Local Ultraviolet B Irradiation Impairs Contact Hypersensitivity Induction by Triggering Release of Tumor Necrosis Factor-α from Mast Cells. Involvement of Mast Cells and Langerhans Cells in Susceptibility to Ultraviolet B
| Autor: | Laila A. Hanninen, Pascale Alard, J. Wayne Streilein, Hironori Niizeki |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
skin
Pathology medicine.medical_specialty Necrosis Langerhans cell Ultraviolet Rays inflammatory mediators Dermatology Calcitonin gene-related peptide Dermatitis Contact Immunoglobulin E Radiation Tolerance Biochemistry Cell Degranulation Mice chemistry.chemical_compound medicine Animals Mast Cells dendritic cells Molecular Biology Mice Inbred BALB C Mice Inbred C3H biology Tumor Necrosis Factor-alpha Cell Biology Mast cell Molecular biology Mice Inbred C57BL medicine.anatomical_structure chemistry Langerhans Cells biology.protein Dinitrophenyl Tumor necrosis factor alpha medicine.symptom Antibody |
| Zdroj: | Journal of Investigative Dermatology. 113(6):983-990 |
| ISSN: | 0022-202X |
| DOI: | 10.1046/j.1523-1747.1999.00772.x |
| Popis: | Our laboratory has previously demonstrated that ultraviolet B radiation impairs contact hypersensitivity induction in ultraviolet B susceptible mice through a tumor necrosis factor-alpha-dependent mechanism, involving calcitonin gene related peptide and cutaneous mast cells. This study was designed to test directly whether mast cells are the source of tumor necrosis factor-alpha, to account for the ultra-violet B-susceptible phenotype. As dermal mast cells seem to release tumor necrosis factor-alpha following exposure to ultraviolet B, we investigated whether tumor necrosis factor-alpha released by mast cells could mediate impairment of contact hypersensitivity in a manner similar to that found with ultraviolet B radiation treatment. First, we loaded Fcepsilon receptors of mast cells of ultraviolet B-susceptible (C3H/HeN), ultraviolet B-resistant (C3H/HeJ), and mast-cell deficient (Sl/Sld) mice by intradermal injections of anti-dinitrophenyl immunoglobulin E antibodies. Twenty-four hours later, dinitrophenyl was injected intravenously, and within 30 min oxazolone was painted on injected skin sites. Contact hypersensitivity induction was impaired in ultraviolet B-susceptible mice, but not in ultraviolet B-resistant or Sl/Sld mice, and treatment with anti-tumor necrosis factor-alpha antibodies was able to reverse this impairment of contact hypersensitivity. Second, we have found that ultraviolet B radiation did not impair contact hypersensitivity induction when haptens were painted on irradiated skin of mast cell deficient mice. As ultraviolet B radiation impairs contact hypersensitivity induction through a tumor necrosis factor-alpha-dependent mechanism, we conclude that ultraviolet B radiation triggers the prompt release of tumor necrosis factor-alpha from dermal mast cells, and that mast cell-derived tumor necrosis factor-alpha interferes with generation of the hapten-specific signal required for contact hypersensitivity induction. In addition, we are providing data that indicate that tumor necrosis factor-alpha levels released from mast cells as well as sensitivity of Langerhans cells to tumor necrosis factor-alpha contribute in defining the phenotypes of resistance versus sensitivity to ultra-violet B radiation. |
| Databáze: | OpenAIRE |
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