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Generation & Regulation of Tfh13 cells that drive Pathogenic IgE in Allergy

Award Number: R01AI187460
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: 11/12/2024
PERIOD OF PERFORMANCE END DATE: 10/31/2029

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Generation & Regulation of Tfh13 cells that drive Pathogenic IgE in Allergy - Abstract: Allergies to food and environmental antigens have steeply grown to epidemic proportions. One key determinant of IgE-mediated clinical symptoms is the high-affinity of the IgE antibody for a given allergen which we will refer to as “pathogenic IgE”. A life-threatening complication associated with pathogenic IgE mediated allergic reaction is anaphylaxis, which can lead to the death of otherwise healthy individuals, including children. Follicular helper T cells (Tfh), but not Th2 effector cells, are primarily responsible for directing the affinity, longevity and isotype of antibody produced by B cells, including IgE. The nature of the Tfh cells that drive high-affinity, pathogenic IgE to allergens was unclear. We recently discovered that allergens drive the differentiation of a novel Tfh cell subset namely Tfh13 cells in addition to canonical Tfh2 cells. Tfh13 cells co-produce IL-4 and IL-13, express low levels of IL-21 and are absolutely required for allergen-specific pathogenic IgE production. Importantly, Tfh13 cells are found in patients with food or respiratory allergies but not in healthy individuals. Despite the importance of Tfh13 cells in allergies, currently little is known about how Tfh13 cells differentiate during allergic sensitization. While Tfh2 cells are elicited in response to vaccinations, viral infections, and almost all type 2 responses, Tfh13 cells are specifically generated in allergic disease states. This highlights the existence of vital signals during sensitization that foster Tfh13 cell differentiation, with the possibility of conflicting signals in non-allergic contexts. The goal of our proposal is to fill these gaps in knowledge and thereby elucidate pathways that lead to Tfh13 cell differentiation. The overarching hypothesis that our proposal aims to test is that Tfh2 cells and Tfh13 cells have distinct immunological requirements for their differentiation. We have developed tools including cell specific knockout mice to 1) determine the role of non-conventional antigen presenting cells in promoting Tfh13 cell differentiation to allergens and 2) elucidate the how the balance of type II cytokines and their inhibitory signals determine the Tfh2 versus Tfh13 cell fate decision. The broad impact of our studies could be substantial, enabling the elucidation of the cell extrinsic and intrinsic pathways of Tfh13 cell differentiation that could be leveraged to curtail allergic disease.


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 = $586,250 )
2026	2026	UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL	55 LAKE AVE N	WORCESTER	MA	01655	WORCESTER	USA	Allergy and Infectious Diseases Research	000	2	11/25/2025	NON-COMPETING CONTINUATION	$586,250
														Subtotal = $586,250

Issue Date FY: 2025 ( Subtotal = $586,250 )
2025	2025	UNIVERSITY OF MASSACHUSETTS MEDICAL SCHOOL	55 LAKE AVE N	WORCESTER	MA	01655	WORCESTER	USA	Allergy and Infectious Diseases Research	000	1	11/12/2024	NEW	$586,250
														Subtotal = $586,250

Grand Total All Awards = $1,172,500

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Generation & Regulation of Tfh13 cells that drive Pathogenic IgE in Allergy

Award Number: R01AI187460

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: 11/12/2024

PERIOD OF PERFORMANCE END DATE: 10/31/2029

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