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. 2004 Dec;13(12):740-7.
doi: 10.1111/j.0906-6705.2004.00251.x.

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-alpha and IL-1beta

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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-alpha and IL-1beta

Kristian Reich et al. Exp Dermatol. .

Abstract

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-alpha (TNF-alpha) 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-alpha and IL-1beta 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.

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