Hui Hu, Ph.D.

Assistant Professor
Immunology Program
215-495-6820, Office

Introduction

Research in the Hu laboratory focuses on understanding the transcriptional control of cell development and functional regulation in the immune system.

Research Summary

Research interests in the Hu laboratory include:

• Transcriptional regulatory networks in hematopoiesis/lymphopoiesis
• Transcription factor Foxp1 in early B cell development and mature B cell functions
• Transcriptional regulation of effector and memory T cell functions

Hematopoiesis engages hierarchical regulatory networks of key transcription factors that exert positive and negative impacts on gene transcription by changing chromatin status and structure, and determine cell “fate” at critical developmental and differentiation stages. Key transcription factors also participate in regulating important cellular functions and are regulated by external cell signals via specific signaling pathways.

Recently, Hu and coworkers identified transcription factor Foxp1 as a new essential player in B lymphopoiesis. They are using long-range chromatin structure analysis and BAC recombineering to study the transcriptional regulation and chromatin remodeling of two loci, the Rag locus and the Foxp1 locus, during hematopoiesis. They are also combining gene-targeting, in vitro and in vivo experimental models to explore the functions of Foxp1 in mature B and T cell responses.

Harnessing effective memory responses is essential for immune protection against many infectious diseases and for treating tumors. Immunological memory is also the basis of vaccination. Significant questions about the differentiation of activated T cells to become memory cells, be deleted (leading to tolerance), or become anergic still await conclusive resolution. From the aspect of transcriptional regulation, the Hu laboratory is interested in understanding the molecular mechanisms underlying T cell effector functions, survival, homeostasis, and memory.

Rotation projects available for 2007-2008:

• Transcriptional control and chromatin remodeling of the Rag locus and the Foxp1 locus in hematopoiesis
• Molecular mechanism(s) of Foxp1 in early B cell development
• Transcriptional regulation of effector and memory T cell functions

Selected Publications

Hu, H., Djuretic, I., Sundrud, M.S. and Rao, A. (2007) Transcriptional partners in regulatory T cells: Foxp3, Runx and NFAT. Trends. Immunol. 28, 329-332

Hu, H., Wang, B., Border, M., Nardone, J., Maika, S., Allred, L., Tucker, P.W. and Rao, A. (2006) Foxp1 is an essential transcriptional regulator of B cell development. Nature Immunology. 7, 819-826

Ge, Q., Hu, H., Eisen, H.N. and Chen, J (2002) Different contributions of thymopoiesis and homeostasis-driven proliferation to the reconstitution of naïve and memory T cell compartments. Proc.Natl. Acad. Sci. USA 99, 2989-2994

Ge, Q., Hu, H., Eisen, H.N. and Chen, J (2002) Naïve to memory T-cell differentiation during homeostasis-driven proliferation. Microbes & Infection. 4, 555-558

Hu, H., Huston, G., Duso, D., Lepak, N., Roman, E. and Swain, S.L. (2001) CD4 T cell effectors can become memory cells with high efficiency and without division. Nature Immunology. 2, 705-710

Whitehurst, C. E., Hu, H., Ryu, C. J., Rajendran, P., Schmidt, T. and Chen, J. (2001) V(D)J recombination and expression of TCR b occurs normally in the absence of the Jb2-Cb2 intronic Cis element. Mol. Immunol. 38, 55-63

Swain, S. L., Hu, H. and Huston, G.  (1999) Class II independent generation of CD4 memory T cells from effectors.  Science. 286, 1381-1383

Hu, H., Moller, G. and Abedi-Valugerdi, M. (1999) Mechanism of mercury-induced autoimmunity: both T helper 1- and T helper 2-type responses are involved. Immunology. 96, 348-357

Abedi-Valugerdi, M., Hu, H. and Moller, G. (1999) Mercury-induced anti-nucleolar autoantibodies can transgress the membrane of living cells in vivo and in vitro. Int. Immunol. 11(5), 605-615

Hu, H., Abedi-Valugerdi, M. and Moller, G. (1998) Non-responsiveness of mercury-induced autoimmunity in resistant mice is not due to immunosuppression or biased Th1-type response. Scand. J. Immunol. 48, 515-521

Abedi-Valugerdi, M., Hu, H. and Moller, G. (1997) Mercury-induced renal immune complex deposits in young (NZBxNZW)F1 mice: Characterization of antibodies/autoantibodies. Clin. Exp. Immunol. 110, 86-91

Hu, H., Moller, G. and Abedi-Valugerdi, M. (1997) Major histocompatibility complex Class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro. J. Autoimmun. 10, 441-446

Hu, H., Moller, G. and Abedi-Valugerdi, M. (1997) Thiol compounds inhibit mercury-induced immunological and immunopathological alterations in susceptible mice. Clin. Exp. Immunol. 107, 68-75

Hu, H., Abedi-Valugerdi, M. and Moller, G. (1997) Pretreatment of lymphocytes with mercury in vitro induces a response in T cells from genetically determined low-responders and a shift of the interleukin profile. Immunology. 90, 198-204

Hu, H. and Moller, G. (1993) Lipopolysaccharide-stimulated events in B cell activation. Scand. J. Immunol. 40, 221-227