ArticleImmunity2024
Skin immune-mesenchymal interplay within tertiary lymphoid structures promotes autoimmune pathogenesis in hidradenitis suppurativa.
Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Mature tertiary lymphoid structures in pilonidal sinus disease.JID innovations : skin science from molecules to population health · 2026Article
- Review
- Regulatory T cells in the skin: Origin, function, and plasticity.JID innovations : skin science from molecules to population health · 2026Review
- Spatial transcriptomics maps early B-cell and T-cell activation in hidradenitis suppurativa.The Journal of investigative dermatology · 2026Article
- Integrated Proteogenomics and Single-Cell Transcriptomics Prioritize Putative Protective Plasma Proteins for Hidradenitis Suppurativa.Experimental dermatology · 2026Article
- Single-cell spatial profiling identifies a mucosal-like epithelial signature in Hidradenitis suppurativa tunnels.JCI insight · 2026Article
- Tertiary Lymphoid Structure: A Potential Therapeutic Target Affecting Immune Response in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2026Review
- Modeling development of tertiary lymphoid structures in pulmonary tuberculosis by 3D profiling and trajectory analysis.bioRxiv : the preprint server for biology · 2026Article
- A phenotype-to-mechanism framework links phenome-wide comorbidity architecture to molecular mechanisms and therapeutic discovery in complex diseases.medRxiv : the preprint server for health sciences · 2026Article
- Local IgG autoantibody profiles in hidradenitis suppurativa and their associations with disease features and anti-TNF therapy.JID innovations : skin science from molecules to population health · 2026Article
- A skin colonizer disrupts inflammatory and humoral immune defenses in hidradenitis suppurativa.EMBO molecular medicine · 2026Article
- Single-cell spatial transcriptomic analysis of human skin anatomy.Nature genetics · 2026Article
- Disease context dictates the cellular targets of IL-17 in inflammatory skin disease.bioRxiv : the preprint server for biology · 2026Article
- Adalimumab Treatment Modulates Vascular Changes in Hidradenitis Suppurativa Lesions in a Sex-Dependent Manner.Biomedicines · 2026Article
- IgA autoantibodies promote inflammation, Th17 polarization and fibrotic responses in hidradenitis suppurativa.Nature communications · 2026Article
- When Checkpoint Inhibitors Break Barriers: Mechanisms and Challenges of irAEs of the Skin, Gastrointestinal Tract, and Lung.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Review
- Advances in Bioprinting to Model Immune-Mediated Skin Diseases.Advanced healthcare materials · 2026Review
- Recent Advances in Microfluidic Chip Technology for Laboratory Medicine: Innovations and Artificial Intelligence Integration.Biosensors · 2026Review
- Indolent primary cutaneous B-cell lymphomas resemble persistent antigen reactions without signs of dedifferentiation.Nature communications · 2026Article
- Personalized Models of Biological Barriers and Their Diseases: Recent Progress with Organs-On-Chips.Advanced biology · 2026Review
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26 authors.
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Abstract
Hidradenitis suppurativa (HS) is a chronic, debilitating inflammatory skin disease characterized by keratinized epithelial tunnels that grow deeply into the dermis. Here, we examined the immune microenvironment within human HS lesions. Multi-omics profiling and multiplexed imaging identified tertiary lymphoid structures (TLSs) near HS tunnels. These TLSs were enriched with proliferative T cells, including follicular helper (Tfh), regulatory (Treg), and pathogenic T cells (IL17A+ and IFNG+), alongside extensive clonal expansion of plasma cells producing antibodies reactive to keratinocytes. HS fibroblasts express CXCL13 or CCL19 in response to immune cytokines. Using a microfluidic system to mimic TLS on a chip, we found that HS fibroblasts critically orchestrated lymphocyte aggregation via tumor necrosis factor alpha (TNF-α)-CXCL13 and TNF-α-CCL19 feedback loops with B and T cells, respectively; early TNF-α blockade suppressed aggregate initiation. Our findings provide insights into TLS formation in the skin, suggest therapeutic avenues for HS, and reveal mechanisms that may apply to other autoimmune settings, including Crohn's disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.