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Arnob  Banerjee
 

Arnob Banerjee M.D., Ph.D.

Academic Title: Assistant Professor
Primary Appointment: Medicine
abanerjee@som.umaryland.edu
Location: HSF-II, S111
Phone: (401)-706-2245
Lab: (410)-706-2248

Personal History:

I received my undergraduate degree in Chemistry from Brown University. As a student in the Medical Scientist Training Program at the Columbia University College of Physicians and Surgeons, I pursued my Ph.D. thesis research in the area of cytokine signal transduction under the mentorship of Dr. Paul Rothman. I received my M.D. and Ph.D. degrees in 2002, and went on to clinical Internal Medicine residency and subsequent clinical Hematology and Oncology fellowship at the University of Pennsylvania. As a fellow, I completed postdoctoral research training in the laboratory of Dr. Steven Reiner, where I studied the regulation of gene expression and cell fate decisions in T cells during immune responses. In 2010, I joined the faculty of the University of Maryland School of Medicine and started my own lab.

Research Interests:

My laboratory team is interested in the molecular mechanisms governing gene expression patterns and differentiation in T lymphocytes both in the setting of anti-cancer immune responses and in the setting of T cell leukemia and lymphoma. We anticipate that our studies of T cells in these two different contexts, described in more detail below, will be complementary with our knowledge of non-malignant and malignant T cell biology each informing our research on the other.

  1. T cell differentiation in anti-cancer immune responses. By the time a cancer reaches clinical significance, it has escaped the control of the immune system. The mechanisms by which T cells lose their anti-cancer activity remain incompletely defined. Antibodies directed against surface molecules including CTLA4, PD-1, and 4-1BB have all been shown to induce clinically significant T cell responses, however the inability to maintain a highly active and durable anti-cancer response remains a barrier to longstanding clinical success. We believe that mechanistic insights into the loss of activity in T cells within tumors, and into the induction of anti-cancer activity with current approaches will guide the design of novel immuno-therapeutic strategies.

    Our goal in this project is to define the molecular mechanisms that influence T cell differentiation during both effective and ineffective anti-cancer immune responses. Our experiments are focused on the activities of two partially homologous transcription factors that are both members of the T-box gene family, T-bet and Eomesodermin (Eomes). While both factors are important in generating cell-mediated immune responses, we have recently described their opposing roles in effector versus memory differentiation. While T-bet stimulates terminal effector differentiation, Eomes supports long-term persistence as memory. We are currently determining the contributions of these transcriptional regulators to T cell fate in anti-cancer immunity.

  2. Identification of novel therapeutic targets in T cell malignancies. T cell malignancies are notable for their poor prognosis with a lack of consensus on optimal management. In a second project, we are determining whether T-bet and Eomes, as regulators of differentiation in T cells, play a role in the biology of T cell leukemias and lymphomas. We have also initiated a project to identify mutations in all exons (exome) in peripheral T cell lymphoma (PTCL) and to conduct functional molecular studies to determine the contributions of specific mutations to PTCL biology.

Clinical Speciality:

Hematology


Publications:

Banerjee, A., Gordon, S.M., Intlekofer, A.M., Paley, M.A., Mooney, E.C.,Lindsten T., Wherry, E.J., and Reiner, S.L.: The Transcription Factor Eomesodermin Enables CD8+ T Cells to Compete for the Memory Cell Niche. The Journal of Immunology 185: 4988-4992, 2010.

Banerjee, A., Schambach, F., DeJong, C.S., Hammond, S.M., and Reiner, S.L.: Micro-RNA-155 Inhibits IFN-γ Signaling in CD4+ T cells. The European Journal of Immunology, 40: 225-31, 2010.

Jenne, C.N., Enders, A., Rivera, R., Watson, S.R., Bankovich, A.J., Pereira, J.P., Xu, Y., Roots, C.M., Beilke, J.N., Banerjee, A., Reiner, S.L., Miller, S.A., Weinmann, A.S., Goodnow, C.C., Lanier, L.L., Cyster, J.G., and Chun, J.: T-bet dependent S1P5 expression in NK cells promotes egress from lymph nodes and bone marrow. The Journal of Experimental Medicine 206(11): 2469-81, 2009.

Intlekofer, A.M., Banerjee, A., Takemoto, N., Gordon, S.M., DeJong, C., Hunter, C.A., Wherry, E.J., Lindsten, T., and Reiner, S.L.: Anomalous Type 17 Response to Viral Infection by CD8+ T Cells Lacking T-bet and Eomesodermin. Science 321: 408-11, 2008.

Intlekofer, A.M., Takemoto, N., Kao, C., Banerjee, A., Schambach, F., Northrop, J.K., Shen, H., Wherry, E.J., and Reiner, S.L.: Requirement for T-bet in the aberrant differentiation of unhelped memory CD8+ T cells. The Journal of Experimental Medicine 204(9): 2015-21, 2007.

Chang, J.T., Palanivel, V.R., Kinjyo, I., Schambach, F., Intlekofer, A.M., Banerjee, A., Longworth, S.A., Vinup, K.E., Mrass, P., Oliaro, J., Killeen, N., Orange, J.S., Russell, S.M., Weninger, W., and Reiner, S.L.: Asymmetric T Lymphocyte Division in the Initiation of Adaptive Immune Responses. Science 315: 1687-91, 2007.

Banerjee, A., Rothman, P.: IL-7 reconstitutes multiple aspects of v-Abl mediated signaling. The Journal of Immunology 161:4611-7, 1998, A., Banks, A.S., Nawijn, M.C., Chen, X.P., Rothman, P.B.: Suppressor of Cytokine Signaling (SOCS)-3 inhibits activation of NFATp. The Journal of Immunology 168: 4277-81, 2002.

Banerjee, A., Rothman, P.: IL-7 reconstitutes multiple aspects of v-Abl mediated signaling. The Journal of Immunology 161:4611-7, 1998.