Hui Hu, Ph.D.

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Wistar Institute Assistant Professor of Pathology and Laboratory Medicine
Department: Pathology and Laboratory Medicine
Graduate Group Affiliations

Contact information
The Wistar Institute
3601 Spruce Street
Philadelphia, PA 19104
Office: (215) 495 6820
Fax: (215) 898 0847
Education:
Licentiate (Immunology)
Stockholm University, 1997.
Ph.D. (Immunology)
Stockholm University, 1998.
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Description of Research Expertise

Research Interests
Transcriptional regulation of cell development and function in the immune system.

Cellular quiescence is a state characterized by small cell size, lack of spontaneous proliferation, and reduced metabolic rate. Even in the absence of overt antigen challenge, circumstances such as lymphopenia, or the ablation of inhibitory receptors or regulatory T (Treg) cells, can drive quiescent naive T cells to undergo proliferation, gain effector functions and often lead to autoimmune diseases. These observations indicate that lymphocyte quiescence does not occur by default, but is actively maintained by both extrinsic and intrinsic mechanisms, which are poorly understood at the molecular level. Recently we have identified forkhead box (FOX) transcription factor Foxp1 as an essential regulator in maintaining mature T cell quiescence, providing direct evidence that lymphocyte quiescence is actively controlled at the transcriptional level. One goal of the laboratory is to identify novel regulatory genes/networks of T cell quiescence and determine their roles in T cell homeostasis, tolerance, and immune responses.

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. This line of the research in our laboratory is to understand the hierarchical transcriptional regulation in hematopoiesis/lymphopoiesis.

Our laboratory utilizes a broad variety of techniques including cellular immunology, molecular biology, biochemistry, gene-targeting (knockout and knockin), functional genomics, and in vivo animal models to address the questions that we are interested in.

Research projects in the laboratory include:
1) Foxp1 transcriptional network in maintaining mature T cell quiescence.
2) Crosstalk between the mechanism of T cell quiescence and the mechanism of agonist-induced T cell activation, and the impact of such interactions on T effector differentiation and memory formation in infectious disease models.
3) Tumor microenvironmental regulation of T cell unresponsiveness/quiescence.
4) Transcriptional regulation in early B cell development and mature B cell functions.
5) Transcriptional regulatory networks in hematopoiesis/lymphopoiesis.

Selected Publications

Feng, X., Wang, H., Takada, H., Day, T., Willen, J. and Hu, H. (2011) Transcription factor Foxp1 exerts essential cell-intrinsic regulation of the quiescence of naive T cells. Nature Immunology. 12, 544-550 (see News and Views in Nat. Immunol. 12, 522-524; featured as Article of the month)

Feng, X., Ippolito, G. C., Tian, L., Karla, W., Oh, S., Sambandam, A., Willen, J., Bunte, R. M., Maika, S. D., Harriss, J.V., Caton, A. J., Bhandoola, A., Tucker, P. W., and Hu, H. (2010) Foxp1 is an essential transcriptional regulator for the generation of quiescent naïve T cells during thymocyte development. Blood. 115, 510-518

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., Borde, M., Maika, S., Nardone, J., Allred, L., Tucker, P.W. and Rao, A (2006) Foxp1 is an essential transcriptional regulator of B cell development. Nature Immunology. 7, 819-826 (see News and Views in Nat. Immunol. 7, 793-794)

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

Swain, S. L., Hu, H. and Huston, G. (1999) Class II independent generation of CD4 memory T cells from effectors. Science. 286, 1381-1383
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Last updated: 09/19/2011
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