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Resident Memory T cells in the Pathology of Kidney Disease during Autoimmunity

Award Number: K01DK146251
ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP
PERIOD OF PERFORMANCE START DATE: 04/01/2026
PERIOD OF PERFORMANCE END DATE: 03/31/2031

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Resident Memory T cells in the Pathology of Kidney Disease during Autoimmunity - PROJECT SUMMARY/ABSTRACT Kidney disease contributes greatly to the elevated morbidity and mortality of women with systemic lupus erythematosus (SLE), a systemic autoimmune disorder. The problem of kidney disease is twofold. It is not only a direct health burden but also contributes to the progression of hypertension and cardiovascular disease (CVD), which is the leading cause of death in SLE patients. Over 50% of SLE patients have lupus nephritis, a specific kidney disease of SLE, and roughly half of SLE patients have hypertension. Therapeutic regimens for SLE often cause further kidney injury and worsen hypertension, which is already poorly controlled in this population. Because kidney disease contributes directly to patient morbidity and mortality and also worsens the development of hypertension and CVD, a better understanding of the pathological processes at work within the kidneys is necessary. Circulating autoimmune cells have been the focus of many basic and clinical studies, but the role of kidney resident memory T cells (TRMs) and inflammation within the kidney remains poorly understood. Thus, the central goal of this proposal is to identify the contributions of TRMs to kidney inflammation and hypertension in order to improve future care for SLE patients. Past research has broadly focused on CD4+ vs CD8+ T cell distinctions and various circulating cytokines as causal factors in SLE, but studies investigating the role of TRMs in the pathology of SLE-associated inflammation and hypertension are lacking. TRMs by nature exist entirely within a tissue through adhesion to epithelial cells like kidney tubular cells, which TRMs then target with lytic granules and other pro-inflammatory cytokines, causing kidney inflammation. Thus, in this proposal, specific aim 1 will test the hypothesis that TRMs directly mediate glomerular inflammation and injury in SLE through pro-inflammatory cytokine production. Recent research in the DOCA-salt model of hypertension highlighted CD8+ T cells' ability to upregulate tubular sodium transporters and mediate hypertension. Because similar mechanisms may be at work in SLE, Specific aim 2 will test the hypothesis that kidney TRMs mediate SLE-associated hypertension by augmenting renal tubular sodium reabsorption. Specific aim 3 will test the hypothesis that renal tubule derived molecules, namely CD155, IL-15, and TGF-β stimulate kidney TRM differentiation and activation in SLE. Dr. Moore will receive new training in techniques including T cell co-culturing with kidney cells and blood pressure radiotelemetry implantation and analysis and will gain additional experience in immunological and kidney injury analyses in the NZBWF1 female mouse model of SLE. The experiments and goals of this proposal will shed light on the mechanisms by which TRMs mediate kidney inflammation and hypertension in SLE and will provide Dr. Moore with the professional development, technical experience, and key hypothesis-generating data he will need to transition into an independent academic scientist investigating the contributions of the immune system to cardiovascular and kidney 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 = $158,609 )
2026	2026	UNIVERSITY OF ALABAMA AT BIRMINGHAM	701 S 20TH STREET	BIRMINGHAM	AL	35294	JEFFERSON	USA	Diabetes, Digestive, and Kidney Diseases Extramural Research	000	1	3/19/2026	NEW	$158,609
														Subtotal = $158,609

Grand Total All Awards = $158,609

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Resident Memory T cells in the Pathology of Kidney Disease during Autoimmunity

Award Number: K01DK146251

ORGANIZATION: NATIONAL INSTITUTE OF DIABETES & DIGESTIVE & KIDNEY DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: TRAINING/TRAINEESHIP

PERIOD OF PERFORMANCE START DATE: 04/01/2026

PERIOD OF PERFORMANCE END DATE: 03/31/2031

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