Differential suppression of dendritic cell cytokine production by anti-inflammatory drugs

Abstract

The present results give more insight into the pharmacological effects of immunosuppressive drugs on the immune system, and can thereby contribute to a more rational selection of anti-inflammatory drugs for the treatment of inflammatory skin disorders.

Tacrolimus Modulates Dendritic Cell Activation in the Sensitization Phase of Allergic Contact Dermatitis

“…Additionally, we determined that an interval of 24 h represents the adequate time of incubation of the implemented APC with the contact sensitizers TNBS and CAld. Longer periods of incubation led to a significant downregulation of IL-8 expression per se which is in agreement with recent publications also describing 24-30 h as the optimal APC stimulation time and demonstrating that a contact-allergenic hapten escapes in vitro diagnosis if these kinetics are not taken into consideration [27] . As cell lines are thought to be less physiologically relevant than donor-derived DC [36] , we next used human moDC to determine the influence of tacrolimus and betamethasone on DC activation.…”

“…Recent studies suggest that immunosuppressive drugs target DC on multiple levels including maturation, migration and differentiation [26][27][28] . Still, the current knowledge of the effects of tacrolimus on human DC, especially in the context of ACD, remains limited.…”

The cause of the Chinese sofa/chair dermatitis epidemic is likely to be contact allergy to dimethylfumarate, a novel potent contact sensitizer

“…9 However, scientific interest in fumaric acid esters as immunomodulators keeps continuing. [10][11][12] This novel contact sensitizing property of DMF is unexpected and may encourage further studies.…”

The selective COX-2 inhibitor Etoricoxib reduces acute inflammatory markers in a model of neurogenic laryngitis but loses its efficacy with prolonged treatment

“…The increased levels of IL-10 mRNA in the NGI ? VEHIC group can be seen as an immunologic anti-inflammatory response [35,36] that is aborted by Etoricoxib, whereas the increase in IL-6 can be explained by the capacity of selective COX-2 inhibitors to induce IL-6 production [24,25,36]. It is also possible that COX-2 inhibitors can induce IL-1b and IL-6 production and a decrease in the levels of IL-10 by the loss in the activity of protective cellular molecules like hepatocyte growth factor (HGF).…”