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Identifying signaling networks that contribute to Th17-mediated neuroinflammation

Award Number: R01AI195443
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: 04/01/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2031

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Identifying signaling networks that contribute to Th17-mediated neuroinflammation - Project Summary Multiple Sclerosis (MS), a chronic autoimmune inflammatory disease of the Central Nervous System, affects approximately 2.3 million individuals globally, with nearly 1 million cases in the United States. It is more prevalent in females and typically manifests before the age of 30. Certain T helper 17 (Th17) cell populations are responsible for neuroinflammation and disease progression. However, patients with hyper-IgE syndrome and HIV infection are susceptible to infections due to the diminished Th17 cell count. Developing strategies to preserve Th17 cells while simultaneously blocking those that cause neuroinflammation and MS remains paramount. Transcriptional analyses have unveiled regulators of Th17 pathogenicity that facilitate immunomodulatory programs and promote pro-inflammatory programs. Nevertheless, mRNA measurements may not accurately correlate with protein abundance, and post-translational modifications such as phosphorylation play a crucial role in engaging signaling networks that drive autoimmunity, which are inadequately captured by mRNA-based approaches. To address this, we will develop a comprehensive suite of mass spectrometry proteomics tools to characterize protein abundance and phosphorylation in pathogenic Th17 cells at the systems level in the experimental autoimmune encephalomyelitis (EAE) model of MS. By comprehending the distinctive signaling pathways that distinguish pathogenic Th17 cells from other CD4 subtypes, we can identify potential targets for alleviating Th17-mediated autoimmune diseases while preserving non-pathogenic populations. Our preliminary proteomics and phosphoproteomics data has already identified novel drivers of pathogenic Th17 activity in the EAE model, which will be validated through small molecule inhibition and genetic approaches. In pharmacological studies, we will identify combinations of small molecule inhibitors that target multiple stages of pathogenic Th17s, offering superior protection against EAE disease compared to monotherapies. We will pursue mechanistic studies to elucidate the synergistic effects of targeting multiple pathways simultaneously in reducing EAE disease. The successful completion of this proposal will advance our fundamental understanding of autoimmune mechanisms mediated by Th17 cells and provide preclinical targets that could be utilized for future translational studies as therapeutic interventions for MS or other Th17-driven 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 = $762,086 )
2026	2026	UNIVERSITY OF PITTSBURGH - OF THE COMMONWEALTH SYSTEM OF HIGHER EDUCATION	4200 FIFTH AVENUE	PITTSBURGH	PA	15260	ALLEGHENY	USA	Allergy and Infectious Diseases Research	000	1	3/31/2026	NEW	$762,086
														Subtotal = $762,086

Grand Total All Awards = $762,086

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Identifying signaling networks that contribute to Th17-mediated neuroinflammation

Award Number: R01AI195443

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: 04/01/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2031

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