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Department of Pathology & Laboratory Medicine

Nicholas M. Ponzio, Ph.D.


Associate Director, Neurological Institute of New Jersey

Master Educator

Professor

Department of Pathology & Laboratory Medicine
ponzio@njms.rutgers.edu
 

Medical Science Building (MSB)
185 South Orange Avenue Room C-540
Newark, NJ 07101
Phone: (973) 972-5238
Fax: (973) 972-7293

Biography

Education

Ph.D., 1973, State University of New York Downstate Medical Center College of Medicine

 

 

Publications

Relevant Publications:

Simmons WJ, Koneru M, Mohindru M, Thomas R, Cutro S, Singh P, DeKruyff RH, Inghirami G, Coyle A, Kim BS, Ponzio NM: Tim-3+ T-bet+ Tumor-specific TH1 cells co-localize with and inhibit development and growth of murine neoplasms. J Immunol. 174:1405-1415, 2005.
Potian JA, Aviv H, Ponzio NM, Harrison JS and Rameshwar P: Veto-like activity of mesenchymal stem cells (MSC): Functional discrimination between cellular responses to alloantigens and recall antigens. J Immunol. 171:3426-3434, 2003.
Chen K, Shiflett SC, Ponzio NM, He B, Elliott BS and Keller SE: A preliminary study of the effect of external Qigong on lymphoma growth in mice. J Alternative and Complementary Medicine. 8:615-621, 2002.
Wajchman J, Simmons WJ, Klein A, Koneru M and Ponzio NM: Interleukin-12-induced cytotoxicity against syngeneic B cell lymphomas of SJL/J mice. Leukemia Research. 26:577-590, 2002.
Chong SY, Zhang M, Lin Y-C, Coffman F, Garcia Z, Ponzio NM, and Ravechè E. The growth regulatory role of B-cell-specific-activator-protein (BSAP) in NZB malignant B-1 cells. Cancer Immunology and Immunotherapy. 50:41-50, 2001.
Sen N, Simmons WJ, Thomas RM, Erianne G, Zhang DJ, Jaeggli NS, Huang C, Xiong X, Tsiagbe VK, Ponzio NM and Thorbecke GJ: META-controlled, env-initiated transcripts encoding superantigens of murine Mtv29 and Mtv7 and their possible role in germinal center B cell lymphomagenesis. J Immunology. 166:5422-5429, 2001.
Ponzio, NM and Thorbecke, GJ: Requirement for reverse immune surveillance for the growth of germinal center derived murine lymphomas. In: Reverse Immune Surveillance: An adaptive mechanism used by tumor cells to facilitate their survival and growth. (GJ Thorbecke and NM Ponzio, eds.) Seminars in Cancer Biology. 10:331-340, 2000
Erianne G, Wajchman J, Yauch R, Tsiagbe VK, Kim BS and Ponzio NM: B cell lymphomas of C57L/J mice; the role of Natural Killer cells and T helper cells in lymphoma development and growth. Leukemia Research. 24:705-718, 2000.

 

Current Research

Ongoing research projects in the Ponzio laboratory are in the areas of cellular/molecular immunology related to:
- stimulation of the host immune response against viral induced tumor antigens
- development of tumor responsive T cell lines for adoptive cancer immunotherapy

We are studying B cell lymphomas that arise spontaneously in several strains of mice, including SJL and C57L as prototypic models for cancer immunotherapy. These murine germinal center derived B cell lymphomas exhibit a dependence for their growth on cytokines produced by tumor-activated CD4+ T helper (TH) cells, a phenomenon we have termed ?reverse immune surveillance?.

The basis for the strong CD4+ T cell response to these tumors is the expression by the lymphoma cells of a superantigen (vSAg) encoded by the endogenous murine mammary tumor retrovirus, Mtv29. The mRNA encoding for this vSAg is not detected anywhere in normal adult SJL mice, except in Peyer?s patches. The germinal center origin of these lymphomas, frequently in Peyer?s patches, may therefore be related to a dysregulation of this vSAg expression with the ensuing T cell stimulation in chronically proliferating germinal centers along the intestinal tract.

The lymphoma vSAg tumor antigen activates host TH2 cells to produce cytokines, such as IL-4 and IL-5, that promote tumor growth. However, we are using other cytokines, such as IL-12, to change the T cell response to a TH1 rather than TH2 pattern. TH1 cells produce a different pattern of cytokines, including Interferon-gamma, which results in the development of tumor-specific Cytotoxic T Lymphocytes (CTL) that destroy tumor cells and prevent B lymphoma growth. We have developed tumor responsive TH1 cell lines that enhance the ability of naïve lymphocytes to become CTL. After injection of these TH1 cells, SJL mice are able to resist challenge with viable tumor cells. More importantly, TH1 cell-injected mice fail to develop the characteristic primary lymphomas that arise spontaneously at one year of age in 90% of uninjected SJL mice.

This novel form of adoptive cellular immunotherapy shows promise for development of similar strategies that can be used for treatment of cancer patients.



 

 

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