scholarly journals Joint erosion in rheumatoid arthritis: interactions between tumour necrosis factor  , interleukin 1, and receptor activator of nuclear factor  B ligand (RANKL) regulate osteoclasts

2004 ◽  
Vol 63 (4) ◽  
pp. 354-359 ◽  
Author(s):  
D O' Gradaigh
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Nuclear Factor ◽  
Factor B ◽  
Receptor Activator ◽  
Necrosis Factor ◽  
Joint Erosion

Serum zinc and copper in active rheumatoid arthritis: Correlation with interleukin 1? and tumour necrosis factor ?

1998 ◽  
Vol 17 (5) ◽  
pp. 378-382 ◽  
Author(s):  
A. Zoli ◽  
L. Altomonte ◽  
R. Caricchio ◽  
A. Galossi ◽  
L. Mirone ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Active Rheumatoid Arthritis ◽  
Interleukin 1 ◽  
Serum Zinc ◽  
Necrosis Factor

scholarly journals Keratinocyte sensitization to tumour necrosis factor-induced nuclear factor kappa B activation by the E2 regulatory protein of human papillomaviruses

2011 ◽  
Vol 92 (10) ◽  
pp. 2422-2427 ◽  
Author(s):  
Manel Boulabiar ◽  
Samir Boubaker ◽  
Michel Favre ◽  
Caroline Demeret
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Nuclear Factor Kappa B ◽  
Interleukin 1 ◽  
Regulatory Protein ◽  
Cell Signalling ◽  
Human Papillomaviruses ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Necrosis Factor

Human papillomavirus (HPV) life cycle requires extensive manipulation of cell signalling to provide conditions adequate for viral replication within the stratified epithelia. In this regard, we show that the E2 regulatory protein of α, β and μ-HPV genotypes enhances tumour necrosis factor (TNF)-induced activation of nuclear factor kappa B (NF-κB). This activation is mediated by the N-terminal domain of E2, but does not rely on its transcriptional properties. It is independent of the NF-κB regulator Tax1BP1, which nevertheless interacts with all the E2 proteins. E2 specifically activates NF-κB pathways induced by TNF, while interleukin-1-induced pathways are not affected. E2 stimulates the activating K63-linked ubiquitination of TRAF5, and interacts with both TRAF5 and TRAF6. Our data suggest that E2 potentiates TNF-induced NF-κB signalling mediated by TRAF5 activation through direct binding. Since NF-κB controls epithelial differentiation, this activity may be involved in the commitment of infected keratinocytes to proliferation arrest and differentiation, both required for the implementation of the productive viral cycle.

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