# Myeloid Cell Signaling in Allergic Asthma

> **NIH NIH P20** · LOUISIANA STATE UNIV A&M COL BATON ROUGE · 2021 · $259,000

## Abstract

Project Summary 
Allergic asthma affects over half of the 24 million asthmatics in the United States. Interleukins 4 (IL4) and 13 
(IL13) are known to play an essential role in the pathogenicity of allergic asthma. Germ-line deletion of their 
common receptor, i.e. Interleukin-4 receptor alpha (IL4Rα), provides complete protection against allergic 
asthma suggesting its indispensable role. Accordingly, pharmacological agents blocking IL4Rα are currently 
under clinical trials for management of human allergic asthma. The responses are, however, not very 
promising, perhaps due to the inefficient targeting of a freshly recruited IL4Rα-bearing cell-type involved in the 
pathogenesis of allergic asthma. This is because the cell-type specific role of IL4Rα-mediated signaling in 
allergic asthma has remained unclear. Identification of a key cell-type that employs IL4Rα-mediated signaling 
in pathogenic manifestation of allergic asthma may, therefore, lead to a more effective therapeutic intervention 
in allergic asthma. The overall objective of this proposal is to delineate the cell-specific role of IL4Rα signaling 
in eosinophil recruitment and allergic asthma and to identify the cellular source and molecular identity of 
soluble and vesicle-bound mediators of allergic inflammation in airspaces (airway and alveolar airspaces). 
Outstanding collaborations have been established with experts, including an asthma specialist, an exosomes 
proteomics specialist, a molecular pathologist, an eosinophil biology expert, and an IL4Rα biology expert. 
Innovative tools, including novel transgenic mouse strains, have been developed that will allow a feasible and 
productive investigation. Our central hypothesis is that myeloid-specific IL-4Rα signaling is essential for 
recruitment of eosinophils and manifestation of allergic asthma-relevant outcomes and that exosomes carry the 
mediators of eosinophil recruitment. This hypothesis will be tested under three specific aims. Aim 1 will Test 
the hypothesis that myeloid IL4Rα is essential for eosinophil recruitment; in Aim 2 we will Test the hypothesis 
that myeloid-IL4Rα is essential for allergic asthma outcomes in a mixed allergen challenge model. The findings 
from our studies will have a transformative impact on our mechanistic understanding of the pathophysiology of 
allergic asthma. Eventually, our findings may be applied towards the development of cell-specific therapeutics 
against allergic airway and other eosinophilic disorders.

## Key facts

- **NIH application ID:** 10078643
- **Project number:** 5P20GM130555-03
- **Recipient organization:** LOUISIANA STATE UNIV A&M COL BATON ROUGE
- **Principal Investigator:** Yogesh Saini
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $259,000
- **Award type:** 5
- **Project period:** 2019-01-02 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10078643

## Citation

> US National Institutes of Health, RePORTER application 10078643, Myeloid Cell Signaling in Allergic Asthma (5P20GM130555-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10078643. Licensed CC0.

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