# KIF3A in Allergic Inflammation - Atopic Dermatitis to Asthma

> **NIH NIH U19** · CINCINNATI CHILDRENS HOSP MED CTR · 2020 · $251,169

## Abstract

Allergic disorders are a major global health concern affecting 150 million people worldwide. Recently, epithelial
cells have emerged as central participants in the pathogenesis of allergic inflammation. Defining the key
epithelial drivers of the development, persistence, and progression of allergic inflammation is the focus of this
application. Although epithelial cells are increasingly recognized as critical participants in the initiation and
propagation of allergic inflammation, therapies that specifically target the epithelium are lacking. There are
substantial gaps in understanding the mechanisms by which epithelial pathways converge to promote allergic
inflammation that must be filled before interventions can be designed. Our U19 AADCRC proposal is designed
to help fill this critical knowledge gap. We are uniquely poised for the proposed studies because of resources
and collaborations that we have developed over the past 2 decades. Through the synergistic projects, we will
explore the immunological mechanisms, which underpin initiation, persistence, and progression of allergic
disease and provide novel insights into a key unanswered question in the allergy field: Why is allergic
inflammation restricted to one tissue in some cases, while it progresses to involve additional tissues in other
individuals? The projects are:
Project 1 – To elucidate endotypes of AD that are predictive of progression to asthma and dissect the
mechanistic basis of the contribution of epithelial kinesin family member 3A (KIF3A) to allergic inflammation
and disease persistence/progression.
Project 2 – To determine how protease/protease inhibitor imbalance promotes allergic inflammation - dissect
the mechanistic basis by which the epithelial-derived protease inhibitor serine protease inhibitor Kazal-type 7
(SPINK7) promotes allergic inflammation .
Project 3 – To dissect the mechanisms by which a newly described population of mucosal mast cells (MMC9)
that make large amounts of IL-9, IL-13, and mast cell protease 1 (MCPt-1) develops and amplifies allergic
inflammation to promote progression of AD to allergic asthma.
Investigations in this domain will ultimately provide a road map for primary or secondary prevention of
allergic disease. As such, this proposal is highly aligned with the stated programmatic priorities in the
RFA-AI-15-032.

## Key facts

- **NIH application ID:** 10243032
- **Project number:** 3U19AI070235-15S1
- **Recipient organization:** CINCINNATI CHILDRENS HOSP MED CTR
- **Principal Investigator:** Gurjit K. Khurana Hershey
- **Activity code:** U19 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $251,169
- **Award type:** 3
- **Project period:** 2006-07-01 → 2021-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10243032

## Citation

> US National Institutes of Health, RePORTER application 10243032, KIF3A in Allergic Inflammation - Atopic Dermatitis to Asthma (3U19AI070235-15S1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10243032. Licensed CC0.

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