Quinacrine Suppresses Tumor Necrosis Factor-α and IFN-α in Dermatomyositis and Cutaneous Lupus Erythematosus.
J Investig Dermatol Symp Proc
; 18(2): S57-S63, 2017 10.
Article
em En
| MEDLINE
| ID: mdl-28941496
ABSTRACT
Antimalarials are used to treat dermatomyositis (DM) and cutaneous lupus erythematosus (CLE). Although hydroxychloroquine (HCQ) is frequently used, addition of quinacrine (QC) has shown additional clinical effects when combined with HCQ. To quantify the effects of HCQ versus QC in suppressing secretion of tumor necrosis factor-α (TNF-α) and IFN-α from the peripheral blood mononuclear cells of DM and CLE patients, lipopolysaccharide-stimulated and control peripheral blood mononuclear cells from DM and CLE patients and control subjects were analyzed for the effect of HCQ and QC on TNF-α and IFN-α production using ELISA testing. Flow cytometry showed the effects of these therapies on intracellular TNF-α in myeloid dendritic cells and monocytes of DM patients and control subjects. QC significantly suppressed TNF-α relative to HCQ from unstimulated and lipopolysaccharide-stimulated peripheral blood mononuclear cells of DM and CLE patients (P < 0.0001). It suppressed IFN-α as significantly as HCQ from cytosine phosphodiester guanine-stimulated peripheral blood mononuclear cells of DM and CLE patients (P < 0.0001). Flow cytometry showed that QC significantly suppressed intracellular expression of TNF-α from the lipopolysaccharide-stimulated myeloid dendritic cells and monocytes of DM patients (P-values ≤ 0.0008). In conclusion, QC likely has a different mechanism of action than HCQ, given the broader inhibition of proinflammatory cytokines, including both TNF-α and IFN-α.
Texto completo:
1
Coleções:
01-internacional
Contexto em Saúde:
3_ND
Base de dados:
MEDLINE
Assunto principal:
Quinacrina
/
Lúpus Eritematoso Cutâneo
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Fator de Necrose Tumoral alfa
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Interferon-alfa
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Dermatomiosite
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Hidroxicloroquina
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Antimaláricos
Limite:
Humans
Idioma:
En
Revista:
J Investig Dermatol Symp Proc
Ano de publicação:
2017
Tipo de documento:
Article