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Leveraging Human Skin Dendritic Cells to Unravel Immune Mechanisms and Advance Therapies for Skin Inflammation

Award Number: R01AR087006
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: 07/06/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2031

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Leveraging Human Skin Dendritic Cells to Unravel Immune Mechanisms and Advance Therapies for Skin Inflammation - PROJECT ABSTRACT The skin serves as a critical immune barrier, maintaining a delicate balance between protection and tolerance. This equilibrium is orchestrated largely by dendritic cells (DCs), which regulate T cell activation and immune suppression. When DC composition is altered, a break in tolerance may occur, leading to autoimmune inflammation. Psoriasis is a chronic autoimmune inflammatory condition of the skin affecting 125 million people worldwide and exemplifies how DC misbalance fuels chronic T cell activation, with similar mechanisms implicated in cutaneous immune-related adverse effects (irAE) and graft-versus-host disease (GVHD). The skin DC system is comprised of distinct subsets, each with unique receptors for inducing either immune responses or immune tolerance. We have identified a DC subset, which we denote as ‘CD5+ DCs’ that tilts this balance, via CD5, toward autoimmune activation by driving pathogenic T cell responses (CTLs, TH1, TH17, TH22). The CD5+ DCs accumulate in psoriatic lesions, and our central hypothesis is that CD5+ DCs drive autoimmune skin inflammation by forming inflammatory hubs with T cells and thereby disrupting tolerance. We propose that elucidating the differentiation, function, and spatial organization of CD5+ DCs will reveal new strategies to restore immune balance. In Aim 1, we will define molecular pathways governing CD5+ DC differentiation in autoimmunity using transcriptomics, in vitro differentiation assays, and in vivo models. Aim 2 will investigate how CD5+ DCs handle and present antigens to drive autoreactive T cells, and Aim 3 will identify immune pathways regulating CD5+ DC-driven psoriasis by comparing treatment responders and non-responders through spatial proteomics and transcriptomics; we will map interactions between CD5+ DCs, other DC subsets, and inflammatory T cells, with the goal of discovering therapeutic targets. Collectively, by defining how CD5+ DCs contribute to autoimmune inflammation, this work will provide novel insights into DC-driven autoimmunity and guide targeted therapies for psoriasis, immune checkpoint blockade–induced cutaneous inflammation, and other chronic inflammatory 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 = $483,286 )
2026	2026	WASHINGTON UNIVERSITY, THE	1 BROOKINGS DR	SAINT LOUIS	MO	63130	SAINT LOUIS	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	7/7/2026	NEW	$483,286
2026	2026	WASHINGTON UNIVERSITY, THE	1 BROOKINGS DR	SAINT LOUIS	MO	63130	SAINT LOUIS	USA	Arthritis, Musculoskeletal and Skin Diseases Research	001	1	8/11/2026	NEW	$0
														Subtotal = $483,286

Grand Total All Awards = $483,286

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Leveraging Human Skin Dendritic Cells to Unravel Immune Mechanisms and Advance Therapies for Skin Inflammation

Award Number: R01AR087006

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: 07/06/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2031

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