About

Allison M. Weis, PhD, is a faculty member at the Spencer Fox Eccles School of Medicine, primarily within the Department of Internal Medicine and as an adjunct in the Department of Pathology. Her educational background includes a BA from Lewis & Clark College, a PhD from the University of California, Davis, and postdoctoral training at the University of Utah Spencer Fox Eccles School of Medicine and Huntsman Cancer Institute. Her research focuses on microbiota-host interactions, gut microbiota, and their roles in health and disease, including cancer immunology, metabolic health, and inflammatory conditions. Dr. Weis has contributed to understanding how microbiota components influence immune responses, gut homeostasis, and disease processes, as evidenced by her extensive publication record in these areas.

Research topics

• Biology
• Cell biology
• Immunology
• Genetics
• Computational biology
• Microbiology
• Fishery
• Evolutionary biology
• Ecology

Selected publications

• Training Tomorrow’s Leaders in Cancer Immunology

  Cancer Immunology Research · 2026-01-12

  articleOpen access

  The transition from trainee to independent investigator is one of the most challenging and formative phases of a scientific career. It requires not only scientific expertise but also the skills to lead, mentor, manage, and communicate effectively. The Arthur and Sandra Irving Cancer Immunology Symposium serves as a platform for established investigators to mentor trainees and early-career faculty as they navigate this transition to independence. Through sharing personal experiences and lessons from their own careers, senior leaders provide guidance on the scientific, professional, and personal challenges that shape a successful career in cancer immunology-emphasizing how curiosity, persistence, and a translational mindset can make a lasting real-world impact. This commentary highlights key themes, including leadership, communication, recruitment, and fundraising. Altogether, these insightful thoughts provide a framework for the next generation of cancer immunologists as they establish their independent careers as future leaders in the field.

  PublisherOA PDFDOI

• Isolation of a highly virulent colibactin-positive tumor-promoting strain of <i>Escherichia coli</i> from the gut microbiota of an adult

  mSphere · 2026-05-07

  articleOpen access1st authorCorresponding

  ABSTRACT Recent studies have pointed to critical roles for microbes in both exacerbation of and protection from the development of colon cancer. While much has been learned, the field remains understudied, with functional studies available for only a handful of bacteria. To identify novel microbes associated with colorectal cancer (CRC) development, we employed a preclinical chemical carcinogenesis CRC mouse model using germ-free mice that were colonized with human microbiotas. During the course of these studies, we identified a microbiota that exacerbated CRC, from which we isolated an Escherichia coli strain that had disseminated to the mouse kidneys. This strain, which we designated as AW001, was genetically similar to the reference adherent-invasive E. coli (AIEC) strain NC101 and encoded the DNA-damaging toxin colibactin. In relevant animal models, AW001 worsened both colitis and sepsis, making it a colitogenic AIEC-like strain with the capacity to cause invasive systemic infections similar to extraintestinal pathogenic E. coli (ExPEC). This strain will be a relevant tool to study human-associated intestinal E. coli strains capable of causing disease in mice. IMPORTANCE Colorectal cancer (CRC) is a significant burden on human health. A growing body of work has pointed to critical roles for microbes in the exacerbation of and protection from the development of CRC. Specific Escherichia coli strains can produce colibactin, a genotoxin that has been implicated in exacerbating CRC. In this study, we tested human microbiotas in a mouse model of CRC and isolated a colibactin - positive Escherichia coli strain that led to tumorigenesis, disseminated from the gut to the mouse kidneys, caused death, and worsened both colitis and sepsis in murine models. Identification of this strain enhances our collective knowledge and adds an important tool for future studies on the role of microbes and CRC tumorigenesis.

  PublisherDOI

• A microRNA-regulated transcriptional state defines intratumoral CD8+ T cells that respond to immunotherapy

  Cell Reports · 2025-02-01 · 10 citations

  articleOpen access

  T cell-dependent cancer immunity and ICI responses that may be leveraged for future therapeutics.

  PublisherDOI

• Dietary fat disrupts a commensal-host lipid network that promotes metabolic health

  Cell Metabolism · 2025-11-06 · 8 citations

  articleOpen access
  PublisherOA PDFDOI

• 1137 A human-derived bacterium’s capsular polysaccharide activates a Lag-3-NK cell axis to restrain colon cancer and augment immunotherapy

  Regular and Young Investigator Award Abstracts · 2025-11-01

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• A capsular polysaccharide from a member of the healthy human microbiota activates NK cells to restrain colon cancer and aument immunotherapy 4789

  The Journal of Immunology · 2025-11-01

  articleOpen access1st authorCorresponding

  Abstract Description Colorectal cancer (CRC) is the third leading cause of death in the US and is increasing globally. The microbiota is a driver of CRC pathogenesis, however, there are few microbes that are known to restrain CRC. Using transplantation of the microbiota from patients with or without CRC into germfree mice, we found that the microbiota harbored by non-diseased individuals reduced tumor formation, and we identified Bacteriodes uniformis as protective. Proactive treatment with B. uniformis slowed tumor growth in mice and increased tumor infiltrating T and Natural Killer (NK) cells, by single cell sequencing and flow cytometry. Surprisingly, NK cells, but not T-cells, were required for B. uniformis-mediated protection and B. uniformis directly upregulated NK effectors. CRC is recalcitrant to immunotherapies for unknown reasons; however, we also show that animals colonized with CRC microbiotas failed to respond to a-CTLA-4 treatment, and addition of B. uniformis restores this response, which is dependent on NK cells. We further identified that a specific B. uniformis polysaccharide capsule molecule was essential for the tumor protection and NK activation, thus identifying the relevant immunomodulatory molecule. Taken together, we have determined that healthy individuals possess tumor suppressor microbes that prevent cancer by enhancing NK immunosurveillance and anti-tumor immunity via their capsule molecules. Funding Sources This work was supported by National Institutes of Health Grants (F32CA243501) to A.M.W. University of Utah III Initiative Seed grant to JLR and NU. R01DK124336, R01DK124317 and R01AT011423, grants from the Helmsley Foundation, Burrough’s Wellcome Foundation, and the Keck Foundation to J.L.R. also supported this work. Topic Categories Tumor Immunology: Cellular Responses and Tumor Microevironment (TIME)

  PublisherOA PDFDOI

• Neonatal fungi promote lifelong metabolic health through macrophage-dependent β cell development

  Science · 2025-03-06 · 21 citations

  articleOpen access

  Loss of early-life microbial diversity is correlated with diabetes, yet mechanisms by which microbes influence disease remain elusive. We report a critical neonatal window in mice when microbiota disruption results in lifelong metabolic consequences stemming from reduced β cell development. We show evidence for the existence of a similar program in humans and identify specific fungi and bacteria that are sufficient for β cell growth. The microbiota also plays an important role in seeding islet-resident macrophages, and macrophage depletion during development reduces β cells. Candida dubliniensis increases β cells in a macrophage-dependent manner through distinctive cell wall composition and reduces murine diabetes incidence. Provision of C. dubliniensis after β cell ablation or antibiotic treatment improves β cell function. These data identify fungi as critical early-life commensals that promote long-term metabolic health.

  PublisherOA PDFDOI

• A capsular polysaccharide from a healthy human microbiota member activates a Lag-3-NK cell axis to restrain colon cancer and augment immunotherapy

  Cell Reports · 2025-08-23 · 5 citations

  articleOpen access1st authorCorresponding

  Colorectal cancer (CRC) is increasing globally, making identification of preventative measures necessary. Transplantation of the microbiota from CRC and non-CRC patients into mice demonstrates that non-diseased individuals possess organisms that reduce tumor formation and highlights Bacteriodes uniformis as protective. B. uniformis is reduced in humans with CRC, and proactive treatment with B. uniformis slows tumor growth in mice. Natural killer (NK) cells, but not T cells, are required for B. uniformis-mediated protection. CRC is recalcitrant to immunotherapies; however, addition of B. uniformis restores response to α-CTLA-4 treatment in an NK cell-dependent manner. We report that high Lag-3 expression is associated with greater survival in CRC patients and that B. uniformis-mediated protection is reliant on Lag-3 in innate cells. Induction of NK cell activity and reduced tumor growth is dependent on a specific B. uniformis capsular polysaccharide. Thus, healthy individuals possess tumor suppressor microbes that prevent cancer development and can be harnessed therapeutically.

  PublisherDOI

• Clec12a controls colitis by tempering inflammation and restricting expansion of specific commensals

  Cell Host & Microbe · 2025-01-01 · 6 citations

  articleOpen access
  PublisherOA PDFDOI

• Draft genome of a human-derived <i>pks+ E. coli</i> that caused spontaneous disseminated infection in a mouse

  Microbiology Resource Announcements · 2024-06-04

  articleOpen access1st authorCorresponding

  ABSTRACT We present the draft genome of a novel human-derived Escherichia coli strain isolated from a healthy control human microbiota that, when put into a mouse, spontaneously disseminated from the gut to the kidneys.

  PublisherDOI

Frequent coauthors

• Bart C. Weimer

  University of California, Davis

  28 shared

• June L. Round

  Huntsman Cancer Institute

  18 shared

• Andrea K. Townsend

  Hamilton College

  14 shared

• Bihua C. Huang

  University of California, Davis

  14 shared

• Conor C. Taff

  Cornell University

  14 shared

• W. Zac Stephens

  University of Utah

  12 shared

• Walter M. Boyce

  University of California, Davis

  12 shared

• Barbara A. Byrne

  University of California, Davis

  12 shared

Education

• B.A.

  Lewis & Clark College

• Ph.D.

  University of California, Davis

• Other

  University of Utah Spencer Fox Eccles School of Medicine, Huntsman Cancer Institute