From reductionist mechanisms to models of autoimmunity in humans

We combine human skin cohorts, spatial and single-cell genomics, perturbation, and regulatory modeling to understand the stromal, mesenchymal, and immune-cell interactions that drive autoimmune reactions.

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Spatial transcriptomics of human skin — MMP9+ myeloid cells and LYVE1+ populations at the epidermal-dermal boundary

What we work on

Skin as a human model of autoimmunity and autoinflammatory conditions

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Spatial tissue panels comparing psoriasis, dermatomyositis, and cutaneous lupus samples

Comparative disease biology

Why compare across autoimmune skin diseases?

Inflammatory skin diseases often reuse overlapping cytokine pathways and immune-cell and tissue-cell states, but differ in where, when, and in which cells those programs are activated. This can produce overlapping clinical or histologic patterns—as in atopic dermatitis and allergic contact dermatitis, psoriasis and psoriasiform cutaneous lupus, or dermatomyositis and cutaneous lupus—even when triggers and treatment responses differ. Comparing diseases helps separate shared inflammatory circuits from disease-defining mechanisms.

Heatmap of gene expression responses to PBS, IFN-gamma, IFN-beta, and TNF-alpha stimulation

Cytokine response atlas

Which cells are responding, and to what signals?

We build a cell-type-specific response atlas by exposing primary human skin cells and ex vivo tissue to defined cytokines. We then use these reference programs to resolve disease signatures into their likely cellular and signaling components.

Response QTL plot showing genotype-dependent gene expression change from PBS to IFN-gamma stimulation

Genetics of cytokine response

Do genetic variants change how cells respond?

Many inflammatory and autoimmune skin diseases are polygenic. As part of the IGVF Consortium, we integrate genotyping with RNA-seq, ATAC-seq, and H3K27ac profiling to map response QTLs—variants whose regulatory effects emerge or change after cytokine stimulation. In melanocytes, this approach has implicated loci near ERAP2 and HLA-DRB5 in IFN-γ-induced antigen-presentation programs.IGVF Consortium

Nature Immunology Volume 27 Issue 6 cover for keratinocyte-fibroblast circuits in photosensitive autoimmunity

A spatially coordinated keratinocyte-fibroblast circuit recruits MMP9+ myeloid cells to drive type I interferon-driven inflammation in photosensitive autoimmunity.

Wang Y, Afshari K, Haddadi NS, Lopes CS, Eng CL, Whiteman LM, Martinez N, Kyawe PP, Anufrieva KS, Wei K, Frieda K, Rosenbach M, Vleugels RA, Gallucci S, Harris JE, Rashighi M, Garber M.

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August 2026Award

LEO Foundation Research Grant to continue the photosensitivity work

The LEO Foundation awarded DKK 61.9 million across 16 international skin research projects, ours among them, supporting continued study of photosensitive skin reactions.

LEO Foundation announcement

May 2026People

Yuqing Wang graduated

Yuqing defended her thesis on the mechanisms of photosensitivity in autoimmune skin disease, and is now a Bioinformatics Scientist at New England Biolabs.

April 2026Paper

Our photosensitivity paper is out in Nature Immunology, with the cover

A spatially coordinated keratinocyte-fibroblast circuit recruits MMP9+ myeloid cells to drive IFN-I-driven inflammation in photosensitive autoimmunity.

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