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Inflammatory cell death in systemic lupus erythematosus

Award Number: R21AR085967
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 04/30/2028

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Inflammatory cell death in systemic lupus erythematosus - PROJECT SUMMARY/ABSTRACT Cell death plays a central role in the pathogenesis and exacerbations of systemic lupus erythematosus (SLE). Many of the best recognized autoantigens in SLE are intracellular nucleic acid-binding proteins, some of them located in the cell nucleus. While early work focused on apoptosis, the first known form of programmed cell death, attention has shifted in recent year to several more inflammatory types of programmed cell death resulting in exposure of cellular contents together with alarmins, danger signals, and damage-associated molecular patterns (DAMPs), which stimulate antigen-presenting cells to provoke a much stronger immune response. Inflammatory modes of cell death include NETosis, pyroptosis, ferroptosis, and necroptosis. These newer inflammatory pathways of cell death have been proposed to be important in SLE, but it is not known if they even occur in patients. Progress is hampered by a lack of established assays for measuring their occurrence in vivo in patients. We will use targeted, as well as unbiased, approaches to establish assays (biomarkers) that can selectively measure the presence of pyroptosis, necroptosis, and ferroptosis in patient blood samples (compared to NETosis). In brief, neutrophils and monocytes will be induced to undergo programmed inflammatory cell death and cellular and soluble constituents analyzed by microscopy, ELISA, and mass spectrometry. Our preliminary data suggest that ferroptosis is much increased in neutrophils from SLE patients. Ferroptosis will be assessed using fluorescent markers of lipid peroxides and iron accumulation and the degree of ferroptosis will be related to demographics, sex, and clinical phenotype, including disease activity. Levels of soluble ferroptosis biomarkers will be assessed by ELISA and associated with neutrophil ferroptosis as well as with clinical markers of disease activity. This is a high-risk, but high-reward proposal: a reliable quantification of the inflammatory programmed cell death pathways pyroptosis, ferroptosis, and necroptosis would have significant utility as biomarkers for patient stratification and to fill gaps in our understanding of the molecular pathology of SLE. These biomarkers would have similar utility in many additional autoimmune and autoinflammatory conditions. At present, these cell death pathways are well defined in vitro, but their presence in vivo remains a black box.


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 = $412,569 )
2026	2026	UNIVERSITY OF WASHINGTON	4333 BROOKLYN AVE NE	SEATTLE	WA	98195	KING	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	4/22/2026	NEW	$412,569
														Subtotal = $412,569

Grand Total All Awards = $412,569

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Inflammatory cell death in systemic lupus erythematosus

Award Number: R21AR085967

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 04/30/2028

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