Faculty Detail   
Name HUI HU
 
Campus Address BBRB 859 Zip 2170
Phone  205-996-1820
E-mail  huihu@uab.edu
Other websites PubMed
Hu Lab
    

 Education

Graduate  Stockholm University, Stockholm, Sweden      Licentiate  
Graduate  Stockholm University, Stockholm, Sweden      Ph.D. 

Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Microbiology  Microbiology Associate Professor
Center  Center for AIDS Research  Center for AIDS Research Associate Professor
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Associate Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Associate Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Molecular Genetics Program 
Cancer Biology 
Cell, Molecular, & Developmental Biology 
Cellular and Molecular Biology Program 
Immunology 
Medical Scientist Training Program 
Microbiology 
Molecular and Cellular Pathology Program 

Biographical Sketch 
Hu joined the Department of Microbiology at UAB in May, 2014. He was an Associate Professor at the Wistar Institute, Philadelphia. Before Hu moved to the Wistar Institute, he was an instructor in the Department of Pediatrics at Harvard’s Children’s Hospital, Boston, and a postdoctoral associate at the CBR Institute for Biomedical Research (IDI) at Harvard Medical School. Prior to joining Harvard in 2002, he worked as a postdoctoral associate at the Center for Cancer Research at MIT and as a postdoctoral fellow at the Trudeau Institute. Hu received his doctorate from Stockholm University, Stockholm, Sweden.

Society Memberships
Organization Name Position Held Org Link
American Association of Immunologists (AAI)     
 

Research/Clinical Interest
Title
Transcriptional Regulation of Adaptive Immunity
Description
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.

I. Tfh cell differentiation and humoral immunity
The humoral immune response is one of the two effector arms of the immune system. Studies have shown that CD4+ T follicular helper (Tfh) cells are essential for long-lived, high affinity antibody responses. Yet the complex regulation that determines the initial development of Tfh cells, their developmental progression in germinal centers (GC), and their fates after an immune response dissolves, is still not fully understood. In this research direction, our long-term goals are to identify novel pathways underlying the differentiation of Tfh cells in humoral responses, and design new strategies to manipulate humoral responses for treatment of infectious diseases and autoimmune disorders.
Recently, we find that Foxp1 is a rate-limiting and essential negative regulator of Tfh cell differentiation, drastically affecting GC and antibody responses (Nat. Immunol. 2014).

Rotation/research projects:
1. Elucidate the molecular mechanisms by which the Foxp1 pathway regulates the differentiation and function of Tfh cells.
2.Further dissect how the Foxp1 pathway in T cells may regulate the key steps of mature B cell differentiation in GC responses.
3. Determine how the Foxp1 pathway in T cells may regulate other important components including innate immunity in a GC response.
4. Determine how we may manipulate the Foxp1 pathway (by utilizing a Foxp1-mCherry reporter mouse*) to boost humoral responses and vaccine efficacy by combining with different types of vaccinations.

II. Negative regulatory pathways in controlling T cell quiescence and responses
Much of our understanding of molecular mechanisms regulating immune responses is centered on pathways and processes that promote cell activation, division and differentiation. Recently we have demonstrated that cell-intrinsic signaling pathways are required to maintain mature T cells in a quiescent state (Nat. Immunol. 2011). If these pathways are disrupted, resting T cells become aberrantly activated even in the absence of antigen challenge. In this research direction, our long-term goals are to identify regulatory genes and pathways that actively restrain T cell activation, and define the roles of such negative regulatory pathways in controlling T cell quiescence, effector responses, memory maintenance, and tumor immunology.

Rotation/research projects:
1. Elucidate the molecular mechanisms underlying T cell quiescence.
2. Determine how quiescence pathways regulate effector T cell responses and T cell memory by using various infectious disease models.
3. Develop new adoptive T-cell immunotherapies in treatment of cancer.

III. Transcriptional regulation of mature B cell differentiation and B lymphomagenesis
After activation, mature B cells go through various differentiation stages to elicit successful antibody responses. At each differentiation step, distinct regulatory networks are engaged to regulate the B cell proliferation, survival and differentiation. Not co-incidentally, the genetic aberrations, molecular pathogenesis and oncogenic programs in B cell lymphomas are considerably dependent on the differentiation state of the B cells from which the lymphomas arise. In this direction of research, our long-term goals are to identify novel differentiation stage-specific pathways that regulate the proliferation, survival and differentiation of mature B cells, with particular interests in the ones that will link to the recurrent genetic aberrations in B lymphomas, for which we will define their roles and contributions in the malignant transformation of B cells.

Rotation/research projects:
1. Elucidate the molecular mechanism underlying a novel regulatory pathway we have recently identified in GC B cell differentiation.
* By utilizing a Foxp1-mCherry reporter mouse, we will determine the expression pattern of Foxp1 in various tissues and study the signaling pathways that regulate Foxp1 levels.

Selected Publications 
Wang, H., Geng J., Wen, X., Bi, E., Kossenkov, A. V., Wolf, A. I., Tas, J., Choi, Y.S., Takata, H., Day, T. J., Chang, L-Y., Sprout, S. L., Becker, E. K., Willen, J., Li, T., Wang, Xin., Xiao C., Jiang, P., Crotty, S., Victora, G.D., Showe, L. C., Tucker, H. O., Erikson, J. and Hu, H. (2014) The transcription factor Foxp1 is a critical negative regulator of T follicular helper cell differentiation. Nature Immunology. 15, 667-675 (see News and Views in Nat. Immunol. 15, 597-599)

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).

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.
 
 
 

Keywords
Tfh cell differentiation, GC responses, CD8+ T cell quiescence/activation, T cell responses, immune memory, vaccines