Headshot of Diana Goode

Diana J. Goode, Ph.D.

Assistant Professor, Department of Biomedical Sciences, COM


Pickus Center for Biomedical Research 210
Biddeford Campus
Eligible for Student Opportunities

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. 



Johns Hopkins University, School of Medicine
University of New Hampshire


Cell culture
Neuropathic pain
Tumor immunology

Post-Doctoral 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


Selected publications

1. Goode DJ, Molliver DC. Regulation of mitochondrial function by Epac2 contributes to acute inflammatory hyperalgesia. J Neurosci. 2021 Feb 12;. doi: 10.1523/JNEUROSCI.2368-20.2021. [Epub ahead of print] PubMed PMID: 33593853.

2. Goode DJ, Molliver DC. Phospho-substrate profiling of Epac-dependent protein kinase C activity. Mol Cell Biochem. 2019 Jun;456(1-2):167-178. doi: 10.1007/s11010-019-03502-1. Epub 2019 Feb 9. PubMed PMID: 30739223; PubMed Central PMCID: PMC7269517.

3. Goode D, Truong R, Villegas G, Calenda G, Guerra-Perez N, Piatak M, Lifson JD, Blanchard J, Gettie A, Robbiani M, Martinelli E. HSV-2-driven increase in the expression of α4β7 correlates with increased susceptibility to vaginal SHIV(SF162P3) infection. PLoS Pathog. 2014 Dec;10(12):e1004567. doi: 10.1371/journal.ppat.1004567. eCollection 2014 Dec. PubMed PMID: 25521298; PubMed Central PMCID: PMC4270786.

4. Goode D, Aravantinou M, Jarl S, Truong R, Derby N, Guerra-Perez N, Kenney J, Blanchard J, Gettie A, Robbiani M, Martinelli E. Sex hormones selectively impact the endocervical mucosal microenvironment: implications for HIV transmission. PLoS One. 2014;9(5):e97767. doi: 10.1371/journal.pone.0097767. eCollection 2014. PubMed PMID: 24830732; PubMed Central PMCID: PMC4022654.

5. 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. HIV-1 envelope protein binds to and signals through integrin alpha4beta7, the gut mucosal homing receptor for peripheral T cells. Nat Immunol. 2008 Mar;9(3):301-9. doi: 10.1038/ni1566. Epub 2008 Feb 10. PubMed PMID: 18264102.

Funded grants

Ongoing Research Support

P20GM103643     Pilot Project:  01/01/20 - 05/31/22
The overall goal of this COBRE award is to establish a group devoted to the study of pain.  The major goal of my Pilot Project specifically is to study “Novel expression of MHC class II on DRG neurons can directly activate CD4+ T cells contributing to the resolution of neuropathic pain”

Role:  Pilot Project Leader

Invited plenary presentation

2013    Keystone Symposia Invited Talk, Keystone Symposia
2016    HIV/AIDS Guest Lecturer, University of Southern Maine
2019    Neurobiology and Behavior Invited Talk, North East Regional IDeA Conference

Research interests

Neuro-immune communication in neuropathic pain syndromes

Research topics

COM Neuroscience and Pain