA acetylation. Biochem J. 417:583-91, 2009 Ha UH, Lim JH, Kim HJ, Wu W, Jin S, Xu H, Li JD. MKP1 regulates the induction of MUC5AC Mucin by S. pneumoniae Pneumolysin by inhibiting the PAK4-JNK signaling pathway. J Biol Chem. 83:30624-31, 2008. Lim JH, Ha UH, Woo CH, Xu H, Li JD. CYLD is a crucial negative regulator of innate immune response in Escherichia coli pneumonia. Cell Microbiol. 10:2247-56, 2008. Koga T, Lim JH, Jono H, Ha UH, Xu H, Ishinaga H, Morino S, Xu X, Yan C, Kai H, Li JD. Tumor suppressor cylindromatosis acts as a negative regulator for Streptococcus pneumoniae-induced NFAT signaling. J Biol Chem. 283:12546-54, 2008. Lim JH, Jono H, Koga T, Woo CH, Ishinaga H, Bourne P, Xu H, Ha UH, Xu H, Li JD. Tumor Suppressor CYLD Acts as a Negative Regulator for Nontypeable Haemophilus influenza-Induced Inflammation in the Middle Ear and Lung of Mice. PLoS ONE, 2(10):e1032, 2007. Lim JH, Stirling B, Derry J, Koga T, Jono H, Woo CH, Xu H, Ha UH, Andalibi A, Feng XH, Briles DE, Zhu, H., Huang, Y, Zhang, W, Weng, X, Yin, Z, Davis RJ, Flavell RA, Li JD. Tumor Suppressor CYLD Acts as a Crucial Regulator of Acute Lung Injury in Lethal Streptococcus pneumoniae Infections. Immunity, 27(2):349-60, 2007. Ishinaga, H, Jono H, Lim JH, Kweon SM, Xu H, Ha UH, Xu H, Koga T, Yan C, Feng XH, Chen LF, & Li J.D. TGF-b Induces p65 Acetylation to Enhance Bacteria-induced NF-kB Activation. EMBO J, 26, 150-1162, 2007. Ha,U.H., Lim, J.H., Jono, H., Srivastava, A., Malley, R., Pagès, G., Jacques Pouysségur, P. & Li J.D. A Novel Role for IKKa and IKKb in ERK-dependent Innate Mucosal Defense Response against Streptococcus pneumoniae. J. Immunol. 178, 1736-1747, 2007. Mikami F, Lim JH, Ishinaga H, Ha UH, Gu H, Koga T, Jono H, Kai H, Li JD. Li JD. TGF-b-Smad3/4 Signaling Pathway Acts as a Positive Regulator for TLR2 Induction by Bacteria via a Dual-mechanism Involving Functional Cooperation with NF-kB and MAPK Phosphatase 1-dependent Negative Cross-talk with p38 MAPK. J. Biol. Chem. 281, 22397-22408. 2006. Yoshida, H, Jono, H, Kai, H, Li JD. The tumor suppressor CYLD acts as a negative regulator for toll-like receptor 2 signaling via negative cross-talk with TRAF6 and TRAF7. .J Biol Chem. 280:41111-41121, 2005. Mikami, F, Gu, H, Jono, H, Andalibi, A, Kai, H, Li JD. Epidermal growth factor receptor acts as a negative regulator for bacterium nontypeable Haemophilus influenzae-induced Toll-like receptor 2 expression via an Src-dependent p38 mitogen-activated protein kinase signaling pathway. J Biol Chem. 280:36185-94, 2005 Watanabe, T., Jono, H., Han, J., Lim, D.J. and Li, J.D. Synergistic Activation of NF-kB by Nontypeable Haemophilus influenzae and Tumor Necrosis Factor-a. Proc. Natl. Acad. Sci. USA, 101:3563-8, 2004. Jono, H, Lim, JH, Chen, L.F. Xu, H, Trompouki, E., Pan, ZK, Mosialos, G, Li, J.D. NF-kB Is Essential for Induction of CYLD, the Negative Regulator of NF-kB. J. Biol. Chem. (Accelerated Publication) 279, 36171-36174, 2004. Jono, H., Xu, H., Kai, H., Lim, D.J., Kim, Y.S., Feng, X.H. and Li, J.D. TGF-b-Smad Signaling Pathway Negatively Regulates Nontypeable Haemophilus influenzae-induced MUC5AC Mucin Transcription via MAPK Phosphatase-1-dependent Inhibition of p38 MAPK. J. Biol. Chem. 278, 27811-27819, 2003. Imasato, A., Desbois-Mouthon, C., Han, J., Kai, H., Cato, A.C., Akira, S., Li, J.D. Inhibition of p38 MAPK by glucocorticoids via induction of MAP kinase phosphatase-1 enhances nontypeable Haemophilus influenzae-induced expression of toll-like receptor 2. J. Biol. Chem. 277:47444-47450, 2002. Jono, H., Shuto, T., Xu, H., Kai, H., Lim, D.J., Gum, J.R., Kim, Y.S., Yamaoka, S, Feng, X.H. and Li, J.D. Transforming Growth Factor-b-Smad Signaling Pathway Cooperates with NF-kB to Mediate Nontypeable Haemophilus influenzae-induced MUC2 Mucin Transcription. J. Biol. Chem. 277:45547-45557, 2002. Shuto, T., Imasato, I., Jono, H., Xu, H., Watanabe, T., Kai, H., Andalibi, A., Linthicum, F., Guan, Y.L., Han, J., Cato, A.C., Akira, S., Lim, D.J. and Li, J.D. Glucocorticoids synergistically enhance Nontypeable Haemophilus influenzae-induced Toll-like receptor 2 expression via a negative cross-talk with p38 MAP kinase. J. Biol. Chem. 277:17263-17270, 2002. Wang, B., Lim, D.J., Han, J., Kim, Y.S., Basbaum, C.B. and Li, J.D. Novel Cytoplasmic Proteins of Nontypeable Haemophilus influenzae Up-regulate Human MUC5AC Mucin Transcription via a Positive p38 MAP Kinase Pathway and a Negative PI 3-Kinase-Akt Pathway. J. Biol. Chem. 277:949-957, 2002. Shuto, T., Xu H., Wang, B, Han, J., Kai, H., Gu, X.X., Murphy, T., Lim, D.J. and Li, J.D. Activation of NF-kB by Nontypeable Haemophilus influenzae is mediated by Toll-like Receptor-2-TAK1-dependent NIK-IKKa/b-IkBa and MKK3/6-p38 MAP kinase signaling pathways. Proc. Natl. Acad. Sci. USA, 98:8774-8779, 2001.