Thomas Griffith

About

Thomas S. Griffith earned his Ph.D. from Washington University in 1996, where he examined the cellular and molecular mechanisms of ocular immune privilege. He was a postdoctoral scientist at Immunex Corporation from 1997 to 1999, contributing to the initial characterization of TRAIL (TNF-related apoptosis-inducing ligand). In 1999, Dr. Griffith moved to the Department of Urology at the University of Iowa, where he continued evaluating TRAIL as an antitumor therapeutic. He joined the University of Minnesota Department of Urology as an associate professor in August 2011 and has since been promoted to professor. Dr. Griffith is also a member of the Masonic Cancer Center, the Center for Immunology, and the Microbiology, Immunology, and Cancer Biology Graduate Program at the University of Minnesota. His research focuses on tumor immunology and apoptosis, specifically studying the therapeutic potential of apoptotic cell death in cancer treatment. His laboratory investigates the use of TRAIL as a potent inducer of tumor cell apoptosis that is non-toxic to normal tissues, employing gene delivery systems such as recombinant adenoviral vectors to induce tumor cell death and activate systemic antitumor immunity. Additional studies explore how apoptotic cells influence immune responses using experimental models of tolerance and sepsis.

Research topics

• Biology
• Medicine
• Immunology
• Internal medicine
• Endocrinology

Selected publications

• CD4 T Cell Responses and the Sepsis-Induced Immunoparalysis State

  Frontiers in Immunology · 2020 · 176 citations

  Senior authorCorresponding

  Sepsis remains a major cause of death in the United States and worldwide, and costs associated with treating septic patients place a large burden on the healthcare industry. Patients who survive the acute phase of sepsis display long-term impairments in immune function due to reductions in numbers and function of many immune cell populations. This state of chronic immunoparalysis renders sepsis survivors increasingly susceptible to infection with newly or previously encountered infections. CD4 T…

  DOI

• Physiological microbial exposure transiently inhibits mouse lung ILC2 responses to allergens

  Nature Immunology · 2022 · 27 citations

  PublisherOA PDFDOI

• The generation of stable microvessels in ischemia is mediated by endothelial cell derived TRAIL

  Science Advances · 2024-10-04 · 16 citations

  articleOpen access

  Reversal of ischemia is mediated by neo-angiogenesis requiring endothelial cell (EC) and pericyte interactions to form stable microvascular networks. We describe an unrecognized role for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in potentiating neo-angiogenesis and vessel stabilization. We show that the endothelium is a major source of TRAIL in the healthy circulation compromised in peripheral artery disease (PAD). EC deletion of TRAIL in vivo or in vitro inhibited neo-angi…

  PublisherDOI

• Determining potential immunomodulatory drug efficacy in sepsis using ELISpot

  Scientific Reports · 2025-04-18 · 6 citations

  articleOpen access

  This study evaluated the ability of ELISpot to identify potential immuno-modulatory drug therapies in sepsis. ELISpot was performed ex vivo on whole blood from septic patients and healthy controls. Innate and adaptive immunity were evaluated by production of TNF-α and IFN-γ, respectively. Drug efficacy was determined by their effects to modulate the both the number of cytokine-producing cells and amount of cytokine produced per cell. The corticosteroid dexamethasone was evaluated for its ability…

  PublisherOA PDFDOI

• FUNCTIONAL IMMUNOPHENOTYPING FOR PRECISION THERAPIES IN SEPSIS

  Shock · 2024-11-20 · 6 citations

  reviewOpen access

  ABSTRACT: Sepsis remains a significant cause of morbidity and mortality worldwide. Although many more patients are surviving the acute event, a substantial number enters a state of persistent inflammation and immunosuppression, rendering them more vulnerable to infections. Modulating the host immune response has been a focus of sepsis research for the past 50 years, yet novel therapies have been few and far between. Although many septic patients have similar clinical phenotypes, pathways affecte…

  PublisherOA PDFDOI

Recent grants

• BLRD Research Career Scientist Award Application

  NIH · 2023–2027

• NIH Grant R56AI077565

  NIH · $372k · 2011

• NIH Grant R01CA109446

  NIH · $2.6M · 2015

Frequent coauthors

• Vladimir P. Badovinac

  University of Iowa

  144 shared

• Tamara A. Kucaba

  University of Minnesota Medical Center

  94 shared

• Isaac J. Jensen

  Columbia University

  50 shared

• Britnie R. James

  University of Minnesota

  49 shared

• Katherine A. Murphy

  39 shared

• Salih Şanlıoğlu

  Akdeniz University

  34 shared

• Jayanth Panyam

  Temple University

  34 shared

• Frances V. Sjaastad

  University of Minnesota

  34 shared

Labs

• Timm-Nelson LabPI

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