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Beh?et's Disease, and the Role of TNF-? and TNF-? Blockers.


ABSTRACT: In this both narrative and systematic review, we explore the role of TNF-? in the immunopathogenesis of Behçet's disease (BD) and the effect of treatment with TNF-? blockers. BD is an auto-inflammatory disease, characterized by recurrent painful oral ulcerations. The pathogenesis of BD is not yet elucidated; it is assumed that TNF-? may play a key role. In the narrative review, we report an increased production of TNF-?, which may be stimulated via TLR-signaling, or triggered by increased levels of IL-1? and IFN-?. The abundance of TNF-? is found in both serum and in sites of inflammation. This increased presence of TNF-? stimulates T-cell development toward pro-inflammatory subsets, such as Th17 and Th22 cells. Treatment directed against the surplus of TNF-? is investigated in the systematic review, performed according to the PRISMA guideline. We searched the Pubmed and Cochrane database, including comparative studies only. After including 11 studies, we report a beneficial effect of treatment with TNF-? blockers on the various manifestations of BD. In conclusion, the pivotal role of TNF-? in the immunopathogenesis of BD is reflected in both the evidence of their pro-inflammatory effects in BD and in the evidence of the positive effect of treatment on the course of disease in BD.

SUBMITTER: van der Houwen T 

PROVIDER: S-EPMC7246873 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Behҫet's Disease, and the Role of TNF-α and TNF-α Blockers.

van der Houwen Tim T   van Laar Jan J  

International journal of molecular sciences 20200427 9


In this both narrative and systematic review, we explore the role of TNF-α in the immunopathogenesis of Behçet's disease (BD) and the effect of treatment with TNF-α blockers. BD is an auto-inflammatory disease, characterized by recurrent painful oral ulcerations. The pathogenesis of BD is not yet elucidated; it is assumed that TNF-α may play a key role. In the narrative review, we report an increased production of TNF-α, which may be stimulated via TLR-signaling, or triggered by increased levels  ...[more]

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