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Investigating the role of Runx2 in CD8+ T cell persistence during infection

Award Number: F31AI188992
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 11/15/2026
PERIOD OF PERFORMANCE END DATE: 11/14/2027

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Investigating the role of Runx2 in CD8+ T cell persistence during infection - PROJECT SUMMARY CD8+ T cells responding to acute infection can differentiate into effector cells that aid in pathogen clearance or long-lived, self-renewing memory cells. However, in response to chronic infection, the pool of responding T cells persist poorly or enter a state of dysfunction. Therefore, understanding the factors that promote the persistence and enduring function of T cells is critical to improving their response to chronic antigen. Our lab previously found that the transcription factor Runx2 is required for the longevity of CD8+ memory T cell populations after acute Lymphocytic Choriomeningitis Virus (LCMV) infection. However, the mechanism by which Runx2 promotes T cell persistence remains unknown. The overall goal of this proposal is to determine the specific molecular functions of Runx2 in CD8+ T cells responding to infection. Preliminary data suggests that Runx2-deficiency in the context of chronic infection leads to a defect in the self-renewing TCF1+ precursor exhausted population and an inability of responding cells to persist. Evidence also suggests that Runx2 may negatively regulate the expression of its family member, Runx3. As Runx3 is a known repressor of TCF1, we propose a model whereby Runx2 represses Runx3, allowing for the upregulation of TCF1 to promote the self-renewing capacity of CD8+ T cells. To test this hypothesis, we will adoptively transfer cells with perturbed Runx protein expression into recipients followed by acute or chronic LCMV infection. Experiments proposed in Aim 1 will assess binding of and potential competition between Runx2 and Runx3, as well as determine the effects of differential Runx protein activity on the epigenome and transcriptome of CD8+ T cells. To further interrogate the function of Runx2, we will assess and compare the impact of Runx2 activity on the response to both acute and chronic infection in Aim 2. We will also determine the capacity of enforced TCF1 expression to rescue the function of Runx2-deficient cells in both acute and chronic infection. Results of the proposed experiments will establish the binding patterns and specific functions of Runx2 in CD8+ T cells responding to both acute and chronic infection. Further, experiments will examine potential competition between Runx proteins in T cells. Findings generated by the proposed work will provide new insight to the impact of Runx transcription factor activity on the development and function CD8+ T cells responding to infection.


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 = $38,798 )
2026	2026	THE REGENTS OF THE UNIVERSITY OF COLORADO	13001 E 17TH PL STE F428	AURORA	CO	80045	ADAMS	USA	Allergy and Infectious Diseases Research	000	1	5/15/2026	NEW	$38,798
														Subtotal = $38,798

Grand Total All Awards = $38,798

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Investigating the role of Runx2 in CD8+ T cell persistence during infection

Award Number: F31AI188992

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 11/15/2026

PERIOD OF PERFORMANCE END DATE: 11/14/2027

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