# Metabolic regulation of innate lymphoid cell function and airway inflammation

> **NIH NIH K22** · WEILL MEDICAL COLL OF CORNELL UNIV · 2021 · $108,000

## Abstract

PROJECT SUMMARY
My goal is to become a leading investigator in pulmonary immuno-metabolism at a top-tier academic research
institution. This K22 Career Transition Award Application describes my training, career goals, plan for
professional development, and an innovative research project that will put me in the ideal position to launch a
successful independent program. Building off the strong scientific foundation I gained during my graduate and
postdoctoral training, and with the full professional support of my mentor and the research communities here at
Weill Cornell, I have identified new scientific challenges detailed in this application that I will address with
cutting-edge tools and creative approaches. Chronic lung diseases such as asthma affect millions of
Americans and yet current treatments can be ineffective, cause undesired side effects, and treat the symptoms
rather than the cause. There is an urgent need to understand the molecular mechanisms controlling lung
inflammation in order to design novel therapeutic strategies. Recent studies have demonstrated the importance
of Group 2 innate lymphoid cells (ILC2s) in driving chronic lung inflammation including asthma; however, the
mechanisms controlling this pro-inflammatory function are not well understood. In particular, whether ILC2
function is affected by changes in cellular metabolism is poorly understood. The central focus of this K22
Research Plan is to understand the cellular and biochemical mechanisms by which metabolic signals control
innate immune-cell mediated lung inflammation. In new preliminary studies, I found that human and mouse
lung ILC2s express a transcription factor called aryl hydrocarbon receptor (Ahr), which is a well-appreciated
metabolic sensor of environmental-, diet-, and microbial-derived metabolites known to influence lung health
and disease. Strikingly, mice deficient in Ahr had dysregulated ILC2 responses that resulted in protection from
allergen-induced lung inflammation. Furthermore, I found that activation or inhibition of Ahr signaling directly
regulated aspects of ILC2 metabolism, raising the hypothesis that Ahr-mediated changes to bioenergetic
programming may underlie the ability of ILC2s to drive lung inflammation. Using cutting-edge techniques in
metabolic profiling and immunobiology, in this proposal I will dissect the ILC2-Ahr-dependent mechanisms
regulating lung tissue inflammation by investigating (1) How Ahr signaling affects ILC2 development,
proliferation, and function in vitro and in vivo, and (2) how Ahr signaling affects ILC2 bioenergetics and the
development of lung inflammation. Critically, this research project will generate rich metabolomic and
sequencing data sets that will contribute to hypothesis generation for future NIH funding applications. Given my
background training, publication record, grantmanship skills, mentorship experience of trainees, cutting-edge
tools, and an extraordinarily supportive mentorship network, I am ideally-...

## Key facts

- **NIH application ID:** 10075220
- **Project number:** 5K22AI141739-02
- **Recipient organization:** WEILL MEDICAL COLL OF CORNELL UNIV
- **Principal Investigator:** Laurel Anne Monticelli
- **Activity code:** K22 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $108,000
- **Award type:** 5
- **Project period:** 2019-12-19 → 2021-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10075220

## Citation

> US National Institutes of Health, RePORTER application 10075220, Metabolic regulation of innate lymphoid cell function and airway inflammation (5K22AI141739-02). Retrieved via AI Analytics 2026-06-14 from https://api.ai-analytics.org/grant/nih/10075220. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*