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Tumor-necrosis factor α-rich environment alters type-I interferon response to viral stimuli in patients with juvenile idiopathic arthritis by altering myeloid dendritic cell phenotype
I. Zentsova, A. Klocperk, M. Bloomfield, H. Kubesova, H. Malcova, D. Cebecauerova, R. Horvath, A. Sediva, Z. Parackova
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
- MeSH
- dendritické buňky MeSH
- fenotyp MeSH
- interferon typ I * MeSH
- juvenilní artritida * farmakoterapie MeSH
- lidé MeSH
- nekróza MeSH
- TNF-alfa MeSH
- virové nemoci * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
The balance between the tumor-necrosis factor α (TNFα) and type-I interferon (T1IFN) pathways is crucial for proper immune function. Dysregulation of either pathway can contribute to autoimmune diseases development. Even though TNFα blockade has shown promising results in various autoimmune diseases, the effect on the balance between TNFα and T1IFN is elusive. We used targeted anti-TNFα therapies in juvenile idiopathic arthritis (JIA) as an experimental approach to study the cross-regulation between TNFα and type-I IFN. We found that TNFα-rich environment affected viral defense through the attenuation of T1IFN responses and affected the phenotype and distribution of myeloid dendritic cells, which are engaged in early viral infections. Anti-TNFα therapy normalized the observed deviations in JIA patients. We hypothesize that the inadequate immune response caused by a high TNFα environment could be projected to more frequent or lengthy viral infections and possibly play a role in the process of JIA disease development.
Citace poskytuje Crossref.org
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- $a Zentsova, Irena $u Department of Immunology, Second Faculty of Medicine, Charles University, University Hospital in Motol, V Uvalu 84, Prague, Czech Republic. Electronic address: irena.zentsova@fnmotol.cz
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- $a The balance between the tumor-necrosis factor α (TNFα) and type-I interferon (T1IFN) pathways is crucial for proper immune function. Dysregulation of either pathway can contribute to autoimmune diseases development. Even though TNFα blockade has shown promising results in various autoimmune diseases, the effect on the balance between TNFα and T1IFN is elusive. We used targeted anti-TNFα therapies in juvenile idiopathic arthritis (JIA) as an experimental approach to study the cross-regulation between TNFα and type-I IFN. We found that TNFα-rich environment affected viral defense through the attenuation of T1IFN responses and affected the phenotype and distribution of myeloid dendritic cells, which are engaged in early viral infections. Anti-TNFα therapy normalized the observed deviations in JIA patients. We hypothesize that the inadequate immune response caused by a high TNFα environment could be projected to more frequent or lengthy viral infections and possibly play a role in the process of JIA disease development.
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