Evidence for a role of Langerhans cell-derived IL-16 in atopic dermatitis
Autor: | Sabine Hugo, Volker Blaschke, Andrea Heine, Kristian Reich, Ruth M. Williams, Peter Middel, Christine Neumann, Carsten Gutgesell |
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Rok vydání: | 2002 |
Předmět: |
Allergy
Langerhans cell medicine.medical_treatment Immunology In situ hybridization Tacrolimus Dermatitis Atopic 030207 dermatology & venereal diseases 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Immunology and Allergy Humans 030304 developmental biology Skin 0303 health sciences Interleukin-16 integumentary system biology Antibodies Monoclonal Atopic dermatitis medicine.disease 3. Good health Cytokine medicine.anatomical_structure chemistry Langerhans Cells Ionomycin biology.protein Antibody Keratinocyte |
Zdroj: | The Journal of allergy and clinical immunology. 109(4) |
ISSN: | 0091-6749 |
Popis: | Background: The factors controlling infiltration of inflammatory cells into atopic dermatitis (AD) lesions remain to be fully explored. Recently, epidermal cells in lesional AD were reported to contain increased messenger (m)RNA levels of IL-16, a cytokine that induces chemotactic responses in CD4 + T cells, monocytes, and eosinophils. Objectives: We sought to determine the expression of IL-16 in epidermal cells in normal skin and skin from AD lesions and to investigate whether Langerhans cell (LC)-derived IL-16 may contribute to the initiation of atopic eczema. Methods: The cutaneous expression of IL-16 was investigated by in situ hybridization and immunohistochemistry. Expression of IL-16 was also investigated in freshly isolated LCs and in keratinocytes by intracellular cytokine staining, quantitative real-time RT-PCR, and ELISA. Results: Low levels of IL-16 mRNA, but no stored IL-16 protein, were detected in keratinocytes and LCs isolated from normal skin. Synthesis, storage, and secretion of IL-16 could be induced in LCs, but not keratinocytes, by activation with phorbol ester and ionomycin. In normal skin (n = 10) neither keratinocytes nor LCs expressed IL-16. In contrast, IL-16 was contained in approximately 40% of CD1a + LCs in patients with active AD (n = 16). IL-16 expression in LCs in patients with AD correlated with the number of infiltrating CD4 + cells ( r = .72, P = .0017) and was completely downregulated parallel to the clinical response of AD lesions to topical treatment with FK506. Conclusion: LC-derived IL-16 may participate in the recruitment and activation of inflammatory cells in AD. (J Allergy Clin Immunol 2002;109:681-7.) |
Databáze: | OpenAIRE |
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