VINCENT K. TSIAGBE, M.S., Ph.D. tsiagbvk@umdnj.edu Phone: 973-972-2612

Associate Professor, Department of Oral Biology and Department of Pathology.

Graduate Education: M.S. (1981); Ph.D. (1986), University of Wisconsin, Madison WI.

PostDoctoral Training: New York University School of Medicine 1986-1993

Our laboratory studies the intricate host-lymphoma relationships that govern the growth of germinal center-derived B-cell lymphomas. We have focused attention on an SJL mouse model for follicular center B-cell lymphomas (RCS) and have shown that the growth of these lymphomas depends on cytokine products (notably IL-2, -4, and -5) of host CD4 + T cells. IL-1 and IFN-γ are required for optimum growth of the lymphoma cells. The production of these cytokines is ensured by presentation of MHC Class II antigen on the lymphoma cells, in conjunction with a lymphoma-encoded antigen, to CD4 + T cells bearing a particular T-cell receptor ( Vβ16 +). This skewed recognition is the hallmark of a superantigen response; and the tumor's dependence on the host for growth is described as "reversed immunological surveillance." We have also shown that the tumor-associated antigen which mediates the superantigen response is encoded by a novel endogenous mouse mammary tumor virus (Mtv) gene (Mtv-29). We sequenced the Mtv and showed that the stimulating moiety resides within the ORF of the 3' Mtv-LTR, in effect serving as an indirect oncogen. The superantigen encoded by Mtv-29 is called vSAg29. We have employed micro-array gene profile analysis to uncover “lymphoma-specific” genes involved in the lymphoma process. Future work focuses attention on the mechanisms involved in the activation of this vSAg29. These studies involve the use of chromatin immunoprecipitation (ChIP-ChIP) tiling arrays to uncover the role of chromatin modification in the transcription of vSAg29. This work is supported by funding from the National Cancer Institute of NIH.

We are also interested in human, germinal center-derived human B-cell lymphomas, that resemble mouse RCS, and contain CD4 T cells. Such lymphomas include Diffuse Large B Cell Lymphomas, and Burkitt's lymphomas. Considering that the human genome is laden with edogenous retroviral genes (HERVs), current efforts are geared towards cloning HERVs that could potentially serve as “superantigen” for host T cells, and thus enhance lymphomagenesis. This work is supported by funding from by the Cancer Research Institute.

RECENT PUBLICATIONS

Murano M, Xiong X, Murano N, Salzer JL, Lafaille JJ, Tsiagbe VK. Latent TGF-beta1-transduced CD4+ T cells suppress the progression of allergic encephalomyelitis. J Leukoc Biol. 2006;79:140-146.

Thomas RM, Haleem K, Siddique AB, Simmons WJ, Tsiagbe VK. Regulation of META env initiated Mtv29 superantigen (vSAg29) transcripts in SJL/J mice lymphomas: role of Ikaros, demethylation, and chromatin structural change in the transcriptional activation of vSAg29. J. Immunol. 2003;170:218-227.

Li, H, Ma X, Moskovits, T, Inghirami G., and Tsiagbe VK.. Identification of oligoclonal CD4 T cells in diffuse large B cell lymphomas. Clin Immunol. 2003;107:160-169.

Tsiagbe VK, Ponzio NM, Erianne GS, Zhang DJ, Thorbecke GJ, Inghirami G. Germinal center derived lymphomas, in: The biology of germinal centers in lymphoid tissue. Eds. G. J., Thorbecke, and V. K. Tsiagbe, Springer-Verlag, New York, NY, 1998; pg. 199-234.

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