ArticleScience translational medicine2016
Filaggrin inhibits generation of CD1a neolipid antigens by house dust mite-derived phospholipase.
Article in Science translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
56 citing papers in PubMed, 88 citations in OpenAlex.
- Article
- Article
- CD1a and Lipids as Mediators of T Cell Activation in the Skin.The Journal of investigative dermatology · 2025Review
- Langerhans cells: Central players in the pathophysiology of atopic dermatitis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Review
- CD1a and skin T cells: a pathway for therapeutic intervention.Clinical and experimental dermatology · 2024Review
- Human Skin T Cells Express Conserved T-Cell Receptors that Cross-React with Staphylococcal Superantigens and CD1a.The Journal of investigative dermatology · 2024Article
- Keratinocyte-derived small extracellular vesicles supply antigens for CD1a-resticted T cells and promote their type 2 bias in the context of filaggrin insufficiency.Frontiers in immunology · 2024Article
- CD1a and bound lipids drive T-cell responses in human skin disease.European journal of immunology · 2023Review
- CD1-mediated immune responses in mucosal tissues: molecular mechanisms underlying lipid antigen presentation system.Experimental & molecular medicine · 2023Review
- CD1 displays its own negative regulators.Current opinion in immunology · 2023Review
- Group AScience immunology · 2023Article
- Excess filaggrin in keratinocytes is removed by extracellular vesicles to prevent premature death and this mechanism can be hijacked by Staphylococcus aureus in a TLR2-dependent fashion.Journal of extracellular vesicles · 2023Article
- Genetic/Protein Association of Atopic Dermatitis and Tooth Agenesis.International journal of molecular sciences · 2023Review
- Article
- CD1a promotes systemic manifestations of skin inflammation.Nature communications · 2022Article
- Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2022Review
- Phospholipase activity of acyloxyacyl hydrolase induces IL-22-producing CD1a-autoreactive T cells in individuals with psoriasis.European journal of immunology · 2022Article
- Atopic Dermatitis: The Fate of the Fat.International journal of molecular sciences · 2022Review
- A simple assay to quantify mycobacterial lipid antigen-specific T cell receptors in human tissues and blood.PLoS neglected tropical diseases · 2021Article
- PPARdelta in Affected Atopic Dermatitis and Psoriasis: A Possible Role in Metabolic Reprograming.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
22 authors at 3 institutions in 3 countries.
Funding
Abstract
Atopic dermatitis is a common pruritic skin disease in which barrier dysfunction and cutaneous inflammation contribute to pathogenesis. Mechanisms underlying the associated inflammation are not fully understood, and although Langerhans cells expressing the nonclassical major histocompatibility complex (MHC) family member CD1a are known to be enriched within lesions, their role in clinical disease pathogenesis has not been studied. We observed that house dust mite (HDM) allergen generates neolipid antigens presented by CD1a to T cells in the blood and skin lesions of affected individuals. HDM-responsive CD1a-reactive T cells increased in frequency after birth in individuals with atopic dermatitis and showed rapid effector function, consistent with antigen-driven maturation. In HDM-challenged human skin, we observed phospholipase A2 (PLA2) activity in vivo. CD1a-reactive T cell activation was dependent on HDM-derived PLA2, and such cells infiltrated the skin after allergen challenge. Moreover, we observed that the skin barrier protein filaggrin, insufficiency of which is associated with atopic skin disease, inhibited PLA2 activity and decreased CD1a-reactive PLA2-generated neolipid-specific T cell activity from skin and blood. The most widely used classification schemes of hypersensitivity suggest that nonpeptide stimulants of T cells act as haptens that modify peptides or proteins; however, our results show that HDM proteins may also generate neolipid antigens that directly activate T cells. These data define PLA2 inhibition as a function of filaggrin, supporting PLA2 inhibition as a therapeutic approach.
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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.