ArticleeLife2023
Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata.
Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Distinctive T Cell Patterns Defining Lymphocytic Alopecia and Alternate Autoimmune and Stem Cell Pathways, Linked to Pleiotropic Functions of Regulatory T Cells Within iSALT.The American Journal of dermatopathology · 2026Review
- Immunopathogenesis and Experimental Models of Alopecia Areata: From Mechanistic Insights to Translational Platforms.Clinical reviews in allergy & immunology · 2026Review
- Resident T cell activation leads to human hair follicle immune privilege lossFrontiers in medicine · 2026Article
- Hair follicle immune privilege in autoimmune and immune-mediated alopecias: paths toward reestablishing immune tolerance.Frontiers in medicine · 2026Review
- Alopecia areata.Nature reviews. Disease primers · 2025Review
- Preclinical Evidence That Mesoglycan Unfolds Complex Anti-Aging Effects in Photoaged Female Facial Skin.International journal of molecular sciences · 2025Article
- From mechanisms to therapies: current advances breakthroughs in alopecia areata immunopathology.Frontiers in immunology · 2025Review
- Alopecia areata: from immunopathogenesis to emerging therapeutic approaches.Frontiers in immunology · 2025Review
- Pathogenesis of Alopecia Areata and Vitiligo: Commonalities and Differences.International journal of molecular sciences · 2024Review
- Blank Spots in the Map of Human Skin: The Challenge for Xenotransplantation.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we have explored the involvement of innate lymphoid cells-type 1 (ILC1) in the pathogenesis of alopecia areata (AA), because we found them to be significantly increased around lesional and non-lesional HFs of AA patients. To further explore these unexpected findings, we first co-cultured autologous circulating ILC1-like cells (ILC1lc) with healthy, but stressed, organ-cultured human scalp hair follicles (HFs). ILClc induced all hallmarks of AA ex vivo: they significantly promoted premature, apoptosis-driven HF regression (catagen), HF cytotoxicity/dystrophy, and most important for AA pathogenesis, the collapse of the HFs physiological immune privilege. NKG2D-blocking or IFNγ-neutralizing antibodies antagonized this. In vivo, intradermal injection of autologous activated, NKG2D+/IFNγ-secreting ILC1lc into healthy human scalp skin xenotransplanted onto SCID/beige mice sufficed to rapidly induce characteristic AA lesions. This provides the first evidence that ILC1lc, which are positive for the ILC1 phenotype and negative for the classical NK markers, suffice to induce AA in previously healthy human HFs ex vivo and in vivo, and further questions the conventional wisdom that AA is always an autoantigen-dependent, CD8 +T cell-driven autoimmune disease.
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Registered trials
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 OpenQuestion graph.