Michelle A. Swanson-Mungerson, Ph.D.

Associate Professor, Department of Microbiology and Immunology


Michelle Swanson-MungersonMidwestern University
Chicago College of Osteopathic Medicine
Department of Microbiology and Immunology
Room 323-J Science Hall
555 31st St.
Downers Grove, IL 60515

Office: (630) 515-6129
e-mail: mswans@midwestern.edu

EDUCATION

B.S. Biology University of Illinois at Urbana-Champaign 1995
Ph.D. Immunology Loyola University of Chicago, Stritch School of Medicine 2002

RESEARCH SUMMARY

Advances in our treatment options for Hodgkin's lymphoma (HL) are critical in light of the fact that the incidence of HL is on the rise, due to an increase of HL in AIDS patients. Virtually all cases of HIV-associated HL tumors are infected with Epstein-Barr Virus (EBV), indicating that EBV is essential for developing the tumor microenvironment in these individuals. This HL tumor microenvironment is absolutely vital for the survival of the malignant Hodgkin-Reed Sternberg (HRS) cells of HL. The current dogma is that EBV infects B cells that are the precursors of the HRS cells, and promotes initial HRS cell survival through the expression of the EBV protein, LMP2A. However, once the microenvironment is established, the ability of LMP2A to contribute to the tumor microenvironment that is vital for HRS survival remains unknown. The long term goal of our laboratory is to understand how EBV influences the tumor microenvironment in HL in order to develop novel strategies to enhance HL treatment success.  Current projects in our lab are addressing two critical areas to investigate how LMP2A directly promotes the generation of a tumor microenvironment that promotes tumor survival and inhibits the anti-tumor immune response.

Research projects

Project I: The cytokine, IL-10, directly promotes the survival of B cell tumors and dampens anti-tumor responses by decreasing the ability of CD8+ T cells to kill tumor cells. Previous work from our laboratory demonstrates that the EBV latency protein, LMP2A, activates the PI3K pathway to enhance IL-10 production. Ongoing experiments in our laboratory are elucidating targets of PI3K used by LMP2A to increase IL-10 production. Additionally, we are testing whether the LMP2A-mediated increase in IL-10 functionally blocks the anti-tumor response of CD8+ T cells. The results of these studies will help us to understand how LMP2A contributes to the creation of a tumor microenvironment that promotes tumor cell survival and blocks that CD8+ T cell mediated anti-tumor response.

Project II: The chemokine, MIP-1α, is an important chemokine for recruiting cells to envelop HRS cells of Hodgkins lymphoma to set up a microenvironment that promotes tumor development and survival. Recent work from our laboratory demonstrates that the EBV latency protein, LMP2A, directly increases MIP-1α. Ongoing projects in our laboratory are analyzing the signal transduction pathway used by LMP2A to increase MIP-1α at the transcriptional and protein levels. Additionally, we are testing whether the LMP2A-mediated increase in MIP-1α enhances the chemotaxis of monocytes in vitro in an effort to understand the effect of enhanced MIP-1α levels in the HL tumor microenvironment. The results from these studies may elucidate novel strategies to disrupt the microenvironment in Hodgkin's lymphoma to increase the efficacy of current treatments for this disease.

Selected Publications

M. Swanson-Mungerson, Vijay Subramaniam, Ryan Incrocci, Philip Williams, Mary Hill, and Alejandro Mayer. "Effects of Cyanobacteria Oscillatoria sp. Lipopolysaccharide on B cell Activation and Function." Manuscript under review.

Ryan Incrocci, Levi Barse, Amanda Stone, Sai Vagvala, Michael Montesano, Vijay Subramaniam, M. Swanson-Mungerson. "Epstein-Barr Virus Latent Membrane Protein 2A (LMP2A) enhances IL-10 production through the activation of Bruton's tyrosine kinase and STAT3." Virology. 500: 96-102, 2017. 

M. Swanson-Mungerson. Adaptive Immunity. In: Primer of Psychoneuroimmunology. Psychoneuroimmunology Research Society, Los Angeles, CA. Editor: Mark R. Opp. ISBN: 978-0-692-70829-3

Samira Hussain, Ryan Incrocci, and M. Swanson-MungersonEpstein-Barr virus Latent Membrane Protein 2A (LMP2A)-mediated changes in Fas expression and Fas-dependent apoptosis: Role of Lyn/Syk activation. Cell Immunol. 2015 Oct;297(2):108-19. PMID: 26255694

Incrocci R, McCormack M, Swanson-Mungerson M. "Epstein-Barr virus LMP2A increases IL-10 production in mitogen-stimulated primary B-cells and B-cell lymphomas." J Gen Virol. 2013 May;94(Pt 5):1127-33  

Swanson-Mungerson M, Bultema R, Longnecker R. "Epstein-Barr virus LMP2A imposes sensitivity to apoptosis." J Gen Virol. 2010 Sep;91(Pt 9):2197-202

Bieging KT, Swanson-Mungerson M, Amick AC, Longnecker R. "Epstein-Barr virus in Burkitt's lymphoma: a role for latent membrane protein 2A." Cell Cycle. 2010 Mar 1;9(5):901-8. 

Bultema R, Longnecker R, Swanson-Mungerson M. "Epstein-Barr virus LMP2A accelerates MYC-induced lymphomagenesis." Oncogene. 2009 Mar 19;28(11):1471-6

Swanson-Mungerson M, Longnecker R. "Epstein-Barr virus latent membrane protein 2A and autoimmunity." Trends Immunol. 2007 May;28(5):213-8.

Swanson-Mungerson M, Bultema R, Longnecker R. "Epstein-Barr virus LMP2A enhances B-cell responses in vivo and in vitro." J Virol. 2006 Jul;80(14):6764-70.

Swanson-Mungerson MA, Caldwell RG, Bultema R, Longnecker R. "Epstein-Barr virus LMP2A alters in vivo and in vitro models of B-cell anergy, but not deletion, in response to autoantigen." J Virol. 2005 Jun;79(12):7355-62.