Diana J. Goode

Education

Ph.D. Johns Hopkins University, School of Medicine 2012
B.S. University of New Hampshire 2004

Brief biography

My laboratory focuses on neuro-immune cell interactions in chronic and neuropathic pain syndromes, specifically studying how T cells impact neuronal responses properties. Skilled in multi-color flow cytometry,  multi-analyte assays, 2D DiGE and 2D Western, phospho-profiling, and mouse behavioral models (Hargreaves, von Frey, thermal choice assay). I earned my Doctor of Philosophy (Ph.D.) in Immunology from The Johns Hopkins University, and received training at the National Institutes of Health, Yale University, and Population Council. I have 5 years’ experience (4yrs graduate, 1yr undergraduate) teaching immunology and microbiology in both a standard classroom and an integrated medical school curriculum coupled with flipped learning.

In 2008 at the National Institutes of Health, I discovered that the HIV envelope protein gp120 binds to integrin α4β7, the gut homing receptor. Expression of integrin α4β7 mediates migration of T cells to the gut where massive CD4+ T cells depletion occurs and subsequent HIV-induced immune dysfunction. We later showed that integrin α4β7 forms a complex with CD4 and defines a T cell subset that is highly susceptible to HIV infection.

In 2014 as a post-doctoral fellow at Population Council, we showed that HSV-2 infection increased the frequency of α4β7+ T cells in the rectal and vaginal mucosa. This increased expression directly correlated with the increased susceptibility to Simian-Human Immunodeficiency virus (SHIV) infection. These experiments highlighted α4β7 as an important risk factor for HIV transmission. Additionally, we analyzed the effect that sex hormones had on α4β7+ T cells and the mucosal microenvironment. Progesterone and estradiol modified the expression and release of inflammatory immune factors directly implicated in HIV transmission. These experiments underscore the importance of understanding the hormone-driven modulation of the mucosal microenvironment and the implementation of contraceptive polices in high-risk communities.

In 2017 as a post-doctoral fellow at the University of New England, my research focused on the roles of exchange proteins activated by cAMP (Epac) signaling pathways in primary sensory neurons and the contribution to the development of acute pain. Our work identified a previously unknown pathway by which tissue injury increases pain by enhancing mitochondrial function through the phosphorylation of the enzyme pyruvate dehydrogenase (Pdha1). An exciting observation is that this mitochondrial mechanism only occurs in male mice, not females, suggesting the need for sex-specific treatments.

My research focuses on neuro-immune cell interactions in chronic and neuropathic pain syndromes, specifically studying the extent CD4+ T cells impact neuronal responses properties. Projects involve multi-color Flow Cytometry, Western blotting, PCR, immunohistochemistry, immunocytochemistry, Phospho-profiling, and mouse behavioral models (Hargreaves, von Frey, thermal choice assay, mechanical conflict system). I earned my Doctor of Philosophy (Ph.D.) in Immunology from The Johns Hopkins University School of Medicine, and received training at NIH, Johns Hopkins University, and Yale University. I have 6 years’ experience (5yrs graduate, 1yr undergraduate) teaching immunology and microbiology in both a standard classroom and an integrated medical school curriculum coupled with flipped learning.

To reach CV press here.

Postdoctoral Training

  • 2012-2015 Post-doctoral fellow in the laboratory of Dr. Martinelli at Population Council, NYC, NY
  • 2016-2019 Post-doctoral fellow in the laboratory of Dr. Molliver at the University of New England, Biddeford, ME
  • 2019 North American Pain School (NAPS) trainee, Montebello, QC, Canada

Research Interests

  • Cancer
  • Immunology / Inflammation / Hematology
  • Neuroscience
  • Chemotherapy-induced peripheral neuropathy

Publications

  • 1) Emily E. Whitaker, Neal E. Mecum, and Diana J. Goode*. Novel expression of major histocompatibility complex II in dorsal root ganglion neurons attenuates paclitaxel-induced cold hypersensitivity in male and female mice. Biorxiv. doi: https://doi.org/10.1101/2023.03.31.535136. *Corresponding author
  • 2) Goode, D. J*. Whitaker, E.E, and Mecum, N. E. (2022) Ovariectomy increases paclitaxel-induced mechanical hypersensitivity and reduces anti-inflammatory CD4+ T cells in the dorsal root ganglion of female mice. Journal of Neuroimmunology. 367(15):577878. doi.org/10.1016/j.jneuroim.2022.577878. *Corresponding author
  • 3) Goode, D.J. and Molliver, D.C. (2021) Regulation of Mitochondrial Function by Epac2 Contributes to Acute Inflammatory Hyperalgesia. J Neurosci. 41(13):2883-2898. doi: 10.1523/JNEUROSCI.2368-20.2021
  • 4) Goode, D.J. and Molliver, D.C. (2019) Phospho-substrate profiling of Epac-dependent protein kinase C activity. Mol Cell Biochem, DOI: 10.1007/s11010-019-03502-
  • 5) Goode D, Truong R, Villegas G, Calenda G, Guerra-Perez N, Piatak M, Lifson J, Blanchard J, Gettie, A. Robbiani M, Martinelli E. (2014) HSV-2 driven increase in the expression of α4β7 correlates with increased susceptibility to vaginal SHIVSF162P3 infection. PLoS Pathog. 10(12):e1004567.
  • 6) Goode D, Aravantinou M, Jarl S, Derby N, Guerra-Perez N, Kenney J, Blanchard J, Gettie A, Robbiani M, Martinelli E. (2014) Sex hormones selectively impact the endocervical mucosal microenvironment: implications for HIV transmission. PLoS One. 9(5):e97767.
  • 7) Arthos J, Cicala C, Martinelli E, Macleod K, Van Ryk D, Wei D, Xiao Z, Veenstra TD, Conrad TP, Lempicki RA, McLaughlin S, Pascuccio M, Gopaul R, McNally J, Cruz CC, Censoplano N, Chung E, Reitano KN, Kottilil S, Goode DJ, Fauci AS. (2008) HIV-1 envelope protein binds to and signals through integrin α4β7, the gut mucosal homing receptor for peripheral T cells. Nat Immunol. 9(3):301-9.
  • 8) Martinelli E, Vegali F, Goode D, Guerra-Perez N, Aravantinou M, Arthos J, Piatak M Jr, Lifson, JD, Blanchard J, Gettie A, Robbiani M. (2013) The frequency of α4β7 (high) memory CD4+ T cells correlates with susceptibility to rectal simian immunodeficiency virus infection. J Acquir Immune Defic Syndr. 64(4):325-31.
  • 9) Cicala C, Martinelli E, McNally JP, Goode DJ, Gopaul R, Hiatt J, Jelicic K, Kottilil S, Macleod K, O’Shea A, Patel N, Van Ryk D, Wei D, Pascuccio M, Yi L, McKinnon L, Izulla P, Kimani J, Kaul R, Fauci AS, Arthos J. (2009) The integrin α4β7 forms a complex with cell-surface CD4 and defines a T-cell subset that is highly susceptible to infection by HIV-1. Proc Natl Sci USA. 106(49):20877-82.
  • 10) Martinelli E, Cicala C, Van Ryk D, Goode DJ, Macleod K, Arthos J, Fauci AS. (2007) HIV-1 gp120 inhibits TLR9-mediated activation and IFN-α secretion in plasmacytoid dendritic cells. Proc Natl Acad Sci USA. 104(9):3396-401.
  • 11) Yao S, Zhu Y, Zhu G, Augustine M, Zheng L, Goode DJ, Broadwater M, Ruff W, Flies S, Xu H, Flies D, Luo L, Wang S, Chen L. (2011) B7-H2 is a costimulatory ligand for CD28 in human. Immunity. 34(5):729-40.