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Graduate School Of Biomedical Sciences Dental

Vincent K. Tsiagbe


Associate Professor


Graduate School Of Biomedical Sciences Dental
tsiagbvk@njms.rutgers.edu
 

Biography

Education

 

 

Publications

Relevant Publications:

Tsiagbe VK; Yoshimoto T; Asakawa J; Cho SY; Meruelo D; Thorbecke GJ ."Linkage of superantigen-like stimulation of syngeneic T cells in a mouse model of follicular center B cell lymphoma to transcription of endogenous mammary tumor virus".EMBO journal.1993;12:2313.
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.
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.
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.
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.

 

Current Research

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-gamma; 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 (Vbeta16+). 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.



 

 

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