About

Professor Bana Jabri is a world-renowned paediatrician and immunologist specializing in the study of autoimmune and inflammatory diseases. She is trained in France and began her career at the Hôpital Necker-Enfants malades in Paris. She later joined the University of Chicago, where she became a full professor in 2005 and was awarded the Sara and Harold Lincoln Thompson Chair of Immunology and Medicine in 2018. Her work has focused on mucosal immunity and celiac disease, earning her numerous awards for scientific excellence. In Chicago, she directed centers for digestive diseases, coeliac diseases, and human immunology. She is returning to the paediatric campus to become Director of the Institut Imagine on 1 January 2025 for a 5-year term. Her appointment aims to broaden understanding of genetic diseases, improve treatments, and foster international collaboration, youth and diversity, ethics and patient involvement, and a holistic approach to genetic diseases. She emphasizes the importance of technological innovation, collaboration with academic, medical, and industrial partners, and inspiring the next generation of scientists and researchers.

Research topics

• Biology
• Medicine
• Immunology
• Endocrinology
• Pathology
• Cell biology
• Microbiology

Selected publications

• immgenT: A Comprehensive Reference of Convergent T-cell States in the Mouse

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-02

  articleOpen access

  Abstract The immgenT collaborative project generated a comprehensive molecular atlas of T cells spanning virtually all mouse organs and disease states, profiling ∼800,000 cells from 750 samples with RNA, 128-plex surface protein, and αβTCR sequence. Applying a deep generative model to joint RNA and protein data defined a finite landscape of T-cell states organized into eight lineages and 110 robust clusters, integrating identical cells from different contexts, and resolving prior nomenclatures. Analysis of effector molecules, transcription factors and modules showed that both immunological functions and regulatory programs are shared across cell states. This framework provides a stable, reusable reference, demonstrated by computationally integrating 16 external datasets from diverse biological contexts. A set of public web tools supports browsing of these data, allows mapping of any dataset onto the immgenT framework. These results propose a molecular classification of T cells organized around a set of shared states reused across immunological contexts.

  PublisherDOI

• Mammary intraepithelial lymphocytes and intestinal inputs shape T cell dynamics in lactogenesis

  Nature Immunology · 2025-07-29 · 7 citations

  articleOpen access
  PublisherOA PDFDOI

• A dendritic cell population responsible for transglutaminase 2-mediated gluten antigen presentation in celiac disease

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-05

  preprintOpen access

  Abstract In celiac disease (CeD), a gluten-dependent autoimmune disorder, transglutaminase 2 (TG2) deamidates selected glutamine residues in gluten peptides, while HLA-DQ2 presents deamidated antigens to inflammatory T cells. The cellular sources of pathogenic TG2 and DQ2 are unclear. Using chemical biology tools, we show that intestinal CD103 + dendritic cells (DCs) couple cell-surface TG2 to the endocytic LRP1 receptor to simultaneously deamidate gluten antigens and concentrate them in lysosomes. In DQ2-transgenic mice, CD103 + DCs loaded with deamidated antigens migrate from intestinal lamina propria and Peyer’s patches into mesenteric lymph nodes, where they engage T cells. In turn, gluten antigen presentation upregulates intestinal TG2 activity. The tool (HB-230) used to establish a role of CD103 + DCs in gluten antigen presentation and TG2 activation in mice also revealed that the TG2/LRP1 pathway is active in human CD14 + monocytes. Within this population of circulating monocytes, a DC subset with the gut-homing β7-integrin marker is elevated in CeD patients with active disease compared to non-celiac controls or patients on a gluten-free diet. Our findings not only inform the cellular basis for gluten toxicity in CeD but they also highlight the immunologic role of an enigmatic protein of growing therapeutic relevance in CeD and other immune disorders.

  PublisherOA PDFDOI

• A dendritic cell population responsible for transglutaminase 2–mediated gluten antigen presentation in celiac disease

  JCI Insight · 2025-08-28 · 2 citations

  articleOpen access

  In celiac disease (CeD), a gluten-dependent autoimmune disorder, transglutaminase 2 (TG2), deamidates selected glutamine residues in gluten peptides, while HLA-DQ2 presents deamidated antigens to inflammatory T cells. The cellular sources of pathogenic TG2 and DQ2 are unclear. Using chemical biology tools, we show that intestinal CD103+ dendritic cells (DCs) couple cell-surface TG2 to the endocytic LRP1 receptor to simultaneously deamidate gluten antigens and concentrate them in lysosomes. In DQ2-transgenic mice, CD103+ DCs loaded with deamidated antigens migrate from intestinal lamina propria and Peyer's patches into mesenteric lymph nodes, where they engage T cells. In turn, gluten antigen presentation upregulates intestinal TG2 activity. The tool (HB-230) used to establish a role of CD103+ DCs in gluten antigen presentation and TG2 activation in mice also revealed that the TG2/LRP1 pathway is active in human CD14+ monocytes. Within this population of circulating monocytes, a DC subset with the gut-homing β7-integrin marker is elevated in patients with CeD with active disease compared with nonceliac controls or patients on a gluten-free diet. Our findings not only inform the cellular basis for gluten toxicity in CeD, but they also highlight the immunologic role of an enigmatic protein of growing therapeutic relevance in CeD and other immune disorders.

  PublisherOA PDFDOI

• A myeloid Tet2-IL-1β axis modulates intestinal inflammation by restricting catecholaminergic stimulation of enterochromaffin cell differentiation

  Immunity · 2025-11-01 · 2 citations

  articleSenior author
  PublisherDOI

• Immunoglobulin A controls intestinal virus colonization to preserve immune homeostasis

  Cell Host & Microbe · 2025-03-29 · 11 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• HDAC5 regulates the activation of cytotoxic CD8+ T cells 4190

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description We are witnessing a significant increase in complex T cell-mediated immune disorders, such as food allergies and autoimmune disease. This trend suggests that the activation threshold for T cells may be altered, and understanding how to modulate this threshold has profound implications for disease treatment. In this study, we demonstrate that the effector program of CD8? T cells (including naïve, circulating memory, and tissue-resident cells) induced by TCR and cytokine stimulation is regulated by the class II histone deacetylase, HDAC5. HDAC5 exhibits little to no deacetylase activity against histone tails, but can function in the cytoplasm as a scaffolding protein or to directly deacetylate protein targets. Using small interfering RNA (siRNA) in cell lines of primary human CD8+ cytotoxic intraepithelial lymphocytes (IE-CTLs), we show that the loss of HDAC5 decreases their activation. Furthermore, inhibiting HDAC5 activity with the HDAC4/5 inhibitor LMK235 reduces the activation potential of ex vivo isolated human intestinal IE-CTLs following stimulation, suggesting that HDAC5 enzymatic activity is required for this effect. Finally, our data indicate that HDAC5 inhibition broadly impacts CD8? T cell activation, including in circulating memory and naïve subsets. This work identifies HDAC5 as a critical enzyme regulating the activation of CD8? T cells and highlights the potential of targeting HDAC5 to modulate CD8? T cell activation thresholds in inflammatory disorders. Funding Sources Supported by NIH BIBIB 2 T32 EB 9412; NSF Graduate Research Fellowship Program; University of Chicago Celiac Disease Research Center. Topic Categories Immune Response Regulation: Molecular Mechanisms (IRM)

  PublisherOA PDFDOI

• Genomic specificity of anti-mouse TCR mAbs determined by single-cell RNAseq

  The Journal of Immunology · 2025-08-01

  articleOpen access

  T cells play a pivotal role in the immune system, relying on their somatically rearranged T cell receptor (TCR) to recognize peptide-MHC complexes. A comprehensive and extensively used set of monoclonal antibodies (mAbs) against TCR variable regions was generated in the previous century. The separate identification of mAb-specific TCR-V proteins and TRV genes has resulted in multiple nomenclatures, making their relationships unclear. To formally re-establish this link and determine patterns of reactivity within TRV subfamilies, we sorted T cells from C57BL/6 mice positive for any one of a panel of 22 anti-V mAbs and determined their TRV genes by single-cell TCRseq. RNAseq data revealed consistently higher expression of repeated elements from the ERV1-family LTR RLTR6Mm (mapping to Gm20400) in cells utilizing TRBV segments encoded within a 66 kb genomic region between TRBV23 and TRBV30. Our findings provide a comprehensive resource for anti-mouse TCR mAb specificity and insight into V-gene usage biases and T cell function.

  PublisherOA PDFDOI

• Author response: Microbes with higher metabolic independence are enriched in human gut microbiomes under stress

  2025-05-16

  peer-reviewOpen access

  Higher biosynthetic capacity of gut microbes in individuals diagnosed with noncommunicable diseases or taking antibiotics suggests that diversity loss and 'dysbiosis' result from microbiome restructuring in response to ecosystem disruption.

  PublisherDOI

• Microbes with higher metabolic independence are enriched in human gut microbiomes under stress

  eLife · 2025-05-16 · 5 citations

  articleOpen access

  A wide variety of human diseases are associated with loss of microbial diversity in the human gut, inspiring a great interest in the diagnostic or therapeutic potential of the microbiota. However, the ecological forces that drive diversity reduction in disease states remain unclear, rendering it difficult to ascertain the role of the microbiota in disease emergence or severity. One hypothesis to explain this phenomenon is that microbial diversity is diminished as disease states select for microbial populations that are more fit to survive environmental stress caused by inflammation or other host factors. Here, we tested this hypothesis on a large scale, by developing a software framework to quantify the enrichment of microbial metabolisms in complex metagenomes as a function of microbial diversity. We applied this framework to over 400 gut metagenomes from individuals who are healthy or diagnosed with inflammatory bowel disease (IBD). We found that high metabolic independence (HMI) is a distinguishing characteristic of microbial communities associated with individuals diagnosed with IBD. A classifier we trained using the normalized copy numbers of 33 HMI-associated metabolic modules not only distinguished states of health vs IBD, but also tracked the recovery of the gut microbiome following antibiotic treatment, suggesting that HMI is a hallmark of microbial communities in stressed gut environments.

  PublisherDOI

Recent grants

• Viral infections and celiac disease pathogenesis

  NIH · $5.4M · 2014–2024

• Transcriptional Regulation of Innate-Like T Cells

  NIH · $8.6M · 2022–2027

• Localizing Pathogenically Relevant Transglutaminase 2 in Celiac Disease

  NIH · $1.8M · 2021–2026

• Innate and adaptive immunity in celiac disease

  NIH · $8.5M · 2005–2025

• NIH Grant R01DK058727

  NIH · $2.4M · 2011

Frequent coauthors

• Christophe Cellier

  Université Paris Cité

  98 shared

• Nicole Brousse

  Hôpital Necker-Enfants Malades

  93 shared

• Claude Matuchansky

  Sorbonne Paris Cité

  91 shared

• A. Murat Eren

  Carl von Ossietzky Universität Oldenburg

  63 shared

• Éric Delabesse

  Centre Hospitalier Universitaire de Toulouse

  60 shared

• R Modigliani

  Hôpital Saint-Louis

  55 shared

• Nadine Cerf‐Bensussan

  Université Paris Cité

  54 shared

• Virginie Verkarre

  Hôpital Européen Georges-Pompidou

  51 shared

Awards & honors

• Sara and Harold Lincoln Thompson Chair of Immunology and Med…