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Ras signaling in type 1 regulatory T cell development and function during allergic airway inflammation

Award Number: R21AI197492
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: 09/14/2026
PERIOD OF PERFORMANCE END DATE: 08/31/2028

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Ras signaling in type 1 regulatory T cell development and function during allergic airway inflammation - Project Summary / Abstract Allergic asthma affects over 300 million individuals worldwide and continues to rise in prevalence, posing a major public health burden. While anti-inflammatory therapies provide symptomatic relief, they fail to address the underlying immune dysregulation that drives disease progression. Allergic airway inflammation is characterized by elevated levels of inflammatory cytokines, particularly those produced by Th2 and Th17 cells. These pro-inflammatory responses are counter-regulated by immune cells with suppressive functions., including Foxp3+ regulatory T (Treg) cells and Foxp3⁻ IL-10⁺ type 1 regulatory (Tr1) cells. While the biology of Treg cells is relatively well understood, little is known about the intracellular signaling pathways that regulate the development and function of Tr1 cells. Tr1 cells are emerging as potent component in immunomodulatory therapy of allergic inflammation. While the biology of Treg cells is relatively well understood, very little is known about the intracellular signaling pathways that regulate the development and function of Tr1 cells. Understanding the mechanisms governing Tr1 cell development, maintenance, and function is critical for developing strategies to expand and sustain these regulatory cells for immunotherapeutic use in treating allergic airway inflammation. Our research has identified the Ras signaling pathway as a central regulator of Tr1 cell development and maintenance. Based on our findings, we hypothesize that Ras signaling orchestrates transcriptional and effector programs in Tr1 cells that can be leveraged for therapeutic benefit in allergic airway inflammation. We will test this hypothesis through two specific aims: (1) define the role and downstream effectors of Ras signaling in murine and human Tr1 cell transcriptional programming and development, and (2) determine the impact of Ras activation on Tr1 function in vitro and in a mouse model of allergic asthma. Using dual-reporter mice, primary murine and human T cells, retroviral tools, and a house dust mite (HDM)-induced asthma model, we will dissect the molecular and functional impact of Ras signaling on Tr1 cells. This work is conceptually innovative in revealing a new immune regulatory role for Ras, technically innovative in its use of precision genetic and signaling tools in primary T cells, and translationally innovative in exploring a path toward Ras-enhanced Tr1 cell-based therapies. Findings from this R21 will provide critical insight into the mechanisms controlling Tr1 cell biology and lay the groundwork for future immunotherapies for allergic and other inflammatory diseases.


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 = $187,500 )
2026	2026	LOUISIANA STATE UNIVERSITY	202 HIMES HALL	BATON ROUGE	LA	70803	EAST BATON ROUGE	USA	Allergy and Infectious Diseases Research	000	1	9/18/2026	NEW	$187,500
														Subtotal = $187,500

Grand Total All Awards = $187,500

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Ras signaling in type 1 regulatory T cell development and function during allergic airway inflammation

Award Number: R21AI197492

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: 09/14/2026

PERIOD OF PERFORMANCE END DATE: 08/31/2028

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