Hui Xu, Ph.D.


Hui_Xu

University of Alabama at Birmingham
VH 566B1530 3RD AVE S
BIRMINGHAM AL 35294-0019

Office: (205)975-2628
xuhui@uab.edu

 

 

 

 

Education

B.M.
      1981. Medicine. Ye-Jing Medical School, Wuhan, P. R. China.
M.S.      1986. Immunology. Tong-Ji Medical School, Wuhan. P. R. China.
Ph.D.    1992. Immunology. University of Goettingen, W. Germany.

 

Academic Affiliations

Professor:    Department of Dermatology
Research Professor:   Department of Pathology
Faculty Member:   Graduate School, University of Alabama at Birmingham

 

 Research Interests

The major research interest of Dr. Xu's laboratory is to investigate regulatory mechanisms for immune responses in inflammatory diseases and tumors. Immune regulation or feedback regulation after activation of the immune system is a crucial mechanism for balancing the level of immune responses and preventing diseases caused by overreaction. The study is of special importance since in many of clinical immune-related disorders, the immune system in patients has been already activated. Understanding of the regulatory mechanism will not only provide clues to pathogenesis of immune-related disorders but may also be exploited to develop new strategies for treatment. Currently, Dr. Xu is focusing on two main projects.

PD-1 and PD-1 ligands. PD-1 is expressed by activated T cells and plays important regulatory roles in immune responses. So far, two ligand molecules for PD-1, B7-H1 and B7-DC, have been identified. Although PD-1 appears to provide negative signals for T cells, the function of its two ligands is controversial. Dr. Xu is investigating the role of B7-H1 in the regulation of immune responses by dendritic cells and as well as by non-antigen presenting cells. The long-term goal is to determine whether targeting PD-1 mediated immunosuppression provides a therapeutic potentials for autoimmune and inflammatory diseases, graft rejection, and tumors.

Slits and Robos. Slits are neuronal repellents and Robos are the transmembrane receptors for Slits, which both are expressed mainly in the brain. The molecules play important roles in axon guidance and the development of the nervous system. However, the role of Slits/Robos in the regulation of immune responses and inflammatory reactions is unexplored. Dr. Xu has two interrelated projects investigating whether Slits are anti-inflammatory factors in the regulation of immune responses and whether they are involved in tumor mediated immunosuppression.

 

Selected Publications

 

 Xu H, Dilulio NA, and Fairchild RL. 1996. T cell populations primed by hapten sensitization in contact sensitivity are distinguished by polarized pattern of cytokine production: IFN-g producing (Tc1) effector CD8+ T cells and IL-4/IL-10 producing (Th2) negative regulatory CD4+ T cells. J. Exp. Med. 183: 1001.

 Abe M, Kondo T, Xu H and Fairchild RL. 1996. Interferon-g inducible protein (IP-10) expression is mediated by CD8+ T cells and is regulated by CD4+ T cells during the elicitation of contact hypersensitivity. (first three authors contributed equally to this work). J. Invest. Dermal. 107: 360.

 Xu H, Banerjee A, DiIulio NA and Fairchild RL. 1997. Development of effector CD8+ T cells in contact hypersensitivity occurs independently of CD4+ T cells. J. Immunol. 158: 4721.

 Xu H, Heeger P and Fairchild RL. 1997. Distinct roles for B7-1 and B7-2 determinants during priming of effector CD8+ Tc1 and regulatory CD4+ Th2 cells for contact hypersensitivity. J. Immunol. 159: 4217.

 Xu H, Bullard D, Hanson J, Slater M and Elmets CA. 2001. The role of ICAM-1 molecules in the migration of Langerhans cells in the skin and regional lymph node. Eur. J. Immunol. 31:3085-3093.

 Guan H, Zu G, Slater M, Elmets CA and Xu H. 2002. Gammadelta T cells regulate the development of hapten specific CD8+ effector T cells in contact hypersensitivity responses. J Invest Dermal. 119:137-141.

 Guan H, Zu G, Xie Y, Tang H, Johnson M, Xu X, Kevil C, Xiong WC, Elmets CA, Rao Y,  Wu JY, and Xu H. 2003. Neuronal repellent Slit2 inhibits dendritic cell migration and the development of immune responses. J Immunol. 171:6519-6526.

 Kim HK, Guan H, Li H, Zu G, Feng X, Elmets CA, Fu YX, and Xu H. 2006. High level expression of B7-H1 molecules by dendritic cells suppresses the function of activated T cells and desensitizes allergen primed animals. J Leukoc Biol. 76:686-695.

 He D, Wu L, Kim HK, Li H, Elmets CA, and Xu H.  2006. CD8+ IL-17 producing T cells are important in effector functions for the elicitation of contact hypersensitivity responses.  J Immunol. 177: 6852-6858 

 Yusuf N, TH. Nasti, CM Huang, BS. Huber, T. Jaleel, HY. Lin, Xu H, and CA. Elmets. 2009. Heat Shock Proteins HSP27 and HSP70 Are Present in the Skin and Are Important Mediators of Allergic Contact Hypersensitivity. J. Immunol. 182: 675-683.

  He D, Wu L, Kim HK, Li H, Elmets CA, Xu H. 2009. IL-17 and IFN-g mediate the elicitation of contact hypersensitivity responses by different mechanisms and both are required for optimal responses.  J Immunol. 183:1463-1470.

 Wang X, M. Fujita, R. Prado, A. Tousson, H-C. Hsu, A. Schottelius, D.R. Kelly, P.A. Yang, Q. Wu, J. Chen, Xu H, C.A. Elmets, J.D. Mountz and C.K. Edwards. 2009. Visualizing CD4 T-cell migration into inflamed skin and its inhibition by CCR4/CCR10 blockades using in vivo imaging model. Br J Dermatol. 162:487-496.

  He D, Li H, Yusuf N, Elmets CA, Jun Li, John Mountz, Hui Xu. 2010. IL-17 promotes tumor development through the induction of tumor promoting microenvironments at tumor sites and myeloid derived suppressor cells. J Immunol. 184:2281-2288.

 Mudit Vaid, Tripti Singh, Anna Li, Nandan Katiyar, Samriti Sharma, Craig A. Elmets, Hui Xu, Santosh K. Katiyar. 2011. Proanthocyanidins inhibit UVB-induced immunosuppression through IL-12-dependent stimulation of CD8+ effector T cells and inactivation of CD4+ suppressor T cells. Cancer Prevention Research. 4:238-47.

  He D, Li H, Yusuf N, Elmets CA, Athar M, Katiyar SK, Xu H. 2012. IL-17 mediated inflammation promotes tumor growth and progression in the skin. PLoS ONE. 72:e32126.

Grant Support

National Cancer Institute
Project Entitled :Prevention of UV Carcinogenesis Through DNA Repair Dependent Immunomodulation
Principal Investigator
Period: 07/01/2010 through12/31/2014 

National Institute of Arthritis and Musculoskelatal and Skin Diseases
Project Entitled: The Role of CD5 in Dendritic Cell Mediated Immune Suppression
Principal Investigator
Period: 07/01/2010 through 04/30/2014(NCE)

 VA Merit Review, Veteran Administration (PI: Craig Elmets)
Project Entitlted: Host Defense Mechanisms in Polyaromatic Hydrogen Carcinogenesis
Co-Investigator
Period: 10/01/2010-09/30/2014