ArticleClinical and experimental immunology2005
The role of interleukin-16 in murine contact hypersensitivity.
Article in Clinical and experimental immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 18 citations in OpenAlex.
- A Comprehensive Assessment of the Biocompatibility and Safety of Diamond Nanoparticles on Reconstructed Human Epidermis.Materials (Basel, Switzerland) · 2023Article
- T-cell positioning by chemokines in autoimmune skin diseases.Immunological reviews · 2019Review
- [Genetics of contact allergy].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2011Review
- Expression of interleukin-16 in sciatic nerves, spinal roots and spinal cords of experimental autoimmune neuritis rats.Brain pathology (Zurich, Switzerland) · 2009Article
- MMP19 is essential for T cell development and T cell-mediated cutaneous immune responses.PloS one · 2008Article
- Functional Th1 cells are required for surgical adhesion formation in a murine model.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Contact hypersensitivity (CHS) is a T-cell-mediated skin inflammatory response. It is controversial whether CD4(+) T cells play an enhancing or regulatory role in the pathogenesis of CHS. Because interleukin (IL)-16 is a chemoattractant cytokine for CD4-expressing cells, we investigated the involvement of IL-16 in the CHS reaction. IL-16 production was induced in the epidermis and dermis during the elicitation phase of the CHS response with trinitrochlorobenzene. In the sensitization phase, the single application of haptens such as trinitrochlorobenzene and oxazolone also induced IL-16, whereas primary irritants or vehicle control did not. IL-16 was produced mainly by CD11c-negative cells in the epidermis during the elicitation phase. Furthermore, treatment of sensitized mice with anti-IL-16 neutralizing MoAb enhanced the ear swelling and reduced the number of infiltrating CD4(+) T cells. These data indicate that IL-16 plays a role in CHS, whereby IL-16 induces CD4(+) T cells and these CD4(+) T cells subsequently exhibit down-regulating properties.
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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.