About

Jenny Gumperz is a Professor of Medical Microbiology & Immunology at the University of Wisconsin–Madison. She earned her B.A. from the University of California at Santa Cruz in 1986 and her Ph.D. from Stanford University in 1996. Following her doctoral studies, she was a Research Fellow at Harvard Medical School from 1996 to 1999. Her research focuses on human innate T lymphocytes, particularly Natural Killer T (NKT) cells, which can influence the functions of many other immune cell types and significantly impact immune responses. Her lab investigates how NKT cells, which can be activated by self lipids and perform functions without infectious challenges, contribute to inflammatory responses and immune regulation. This research is conducted at molecular, cellular, and systemic levels, with particular interest in their roles in graft-vs-host disease after hematopoietic stem cell transplantation and immune responses during Epstein-Barr virus infection. Dr. Gumperz has received several awards, including the Pew Scholar in the Biomedical Sciences in 2005 and the Charles A. King Trust Fellowship in 2001.

Research topics

• Biology
• Internal medicine
• Immunology
• Medicine
• Cell biology
• Pathology
• Molecular biology
• Genetics
• Virology

Selected publications

• Different Human Immune Lineage Compositions Are Generated in Non-Conditioned NBSGW Mice Depending on HSPC Source

  Frontiers in Immunology · 2020 · 37 citations

  Senior authorCorresponding
  • Immunology
  • Biology
  • Cell biology

  long-term HSC subpopulation, suggesting this model promotes mainly short-term HSC activity. Mice transplanted with cord blood HSPCs maintained a diversified human immune compartment for at least 36 weeks after the primary transplant, although mice given adult bone marrow HSPCs had lost diversity and contained only myeloid cells by this time point. Finally, to assess the impact of non-HSPCs on transplantation outcome, we also tested mice transplanted with total or T cell-depleted adult bone marrow mononuclear cells. Total bone marrow mononuclear cell transplants produced significantly lower human chimerism compared to purified HSPCs, and T-depletion rescued B cell levels but not other lineages. Together these results reveal marked differences in engraftment efficiency and lineage commitment according to HSPC source and suggest that T cells and other non-HSPC populations affect lineage output even in the absence of conditioning-associated inflammation.

  DOI

• Early T Cell Activation Metrics Predict Graft-versus-Host Disease in a Humanized Mouse Model of Hematopoietic Stem Cell Transplantation

  The Journal of Immunology · 2020 · 37 citations

  Senior authorCorresponding
  • Immunology
  • Medicine
  • Biology

  Acute graft-versus-host disease (GVHD) is a frequent complication of hematopoietic transplantation, yet patient risk stratification remains difficult, and prognostic biomarkers to guide early clinical interventions are lacking. We developed an approach to evaluate the potential of human T cells from hematopoietic grafts to produce GVHD. Nonconditioned NBSGW mice transplanted with titrated doses of human bone marrow developed GVHD that was characterized by widespread lymphocyte infiltration and organ pathology. Interestingly, GVHD was not an inevitable outcome in our system and was influenced by transplant dose, inflammatory status of the host, and type of graft. Mice that went on to develop GVHD showed signs of rapid proliferation in the human T cell population during the first 1-3 wk posttransplant and had elevated human IFN-γ in plasma that correlated negatively with the expansion of the human hematopoietic compartment. Furthermore, these early T cell activation metrics were predictive of GVHD onset 3-6 wk before phenotypic pathology. These results reveal an early window of susceptibility for pathological T cell activation following hematopoietic transplantation that is not simply determined by transient inflammation resulting from conditioning-associated damage and show that T cell parameters during this window can serve as prognostic biomarkers for risk of later GVHD development.

  DOI

• B cells infected with Type 2 Epstein-Barr virus (EBV) have increased NFATc1/NFATc2 activity and enhanced lytic gene expression in comparison to Type 1 EBV infection

  PLoS Pathogens · 2020 · 42 citations

  • Biology
  • Virology
  • Molecular biology

  Humans are infected with two distinct strains (Type 1 (T1) and Type 2 (T2)) of Epstein-Barr virus (EBV) that differ substantially in their EBNA2 and EBNA 3A/B/C latency genes and the ability to transform B cells in vitro. While most T1 EBV strains contain the "prototype" form of the BZLF1 immediate-early promoter ("Zp-P"), all T2 strains contain the "Zp-V3" variant, which contains an NFAT binding motif and is activated much more strongly by B-cell receptor signalling. Whether B cells infected with T2 EBV are more lytic than cells infected with T1 EBV is unknown. Here we show that B cells infected with T2 EBV strains (AG876 and BL5) have much more lytic protein expression compared to B cells infected with T1 EBV strains (M81, Akata, and Mutu) in both a cord blood-humanized (CBH) mouse model and EBV-transformed lymphoblastoid cell lines (LCLs). Although T2 LCLs grow more slowly than T1 LCLs, both EBV types induce B-cell lymphomas in CBH mice. T1 EBV strains (M81 and Akata) containing Zp-V3 are less lytic than T2 EBV strains, suggesting that Zp-V3 is not sufficient to confer a lytic phenotype. Instead, we find that T2 LCLs express much higher levels of activated NFATc1 and NFATc2, and that cyclosporine (an NFAT inhibitor) and knockdown of NFATc2 attenuate constitutive lytic infection in T2 LCLs. Both NFATc1 and NFATc2 induce lytic EBV gene expression when combined with activated CAMKIV (which is activated by calcium signaling and activates MEF2D) in Burkitt Akata cells. Together, these results suggest that B cells infected with T2 EBV are more lytic due to increased activity of the cellular NFATc1/c2 transcription factors in addition to the universal presence of the Zp-V3 form of BZLF1 promoter.

  DOI

Recent grants

• Understanding the impact of human NKT cells on hematopoiesis

  NIH · $421k · 2015–2018

• NIH Grant R01HL071590

  NIH · $642k · 2008

• NIH Grant R56AI074940

  NIH · $330k · 2009

• NIH Grant R21AI076707

  NIH · $371k · 2012

• Analysis of human NKT cells in GVHD in vivo

  NIH · $414k · 2012–2015

Frequent coauthors

• Gurdyal S. Besra

  University of Birmingham

  35 shared

• Michael B. Brenner

  26 shared

• D. Branch Moody

  Brigham and Women's Hospital

  25 shared

• Petr A. Illarionov

  24 shared

• Peter Parham

  Stanford University

  23 shared

• Tan‐Yun Cheng

  Brigham and Women's Hospital

  23 shared

• Steven A. Porcelli

  Albert Einstein College of Medicine

  22 shared

• David C. Young

  University of Utah

  21 shared

Education

• B.A.

  University of California at Santa Cruz

  1986

• Ph.D.

  Stanford University

  1996

• Other

  Harvard Medical School

  1996

Awards & honors

• Pew Scholar in the Biomedical Sciences (2005)
• The Medical Foundation Charles A. King Trust Fellowship (200…
• Burroughs Wellcome Fellow of the Life Sciences Research Foun…

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