# Transcriptional Mechanisms that Catalyze Dysregulated Type 17 Mucosal Inflammation via Innate Lymphoid Cells

> **NIH AI K08** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2026 · $201,744

## Abstract

Chronic inflammatory diseases, such as inflammatory bowel disease, psoriatic arthritis, and lupus, impose a
significant public health burden. Despite our understanding of type 17 immune responses, the mechanisms by
which aberrant type 17 inflammation is triggered and sustained remain unclear. Given the critical role of group
3 innate lymphoid cells (ILC3s) in immune homeostasis, this project aims to define how ILC3s can cause
sustained inflammation and identify the molecular pathways governing this dysregulation. The findings will
provide fundamental insights into immune regulation, to advance understanding of immune-mediated diseases,
and improve therapeutic strategies. Aim 1 will determine the impact of ILC3 abundance on tissue homeostasis
and inflammation by investigating how ILC3s influence T cell numbers, function, and inflammatory programs,
contributing to tissue homeostasis. Aim 2 will define the role of ZBTB transcription factors in ILC3 maintenance
and type 17 inflammation by examining how they regulate ILC3 populations, modulating immune responses
from a homeostatic type 17 program to a pathogenic inflammatory state. To achieve these aims, the project will
leverage a physiologically relevant A20 knock-in mouse model, which develops spontaneous mucosal
inflammation mimicking human disease. The study will integrate in vivo immune profiling, transcriptomic
analysis, and chromatin mapping to uncover how ILC3s contribute to type 17 dysregulation. By elucidating how
ILC3s and transcription factors drive inflammation, this project will uncover key epigenetic and immune
regulatory mechanisms. Furthermore, these studies open up potentially new therapeutic targets for chronic
inflammatory diseases. These findings will provide a foundation for developing novel interventions that restore
immune balance/homeostasis and prevent pathogenic inflammation.
 Dr. Bowman is a clinical research fellow at the University of California, San Francisco. Prior research
training has g

## Key facts

- **NIH application ID:** 11282077
- **Project number:** 1K08AI196236-01
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Christopher John Bowman
- **Activity code:** K08 (R01, R21, SBIR, etc.)
- **Funding institute:** AI
- **Fiscal year:** 2026
- **Award amount:** $201,744
- **Award type:** 1
- **Project period:** 2026-04-15T00:00:00 → 2031-03-31T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11282077

## Citation

> US National Institutes of Health, RePORTER application 11282077, Transcriptional Mechanisms that Catalyze Dysregulated Type 17 Mucosal Inflammation via Innate Lymphoid Cells (1K08AI196236-01). Retrieved via AI Analytics 2026-07-19 from https://api.ai-analytics.org/grant/nih/11282077. Licensed CC0.

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