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The maturation‐dependent production of interleukin‐16 is impaired in monocyte‐derived dendritic cells from atopic dermatitis patients but is restored by inflammatory cytokines TNF‐α and IL‐1β
Author(s) -
Reich Kristian,
Hugo Sabine,
Middel Peter,
Blaschke Volker,
Heine Andrea,
Neumann Christine
Publication year - 2004
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2004.00251.x
Subject(s) - immunology , tumor necrosis factor alpha , monocyte , cd86 , cytokine , dendritic cell , interleukin , interleukin 20 , thymic stromal lymphopoietin , granulocyte macrophage colony stimulating factor , interleukin 10 , atopic dermatitis , medicine , biology , immune system , interleukin 5 , t cell
Background: Maturation of dendritic cells (DCs) influences important DC functions such as production of cytokines. Recently, DCs were identified as a source of interleukin‐16 (IL‐16), a chemotactic factor for DCs themselves, CD4 + T cells, and eosinophils. There is evidence that DC‐derived IL‐16 may contribute to the pathogenesis of atopic dermatitis (AD). Objective: To investigate the production of IL‐16 during differentiation of monocytes into DCs in healthy individuals and patients with AD. Methods: IL‐16 production was investigated by quantitative real‐time RT‐PCR, intracellular cytokine staining, immunoblotting, and ELISA. Results: DCs generated from peripheral monocytes by 5‐day culture in the presence of IL‐4 and granulocyte/macrophage colony‐stimulating factor acquired the capability to synthesize, store, and secrete IL‐16. Storage and release of IL‐16 was further enhanced during final DC maturation induced by additional 3‐day culture with tumor necrosis factor‐α (TNF‐α) and monocyte‐conditioned medium. Maturation, as determined by up‐regulation of CD83 and CD86 surface expression, and production of IL‐16, but not production of IL‐10 and IL‐12p40 was impaired in day 8 DCs derived from AD patients compared to those from healthy donors. Stimulation of day 8 DCs from AD patients with TNF‐α and IL‐1β enhanced the expression of CD83 and CD86 and restored the production of IL‐16. Conclusions: Signals involved in the activation and maturation of DCs enhance their capacity to produce IL‐16. Functional abnormalities present in patients with AD at the monocyte level may account for impaired maturation and IL‐16 production of monocyte‐derived DCs.