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Baidong Hou, Ph.D, Prof.
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Principal Investigator
Chinese Academy of Sciences Key Laboratory of Infection and Immunity,IBP
Research Interests: Anti-viral antibody response; Antibody response in autoimmunity; Regulation of B cell differentiation; Novel vaccine and immune therapy
Email: baidong_hou@ibp.ac.cn
Tel: 010-64884501
Address: 15 Datun Road, Chaoyang District, Beijing, 100101, China
Chinese personal homepage
- Biography
1989 - 1994 B.S., Beijing Medical University, Beijing, China
1994 - 1997 Medical Resident, Peking Union Medical College Hospital, Beijing, China
1997 - 2001 M.D., Peking Union Medical College, Beijing, China
2001 - 2003 Postdoctoral fellow, Vanderbilt University, Nashville, TN, USA
2003 - 2009 Postdoctoral fellow, University of California, San Francisco, CA, USA
2009 - 2011 Associate specialist, University of California, San Francisco, CA, USA
2011 - Professor, Institute of Biophysics, Chinese Academy of Science, Beijing, China
- Awards
- Membership in Academies & Societies
- Research Interests
1. Anti-viral antibody response
2. Antibody response in autoimmunity
3. Regulation of B cell differentiation
4. Novel vaccine and immune therapy
Antibody is the most important effector molecules of the immune system, which plays critical role in host defense against infection, and is the most commonly used tool in immune therapy. Our research team are focusing on the mechanism by which antibody is generated in viral infection and autoimmune diseases. Our goal is to use the knowledge learnt in the basic research to develop novel vaccines and strategy for immune therapy.
1. The antibody response in viral infection varies from person to person. In clinic, it has been observed that some individual infected by HIV or HCV can develop broadly-neutralizing antibody against these viruses. The mechanism underlying this phenomenon is currently unknown. To facilitate investigation of antibody response in viral infection, we developed a novel model antigen system based on virus-like particle. Examination of the antibody response elicited by this antigen shall shed light on the mechanisms by which antibody response is regulated in viral infection.
2. Immune cells that recognize self-antigen are present even in healthy individual. Under normal circumstance, these cells do not mount overt immune response to self-antigens. However, under circumstance when immune tolerance is broken due to genetic or environmental alterations, they could be inappropriately activated and cause autoimmune diseases. One of our goals is to understand how auto-antibodies are generated in autoimmune diseases.
3. Upon antigen stimulation, responsive B cells can differentiate towards several different cell “fates”, each with distinct functional importance. Previously, the study of B cell differentiation was severely hampered by lack of in vitro culture system. Our lab recently developed novel method to enrich antigen-specific B cells, which would facilitate the dissection of the mechanism by which B cell differentiation is regulated.
4. Novel vaccine and immune therapy: vaccine and immune therapy are promising solutions to the challenge posed by infectious diseases and malignant tumors. Our lab has developed a novel vaccine technology using virus-like particle as platform, and method to obtain high-affinity antibody using single-cell antibody cloning technique. These techniques are currently being employed for developing novel universal vaccine and bnAb for flu.
- Grants
- Selected Publications
1. Guo C, Peng Y, Lin L, Pan X, Fang M, Zhao Y, Bao K, Li R, Han J, Chen J, Song TZ, Feng XL, Zhou Y, Zhao G, Zhang L, Zheng Y, Zhu P, Hang H, Zhang L, Hua Z*, Deng H*, Hou B*. A pathogen-like antigen-based vaccine confers immune protection against SARS-CoV-2 in non-human primates. Cell Rep Med. 2021 Nov 16;2(11):100448. doi: 10.1016/j.xcrm.2021.100448. Epub 2021 Oct 23. PMID: 34723223; PMCID: PMC8536523.
2. Lin X, Twelkmeyer T, Zhu D, Zhang L, Zhao Y, Zhang C, Iwakura Y, Meng G, Hua Z, Yan B, Liu WJ, Luo Z, Gong S, Chen H, Li S*, Hou B*, Tang H*. Homeostatic regulation of T follicular helper and antibody response to particle antigens by IL-1Ra of medullary sinus macrophage origin. Proc Natl Acad Sci U S A. 2021 Apr 27;118(17):e2019798118. doi: 10.1073/pnas.2019798118. PMID: 33875594; PMCID: PMC8092388.
3. Hua Z*, Hou B*. The role of B cell antigen presentation in the initiation of CD4+ T cell response. Immunol Rev. 2020 Apr 18. doi: 10.1111/imr.12859. [Epub ahead of print] Review. PMID:32304104
4. Hong S, Zhang Zhimin, Liu H, Tian M, Zhu X, Zhang Zhuqiang, Wang W, Zhu B, Zhou X, Zhang F, Ge Q, Tang H*, Hua Z*, Hou B*. B cells are the dominant antigen-presenting cells that activate naive CD4+ T cells upon immunization with a virus-derived nanoparticle antigen. Immunity, 2018, Sep 21. pii: S1074-7613(18)30353-4. doi: 10.1016/j.immuni.2018.08.012. [Epub ahead of print]
◆ Selected and recommended by Faculty of 1000.
5. Tian M, Hua Z, Hong S, Zhang Z, Liu C, Lin L, Chen J, Zhang W, Zhou X, Zhang F, DeFranco AL and Hou B*. B Cell-Intrinsic MyD88 Signaling Promotes Initial Cell Proliferation and Differentiation To Enhance the Germinal Center Response to a Virus-like Particle. J Immunol. 2018 February 1. 200 (3) 937-948. PMID: 29282308
6. Liao W, Hua Z, Liu C, Lin L, Chen R, Hou B*. Characterization of T-Dependent and T-Independent B Cell Responses to a Virus-like Particle. J Immunol. 2017 May 15. PMID:28416599
7. Hua Z, Gross AJ, Lamagna C, Ramos-Hernández N, Scapini P, Ji M, Shao H, Lowell CA, Hou B*, DeFranco AL*. Requirement for MyD88 signaling in B cells and dendritic cells for germinal center anti-nuclear antibody production in Lyn-deficient mice. J Immunol. 2014 Feb 1;192(3):875-85. PMID: 24379120
8. Hua Z, Hou B*. TLR signaling in B cell development and activation. Cell. Mol. Immunol., Vol.10, 103-106, 2013. PMID: 23241902
9. DeFranco AL, Rookhuizen D, Hou B. Contribution of TLR signaling to germinal center antibody responses. Immunological reviews. 2012 May;247(1):64-72. PMID: 22500832.
10. Kirkland D, Benson A, Mirpuri J, Pifer R, Hou B, Defranco AL, Yarovinsky F. B Cell-Intrinsic MyD88 Signaling Prevents the Lethal Dissemination of Commensal Bacteria during Colonic Damage. Immunity. 2012 Feb 24;36(2):228-38. PMID: 22306056.
11. Hou B*, Saudan P, Ott G, Wheeler ML, Ji M, Kuzmich L, Lee L, Coffman R, Bachmann M, DeFranco AL*. Selective utilization of TLR/MyD88 signaling in B cells for enhancement of the anti-viral germinal center response. Immunity 2011 Mar 25;34(3):375-84. PMID: 21353603.
◆ Selected and recommended by Faculty of 1000.
12. Hou B*, Benson A, Kuzmich L, DeFranco AL, Yarovinsky F*. Critical coordination of innate immune defense to Toxoplasma gondii by dendritic cells responding via their Toll-like receptors. Proc Natl Acad Sci USA. 2011 Jan 4;108(1):278-83. PMID: 21173242.
13. Hou B, Reizis B, DeFranco AL. Toll-like receptor-mediated dendritic cell-dependent and –independent stimulation of innate and adaptive immunity. Immunity 2008 Aug; 29(2): 272-82. PMID: 18656388.
◆ Highlighted in News View. Immunity 2008
◆ Selected and evaluated for the Faculty of 1000
(From Baidong Hou, December 30, 2021)