معرفی
Diana J. Goode is an Assistant Professor at the Graduate School of Biomedical Science and Engineering (GSBSE) at the University of Maine. She holds a Ph.D. in Immunology from The Johns Hopkins University School of Medicine (2012) and a B.S. from the University of New Hampshire (2004). Her postdoctoral training included roles at the National Institutes of Health (NIH), Population Council (NYC), University of New England, and the North American Pain School (NAPS) in Canada. Her research focuses on neuro-immune cell interactions in chronic and neuropathic pain syndromes, particularly how T cells influence neuronal responses. She has pioneered studies on α4β7 integrin’s role in HIV infection and transmission, as well as sex hormone modulation of pain mechanisms in mice. She has over 6 years of teaching experience in immunology and microbiology, integrating flipped learning into medical curricula.
- Education:
- Ph.D. in Immunology, Johns Hopkins University School of Medicine (2012)
- B.S., University of New Hampshire (2004)
Her research interests span neuro-immune interactions, chronic pain, HIV/HSV-2 transmission, cancer immunology, and sex differences in pain. She employs advanced techniques like multi-color flow cytometry, phospho-profiling, and mouse behavioral models to dissect mechanisms underlying pain hypersensitivity and immune dysfunction. Recent work highlights the role of MHC II in dorsal root ganglion neurons and the impact of ovariectomy on pain sensitivity in female mice, advocating for sex-specific therapeutic approaches.
Publications reflect her commitment to understanding pain pathways and mucosal HIV transmission risks. Key findings include identifying α4β7+ T cells as a critical HIV target and discovering Epac2-dependent mitochondrial regulation in pain signaling. She is actively involved in the GSBSE’s NIH-funded T32 training program, fostering collaborative biomedical research across Maine institutions.
Laboratory work emphasizes translational pain research, with projects exploring how tissue injury amplifies pain via mitochondrial activation. Future directions aim to bridge immunology and neurology to develop precision therapies for pain and infectious diseases.
