About

Dr. Daniel Leung, MD, MSc, is a Professor in the Division of Infectious Diseases at the University of Utah School of Medicine. His work has significantly contributed to the field of global infectious diseases, with a focus on tropical medicine. Dr. Leung's research and training efforts have had a growing impact in these vital areas, reflecting the university's strong presence and leadership in global health and tropical medicine. His distinguished contributions have been recognized with the 2025 Bailey K. Ashford Medal from the American Society of Tropical Medicine and Hygiene, an honor awarded to early- or mid-career investigators whose work has advanced the field of tropical medicine.

Research topics

• Immunology
• Biology
• Medicine

Selected publications

• Targeted multi-omic analysis of human skin tissue identifies alterations of conventional and unconventional T cells associated with burn injury

  eLife · 2023 · 8 citations

  Senior authorCorresponding
  • Medicine
  • Immunology
  • Biology

  Burn injuries are a leading cause of unintentional injury, associated with a dysfunctional immune response and an increased risk of infections. Despite this, little is known about the role of T cells in human burn injury. In this study, we compared the activation and function of conventional T cells and unconventional T cell subsets in skin tissue from acute burn (within 7 days from initial injury), late phase burn (beyond 7 days from initial injury), and non-burn patients. We compared T cell functionality by a combination of flow cytometry and a multi-omic single-cell approach with targeted transcriptomics and protein expression. We found a significantly lower proportion of CD8+ T cells in burn skin compared to non-burn skin, with CD4+ T cells making up the bulk of the T cell population. Both conventional and unconventional burn tissue T cells show significantly higher IFN-γ and TNF-α levels after stimulation than non-burn skin T cells. In sorted T cells, clustering showed that burn tissue had significantly higher expression of homing receptors CCR7, S1PR1, and SELL compared to non-burn skin. In unconventional T cells, including mucosal-associated invariant T (MAIT) and γδ T cells, we see significantly higher expression of cytotoxic molecules GZMB, PRF1, and GZMK. Multi-omics analysis of conventional T cells suggests a shift from tissue-resident T cells in non-burn tissue to a circulating T cell phenotype in burn tissue. In conclusion, by examining skin tissue from burn patients, our results suggest that T cells in burn tissue have a pro-inflammatory rather than a homeostatic tissue-resident phenotype, and that unconventional T cells have a higher cytotoxic capacity. Our findings have the potential to inform the development of novel treatment strategies for burns.

  PublisherDOI

• A subset of follicular helper-like MAIT cells can provide B cell help and support antibody production in the mucosa

  Science Immunology · 2022 · 78 citations

  Senior authorCorresponding
  • Biology
  • Immunology
  • Medicine

  We identify a MAIT cell subset expressing T follicular helper markers and show the ability of MAIT cells to support B cell responses in the mucosa.

  PublisherOA PDFDOI

• Mucosal-associated invariant T (MAIT) cells mediate protective host responses in sepsis

  eLife · 2020 · 33 citations

  Senior authorCorresponding
  • Immunology
  • Biology
  • Medicine

  Sepsis is a systemic inflammatory response to infection and a leading cause of death. Mucosal-associated invariant T (MAIT) cells are innate-like T cells enriched in mucosal tissues that recognize bacterial ligands. We investigated MAIT cells during clinical and experimental sepsis, and their contribution to host responses. In experimental sepsis, MAIT-deficient mice had significantly increased mortality and bacterial load, and reduced tissue-specific cytokine responses. MAIT cells of WT mice expressed lower levels of IFN-γ and IL-17a during sepsis compared to sham surgery, changes not seen in non-MAIT T cells. MAIT cells of patients at sepsis presentation were significantly reduced in frequency compared to healthy donors, and were more activated, with decreased IFN-γ production, compared to both healthy donors and paired 90-day samples. Our data suggest that MAIT cells are highly activated and become dysfunctional during clinical sepsis, and contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.

  PublisherDOI

Recent grants

• Estimating Cholera Burden with Cross-sectional Immunologic Data

  NIH · $3.4M · 2018–2023

• A mobile health tool to improve antibiotic stewardship among village doctors in Bangladesh

  NIH · $383k · 2022–2025

• Development of clinical decision tools for management of diarrhea of children in high and low resource settings

  NIH · $4.0M · 2018–2027

• NIH Grant K08AI100923

  NIH · $686k · 2017

• Mucosal associated invariant T (MAIT) cells in Vibrio cholerae infection and vaccination

  NIH · $1.4M · 2017–2023

Frequent coauthors

• Edward T. Ryan

  Massachusetts General Hospital

  204 shared

• Jason B. Harris

  Harvard University

  164 shared

• Stephen B. Calderwood

  Massachusetts General Hospital

  159 shared

• Richelle C. Charles

  Harvard University

  131 shared

• Regina C. LaRocque

  Harvard University

  129 shared

• Andrew S. Azman

  University Hospital of Geneva

  84 shared

• Firdausi Qadri

  Weill Cornell Medicine

  69 shared

• Taufiqur Rahman Bhuiyan

  International Centre for Diarrhoeal Disease Research

  61 shared

Awards & honors

• Bailey K. Ashford Medal from the ASTMH (2025)

Similar researchers at University of Utah

• Teruo Okanoh-160
• Mario Capecchih-134
• Gerald J. Gleichh-119
• Michael Allen Pulsipherh-110
• Alfred K. Cheungh-106