Dr. Robson is a Professor of Anaesthesia, Harvard Medical School, Department of Anesthesia, Critical Care and Pain Medicine at BIDMC. He is also the Charlotte F. & Irving W. Rabb Distinguished Professor of Gastroenterology and Hepatology, Harvard Medical School, Department of Medicine at BIDMC.

Simon C. Robson is a physician scientist and the newly appointed Director of the Center for Inflammation Research within the Department of Anesthesia, Critical Care and Pain Medicine at Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School. He is also the Director of Liver Research within Gastroenterology and has been a core faculty member of the Transplant Institute at BIDMC. He served as the Chief of Gastroenterology, Hepatology & Endoscopy, through 2015, at BIDMC. He remains active clinically in Hepatology and Liver Transplantation and cares for a diverse population of patients with inflammatory, autoimmune and vascular-type liver diseases; as well as those undergoing liver transplantation.

His major area of basic science and translational research provides the central theme of the newly formed Center for Inflammation Research. This involves innovative work in vascular biology, immunity, immunometabolism and purinergic signaling. Simon’s focus over the past two decades has been on the discovery, characterization and investigations of mammalian ectonucleotidases, which are vascular, myeloid and regulatory lymphoid cell expressed ectoenzymes that hydrolyze extracellular nucleotides, such as ATP and ADP, to adenosine and derivatives. CD39 and other gene family members, expressed on the vasculature and regulatory immune cells, are crucial in the maintenance of homeostasis, and in the control of inflammation and immune responses in transplanted organs; as well in native organs, such as the lungs and liver (see reviews at end).

CD39 and family members are highly relevant to the control of inflammation in human disease and provide innovative therapeutic targets in inflammatory diseases and cancer. Pertinent examples include CD39 and related proteins being solubilized or coupled to biodegradable polymers/liposomes, or expressed in transgenic manner, to boost generation of adenosine. Select investigational agents may be administered systemically to ameliorate inflammatory responses as in ischemia reperfusion injury, graft rejection and systemic inflammatory states as following trauma and surgery.

Purinergic signaling is also a central component of the dysregulated inflammation in cancer. Immune escape of cancer involves heightened suppressive responses to extracellular nucleotides and adenosine, which are also tightly regulated by the ectonucleotidases CD39 and CD73. Therefore, pharmacological blockade of CD39 and CD73, as with neutralizing antibodies or small molecules, can augment host cellular responses and alter vascular homeostasis to specifically target experimental cancers. This bolstering of immunostimulatory effects, by overcoming immune exhaustion and augmenting responses to release of ATP post-chemotherapy, has potential clinical benefits in cancer and other states of immune exhaustion.

Dr. Robson has been funded by NIH, the DoD, AASLD, AHA and other national and international groups as well as BioPharma, since 1996. He has served on NIH, AHA and other Study Sections as a standing charter member. As a member of the AASLD Basic Research Committee, he has organized Liver Fibrosis Special Interest Group (SIG) programs at AASLD, amongst others. He is a thought leader in purinergic signaling area and served as the Chairman of Scientific Committees and International Workshops on Purinergic Signaling, including the past Keystone Symposium in Molecular and Cellular Biology in 2016 and more recently PURINES2018, as well as being an Associate Editor of the journal “Purinergic Signaling.” His diverse life experiences, global perspectives, organizational skills and multiple academic contacts facilitate access to international thought leaders.

Selected Publications

  1. Deaglio S, Dwyer KM, Gao W, Friedman D, Usheva A, Erat A, Chen JF, Enjyoji K, Linden J, Oukka M, Kuchroo VK, Strom TB, Robson SC. Adenosine generation by CD39 and CD73 on T regulatory cells mediates immune suppression. Journal of Experimental Medicine. 2007 Jun 11;204(6):1257-65. PMCID: PMC2118603. >1695 citations.
  2. Eltzschig H, Sitkovsky M & Robson SC. Purinergic signaling during inflammation. New England Journal of Medicine 2012 Dec 13;367(24):2322-33. PMCID: PMC3675791. >420 Citations.
  3. Bai A, Moss A, Rothweiler S, Serena Longhi M, Wu Y, Junger WG, Robson SC. NAD(P)H oxidase-dependent CD39 expression by CD8(+) T cells modulates interferon gamma responses via generation of adenosine. Nat Commun. 2015 Nov 9. PMID: 26549640.
  4. Longhi MS, Vuerich M, Kalbasi A, Kenison JE, Yeste A, Csizmadia E, Vaughn B, Feldbrugge L, Mitsuhashi S, Wegiel B, Otterbein L, Moss A, Quintana FJ, Robson SC. Bilirubin suppresses Th17 immunity in colitis by upregulating CD39. JCI Insight. 2017 May 4;2(9). pii: 92791. doi:  10.1172/jci.insight.92791.
  5. Allard BLonghi MSRobson SC & Stagg J (joint senior/corresponding). The ectonucleotidases CD39 and CD73: Novel checkpoint inhibitor targets. Immunol Rev. 2017 Mar;276(1):121-144. doi: 10.1111/imr.12528.

Complete List of Published Work in My Bibliography