Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

Decoding the neuroimmune control of cutaneous gamma/delta cell function in allergic immunity

Award Number: R01AI195674
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 02/09/2026
PERIOD OF PERFORMANCE END DATE: 01/31/2031

Group Awards By:

View Award Description

Decoding the neuroimmune control of cutaneous gamma/delta cell function in allergic immunity - Project Abstract Allergic diseases result from dysregulated Type-2 immune responses to environmental allergens, with sensory neurons playing a key role in both allergen detection and immune activation. Sensory neurons, specifically TRPV1+ peptidergic (PEP) neurons, detect protease allergens, triggering itch and releasing Substance P, which activates dendritic cells to initiate Type-2 immunity. Recent findings reveal a bidirectional neuroimmune circuit involving sensory neurons and a subset of epidermal  T cells, termed GD3s, which produce IL-3. GD3s reside near free nerve endings, where their IL-3 primes Il3ra-expressing PEP1 neurons to enhance allergen detection and promote allergic immunity. Our long-term goal is to elucidate the mechanisms that regulate GD3 maintenance and function in both model organisms and humans. Type-2 immunity depends on feedback loops between sensory and immune cells that amplify allergic inflammation. Our central hypothesis is that sensory neurons not only respond to IL-3, but also sustain murine GD3s and their human counterparts – epidermal  T cells – through ligand-receptor interactions. Supporting this, we find that PEP1 neurons express Ccl8 and Bdnf, while GD3s express the corresponding receptors Ccr8 and Ntrk2, respectively. GD3s depend on Ccr8 for localization and proliferate in response to BDNF, suggesting that neurons actively regulate GD3 positioning and function. Furthermore, we find that human epidermal  T cells share common transcriptional signatures with murine GD3s, suggesting that epidermal  T cells may serve as the human correlate of GD3s. To test our central hypothesis, we will integrate cellular immunology, neurobiology, and molecular biology approaches across three specific aims: (1) Evaluate the chemokine-mediated pathways driving cutaneous GD3 localization, (2) Determine the neuronal factors driving GD3 function, and (3) Identify the human equivalent of GD3 cells. These studies will establish a fundamental understanding of the neuroimmune interactions that drive allergic immune activation, laying the foundation for therapeutic strategies to prevent allergic sensitization, treat chronic itch, and target chronic allergic inflammatory disorders.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $776,034 )
2026	2026	THE GENERAL HOSPITAL CORPORATION	55 FRUIT ST	BOSTON	MA	02114	SUFFOLK	USA	Allergy and Infectious Diseases Research	000	1	2/9/2026	NEW	$776,034
														Subtotal = $776,034

Grand Total All Awards = $776,034

Top

All Categories

About

Search

Reports

Data Submission

Award Information

Decoding the neuroimmune control of cutaneous gamma/delta cell function in allergic immunity

Award Number: R01AI195674

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 02/09/2026

PERIOD OF PERFORMANCE END DATE: 01/31/2031

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer