Eric Jonas Gapud, M.D., Ph.D. is an Assistant Professor of Medicine, Physician Scientist, and Director of Research for the Vasculitis Center (JHVC) in the Division of Rheumatology. He completed both his M.D. and Ph.D. in Molecular Immunology through the Medical Scientist Training Program at Washington University in St. Louis. He completed a thesis on the necessary functions of DNA damage signals in normal lymphocyte development under the mentorship of the renown immunologist Barry Sleckman and with the renown cancer immunologist Robert D. Schreiber serving as his committee chair. He did his internship and residency in Internal Medicine at Washington University in St. Louis/Barnes Jewish Hospital.
Dr. Gapud subsequently pursued fellowship training in rheumatology at the Johns Hopkins School of Medicine. As a fellow, Dr. Gapud trained extensively in the clinical management of vasculitis under the direct mentorship of Dr. Philip Seo, the current Director of the Vasculitis Center, and Dr. Rebecca Manno, Assistant Director of the Vasculitis Center. In addition, Dr. Gapud also simultaneously completed an intensive research post-doc under the mentorship of Dr. Livia Casciola-Rosen, Professor of Medicine and Dr. Antony Rosen, Director of the Division of Rheumatology and Vice Dean for Research for the School of Medicine. The American College of Rheumatology, the world’s largest professional body of rheumatologists, recognized Dr. Gapud’s achievements during his training by awarding him the 2017 ACR Distinguished Fellow Award, the highest honor that the College can bestow on a fellow in training.
Dr. Gapud joined the Johns Hopkins School of Medicine Faculty in 2017. As a physician scientist, he divides his time seeing patients in the Johns Hopkins Vasculitis Center and continuing to conduct immunology research on autoimmune disease mechanisms. He is a current Jerome L. Greene Scholar awardee and a sitting member of the American College of Rheumatology’s Leadership Committee for Journals and Publications. Because of his clinical sub-specialty and research, he also has been invited as guest faculty to the Asahi General Hospital post-graduate medical training program in Tokyo, Japan for 2018.
The Vasculitis Center is actively recruiting patients to assist with studies that will advance understanding the mechanisms of vasculitis with the intent of using these mechanistic insights to identify new treatment targets and to develop prognostic tools with personalized precision so that disease flares ideally can be detected before clinical symptoms fully manifest. Dr. Gapud and the other experts at the JHVC are advancing this research based on the realization that not all answers for these diseases can come from randomized clinical trials and large population-based studies and that disease names are only approximations of the reality of what patients endure. He believes that only by carefully working together with individual patients to study these diseases that will we be able to truly bring our patients closer to cure. The ultimate goal of the JHVC research programs is personalized medicine.
As Director of Research in the Johns Hopkins Vasculitis Center, Dr. Gapud has specific interests in the molecular disease mechanisms that shape patient outcomes ANCA-Associated Vasculitis, Giant Cell Arteritis, Behcet’s Disease, and Takayasu Arteritis.
He is spearheading new projects to explore the poorly understood role of T cells potentially as apical patho-etiogenic determinants of disease onset and activity in ANCA-Associated Vasculitis. The vast majority of studies of ANCA-Associated Vasculitis have focus on the role of acute inflammatory cells called neutrophils that are seen in the vessel of patients with active disease. Newer evidence has emerged that these acute inflammatory cells do not cause disease manifestations autonomously, but rather that they seem to be directed and sustained in their damage-causing states by T cells.
Dr. Gapud, in studies with Drs. Antony Rosen and Livia Casciola-Rosen, also is seeking to define the patho-etiologic role of granzymes in autoimmune disease. Granzymes are key molecular signals used by T cells normally to kill off infected and cancerous tissues and cells. In particular, he is interested in previously unappreciated off-target effects of these mediators on bystander cells and tissues during normal immune responses and how alterations and perturbations of these off-target responses lead to auto-disease.
- Gapud EJ, Seo P, and Antiochos B. ANCA-Associated Vasculitis Pathogenesis: A Commentary. Curr Rheumatol Rep. 2017. 19(4):15.
- Seung BS, Gapud EJ, Zhang S, Dorsett Y, Bredemeyer A, George R, Callen E, Daniel JA, Osipovich O, Oltz EM, Bassing CH, Nussenzweig A, Lees-Miller S, Hammel M, Chen BPC, and *Sleckman BP. Overlapping Activities of
ATM and DNA-PKcs in Coding End Joining During V(D)J Recombination. 2013. Mol Cell Biol. 33(18):3568-3579.
- Gapud EJ and Sleckman BP. Unique and redundant functions of ATM and DNA-PKcs during V(D)J recombination. 2011. Cell Cycle. 10(12): 1928–1935.
- Gapud EJ, Dorsett Y, Yin B, Callen E, Bredemeyer AL, Mahowald GK, Omi KQ, Bednarski JJ, McKinnon PJ, Nussenzweig A, and Sleckman BP. Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping
activities during chromosomal signal joint formation. 2011. Proc Natl Acad Sci U S A. 108(5): 2022–2027.
- Gapud EJ, Lee BS, Mahowald GK, Bassing CH, and Sleckman BP. Repair of Chromosomal RAG-Mediated DNA Breaks by Mutant RAG Proteins Lacking PI-3-like Kinase Consensus Phosphorylation Sites. 2011. J Immunol. 187(4): 1826–1834.
- Zhang S, Yajima H, Huynh HD, Zheng J, Callen E, Chen HT, Wong N, Bunting S, Lin YF, Li M, Lee KJ, Story M, Gapud E, Sleckman BP, Nussenzeig A, Zhang CC, Chen DJ, and Chen BPC. Congenital bone marrow failure in DNA-PKcs mutant mice
associated with deficiencies in DNA repair. 2011. J Cell Biol. 193(2): 295–305.
- Gonzalez-Suarez I, Redwood AB, Perkins SM, Vermolen B, Lichtensztejin D, Grotsky DA, Morgado-Palacin L, Gapud EJ, Sleckman BP, Sullivan T, Sage J, Stewart CL, Mai S, and *Gonzalo S. Novel roles for A-type lamins in telomere biology and the DNA damage response pathway. 2009. EMBO J. 28(16):2414-27.
- Difilippantonio S, Gapud E, Wong N, Huang CY, Mahowald G, Chen HT, Kruhlak MJ, Callen E, Livak F, Nussenzweig MC, Sleckman BP, and Nussenzeig A. 53BP1 facilitates long-range DNA end-joining during V(D)J recombination. 2008. Nature.
- Bredemeyer AL, Helmink BA, Innes CL, Calderon B, McGinnis LM, Mahowald GK, Gapud EJ, Walker LM, Collins JB, Weaver BK, Mandik-Nayak L, Schreiber RD, Allen PM, May MJ, Paules RS, Bassing CH, and Sleckman BP. DNA double-strand breaks activate a multi- functional genetic program in developing lymphocytes. 2008. Nature. 456(7223):819-823.
- Pettit GR, Anderson CR, Gapud EJ, Jung MK, Knight JC, Hamel E, and Pettit RK. Antineoplastic agents. 515. Synthesis of human cancer cell growth inhibitors derived from 3,4-methylenedioxy-5,4′-dimethoxy-3′-amino-Z-stilbene. 2005. J Nat Prod. 68(8):1191-1197.
- Gapud EJ, Bai R, Ghosh AK, and Hamel E. Laulimalide and paclitaxel: a comparison of their effects on tubulin assembly and their synergistic action when present simultaneously. 2004. Mol Pharmacol. 66(1):113-121.