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Dr. Terry B. Strom, Professor of Medicine and Surgery Harvard Medical School, Boston, MA. USA A Retrospective of a Transplant Visionary, Innovator, and Dedicated Mentor

Li, Xian C., MD, PhD1

doi: 10.1097/TP.0000000000002084
In View: People in Transplantation

1 Immunobiology and Transplant Science Center, Houston Methodist Hospital Texas Medical Center, Houston, TX.

Received 3 January 2018.

Accepted 5 January 2018.

The author declares no funding or conflicts of interest.

Correspondence: Xian C. Li, MD, PhD, Immunobiology and Transplant Science Center, Houston Methodist Hospital Texas Medical Center, Houston, TX 77030. (

Dr. Terry Strom, lovingly called the Big T by his family and friends, had an unusual combination of talents. As Dr. Doug Hanto, former chief of transplantation services at Beth Israel Deaconess Medical Center points out, “Terry is one of the most productive and prolific transplant immunologists of our generation.” Terry’s scientific output has been outstanding and included over 700 papers in all major scientific journals, in addition to more than 50 patents.

A defining attribute about Terry is that he was a curious man who had a genuine interest in seeking answers to all questions. He had a remarkable talent for conceptualizing complicated issues and coming up with testable hypotheses and workable projects. Early in his career, Terry was a leading investigator in searching for surface markers that could separate activated lymphocytes from resting ones, so they could be selectively targeted.1 He pioneered the multidimensional assessments of lymphocytes in the rejecting grafts,2 an approach that we still apply to recent studies.3 His theories on T-cell clone size and transplant outcomes,4 approaches to tipping the balance of T effector cells and T regulatory cells,5 and inflammation that rules immunity over tolerance continue to shape our thinking on how we approach transplant tolerance in the clinic.6

As a highly accomplished nephrologist, Terry was very well versed in clinical applications of laboratory discoveries. He was always at the very forefront of translational studies, long before “translational” became trendy. Terry led the early studies of anti-CD25 in transplant survival,7 which resulted in the clinical development and subsequent FDA approval of the anti-CD25 monoclonal antibody for kidney transplant patients.8 Today, Simulect (the brand name of the Novartis compound) is widely used as a clinical induction reagent.

Terry had great interests in developing Fc-based fusion proteins as clinical therapeutics.9 He also devoted tremendous efforts in his career to identify molecular biomarkers to better serve kidney transplant patients,10 an area of significant importance in further advancement of transplant medicine.

Throughout his career, Terry was very sensitive to new technologies, and very creative in applying them to his research. Even before the time of quantitative reverse transcriptase polymerase chain reactions, his laboratory was already doing quantitative PCR, simply by introducing a target gene-specific competitor during all PCR amplifications.10 His laboratory actively bred double or triple knockout mice for transplant studies, long before genetically modified mice became mainstream tools. Terry had great insights into animal models with color-coded T cells and creatively applied them to the study of transplant tolerance.11 Only a month before his passing, he had advised me on the use of CyTOF, a mass cytometer that is radically different from flow cytometer, and how to incorporate the CyTOF into my own studies.

Terry was a beloved mentor and a great educator. As a prolific investigator in the field, he drew fellows from all over the world to his laboratory, and when I joined Terry’s laboratory in the summer of 1996, his laboratory was truly like a miniaturized United Nations. He allowed fellows the freedom to excise their own talent, but never far in providing guidance and support. I benefited tremendously from this style.

He often said that in scientific research, “you have to respect the data, not the paradigms, because people lie but data never lie.” This gave fellows great confidence in their own intellectual pursuits.

Terry was an inspiring speaker and a motivating communicator. The breadth and depth of his knowledge was always impressive, and whatever the topic was and wherever the conversation was heading, Terry always made talks fun and enjoyable, and left the audience with a profound sense of enlightenment.

Terry was also an enthusiast and an eternal optimist, oftentimes providing encouragement when you needed it the most. When bogged down by rejections of articles and grants, he often said to me, “you have to look at the big picture. Justice is done over a career, not a paper or a grant.” Importantly, he was genuinely kind and generous toward his fellows in terms of his support, time, and advice, even long after leaving his laboratory. In fact, the most significant contributions of Terry’s legacy are the trainees he mentored, who are now at the forefront of transplant science as well as patient care around the world. They will surely carry on his legacy in transplant medicine.

Terry was a visionary who worked tirelessly to advance the promise of transplantation. He had a strong conviction that advancing transplant science will provide ample opportunities for generations to come, and in doing so, patients will become the ultimate winners.

His work has been recognized with numerous awards, including the American Society of Transplantation (AST) mentoring award, AST distinguished achievement award, the Starzl Prize in Transplantation, the Alfred Newton Richards lifetime achievement Award from the International Society of Nephrology, and Homer W. Smith award from the American Society of Nephrology. He also left his marks on many professional societies and had been a founding member of the American Society of Transplant Physicians (ASTP), the predecessor of AST, and served as the Society's first past president.

Terry B. Strom, MD, passed away on December 20, 2017 from complications of a bone marrow transplant at the age of 76. As one of Terry’s trainees, who worked closely with him for almost 16 years, I reflected a lot, often asking myself the question—what makes Terry so special, that his passing has touched so many of us?

For all of us in the transplant community, we certainly feel the pain and a sense of deep loss, as Terry’s career was unparalleled in transplant medicine. He certainly left with us a towering legacy, in which we might find solace. Although the term appears overused at times, Terry was bigger than life; his unique set of talents and expertise combined with enthusiasm, optimism, and dedication made him a gifted scientist, a special mentor, and a beloved physician (Figure 1).



Terry’s beliefs, contributions, and achievements, as well as the extraordinary impact he had on the field, will live on and will continue to inspire us.

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1. Helderman JH, Strom TB. Specific insulin binding site on T and B lymphocytes as a marker of cell activation. Nature. 1978;274:62–63.
2. Strom TB, Tilney NL, Carpenter CB, et al. Identity and cytotoxic capacity of cells infiltrating renal allografts. N Engl J Med. 1975;292:1257–1263.
3. Wu J, Zhang H, Shi X, et al. Ablation of transcription factor IRF4 promotes transplant acceptance by driving allogenic CD4+ T cell dysfunction. Immunity. 2017;47:1114–1128 e1116.
4. Li XC, Strom TB, Turka LA, et al. T cell death and transplantation tolerance. Immunity. 2001;14:407–416.
5. Zheng XX, Sanchez-Fueyo A, Domenig C, et al. The balance of deletion and regulation in allograft tolerance. Immunol Rev. 2003;196:75–84.
6. Strom TB, Koulmanda M. Recently discovered T cell subsets cannot keep their commitments. J Am Soc Nephrol. 2009;20:1677–1680.
7. Kirkman RL, Barrett LV, Gaulton GN, et al. Administration of an anti-interleukin 2 receptor monoclonal antibody prolongs cardiac allograft survival in mice. J Exp Med. 1985;162:358–362.
8. Nashan B, Moore R, Amlot P, et al. Randomised trial of basiliximab versus placebo for control of acute cellular rejection in renal allograft recipients. CHIB 201 International Study Group. Lancet. 1997;350:1193–1198.
9. Zheng XX, Sánchez-Fueyo A, Sho M, et al. Favorably tipping the balance between cytopathic and regulatory T cells to create transplantation tolerance. Immunity. 2003;19:503–514.
10. Lipman ML, Stevens AC, Strom TB. Heightened intragraft CTL gene expression in acutely rejecting renal allografts. J Immunol. 1994;152:5120–5127.
11. Fan Z, Spencer JA, Lu Y, et al. In vivo tracking of 'color-coded' effector, natural and induced regulatory T cells in the allograft response. Nat Med. 2010;16:718–722.
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