ArticleImmunology2001
Interleukin (IL)-18 induces Langerhans cell migration by a tumour necrosis factor-alpha- and IL-1beta-dependent mechanism.
Article in Immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 182 citations in OpenAlex.
- IL-1beta-induced Langerhans' cell migration and TNF-alpha production in human skin: regulation by lactoferrin.Clinical and experimental immunology · 2003Trial
- Requirements for Alternative In Vitro and In Silico Skin Models of Irritant and Allergic Contact Dermatitis.Contact dermatitis · 2025Review
- IL-18 favors Th2 responses in sporotrichosis caused by Sporothrix globosa, prolonging the course of the disease.PLoS neglected tropical diseases · 2025Article
- Langerhans cells regulate immunity in adulthood by regulating postnatal dermal lymphatic development.bioRxiv : the preprint server for biology · 2024Article
- Ethylhexadecyldimethylammonium bromide, a quaternary ammonium compound, controls inflammatory response through NRF2 pathway in a human immortalized keratinocyte cell line.Frontiers in toxicology · 2023Article
- Review
- The Inflammatory Response in Human Keratinocytes Exposed to Cinnamaldehyde Is Regulated by Nrf2.Antioxidants (Basel, Switzerland) · 2022Article
- How cell migration helps immune sentinels.Frontiers in cell and developmental biology · 2022Review
- Titanium salts tested in reconstructed human skin with integrated MUTZ-3-derived Langerhans cells show an irritant rather than a sensitizing potential.Contact dermatitis · 2020Article
- Depletion of langerinImmunology · 2020Article
- Nature and kinetics of redox imbalance triggered by respiratory and skin chemical sensitizers on the human monocytic cell line THP-1.Redox biology · 2018Article
- Skin as an immune organ and clinical applications of skin-based immunotherapy.The World Allergy Organization journal · 2018Review
- Tacrolimus Reverses UVB Irradiation-Induced Epidermal Langerhans Cell Reduction by Inhibiting TNF-α Secretion in Keratinocytes via Regulation of NF-κB/p65.Frontiers in pharmacology · 2018Article
- Langerhans Cells: Sensing the Environment in Health and Disease.Frontiers in immunology · 2018Review
- Dendritic cells enter lymph vessels by hyaluronan-mediated docking to the endothelial receptor LYVE-1.Nature immunology · 2017Article
- Electroporation as a vaccine delivery system and a natural adjuvant to intradermal administration of plasmid DNA in macaques.Scientific reports · 2017Article
- NKG2D-dependent activation of dendritic epidermal T cells in contact hypersensitivity.The Journal of investigative dermatology · 2015Article
- The role of interleukin-18 in glioblastoma pathology implies therapeutic potential of two old drugs-disulfiram and ritonavir.Chinese journal of cancer · 2015Article
- Interleukin-1 loop model for pathogenesis of Langerhans cell histiocytosis.Cell communication and signaling : CCS · 2015Review
- Gingiva Equivalents Secrete Negligible Amounts of Key Chemokines Involved in Langerhans Cell Migration Compared to Skin Equivalents.Journal of immunology research · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following skin sensitization a proportion of epidermal Langerhans cells (LC) are stimulated to leave the skin and to migrate, via afferent lymphatics, to draining lymph nodes where they accumulate as immunostimulatory dendritic cells (DC). It has been demonstrated previously that tumour necrosis factor-alpha (TNF-alpha), an inducible product of epidermal keratinocytes, and interleukin (IL)-1beta, produced exclusively by LC in murine epidermis, provide important signals for the initiation of this response. Recently, it has been demonstrated that IL-18, a cytokine produced by both LC and keratinocytes within the epidermis, may also participate in immune responses induced following skin sensitization. In the present investigations, the ability of IL-18 to contribute to the regulation of LC migration and the accumulation of DC in draining lymph nodes has been examined. It was found that, like IL-1beta, IL-18 administered intradermally to mice resulted in a significant reduction in epidermal major histocompatibility complex (MHC) class II+ LC densities and a marked increase in lymph node DC numbers. Using neutralizing anti-TNF-alpha and blocking anti-type I IL-1 receptor (IL-1RI) antibodies, it was shown also that the induction by IL-18 of both LC mobilization and DC accumulation in regional lymph nodes was dependent upon availability of TNF-alpha and the integrity of IL-1RI signalling. Furthermore, using IL-1beta converting enzyme (caspase-1) knockout mice, IL-18-induced LC migration was found to have a mandatory requirement for active IL-1beta. Importantly, not only was IL-18 able to contribute to the regulation of LC migration, it was found to be essential for the manifestation of these processes in response to topical sensitization with the contact allergen oxazolone.
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