After interleukin-12p40, are interleukin-23 and interleukin-17 the next therapeutic targets for inflammatory bowel disease?

2007 ◽  
Vol 7 (4) ◽  
pp. 409-416 ◽  
Author(s):  
Zili Zhang ◽  
David J. Hinrichs ◽  
Huiying Lu ◽  
Hong Chen ◽  
Wenwei Zhong ◽  
...  
2013 ◽  
Vol 19 (14) ◽  
pp. 1711-1747 ◽  
Author(s):  
Fiorella Biasi ◽  
Gabriella Leonarduzzi ◽  
Patricia I. Oteiza ◽  
Giuseppe Poli

2013 ◽  
Vol 93 (4) ◽  
pp. 378-383 ◽  
Author(s):  
Eoin P Cummins ◽  
Glen A Doherty ◽  
Cormac T Taylor

2010 ◽  
Vol 160 (3) ◽  
pp. 386-393 ◽  
Author(s):  
T. Sugihara ◽  
A. Kobori ◽  
H. Imaeda ◽  
T. Tsujikawa ◽  
K. Amagase ◽  
...  

2008 ◽  
Vol 14 (29) ◽  
pp. 4643 ◽  
Author(s):  
Anna Latiano ◽  
Orazio Palmieri ◽  
Maria Rosa Valvano ◽  
Renata D’Incà ◽  
Salvatore Cucchiara ◽  
...  

2019 ◽  
Vol 37 (6) ◽  
pp. 451-457 ◽  
Author(s):  
Mario Cottone ◽  
Chiara Sapienza ◽  
Fabio Salvatore Macaluso ◽  
Marco Cannizzaro

Background: Inflammatory bowel disease (IBD) and psoriasis (PS) are associated conditions. The reason for this association lies in the sharing of predisposition genes and common immunological mechanisms. Summary: This review will focus on the interplay between IBD and PS, with details on prevalence and phenotype of PS in IBD, genetics, pathogenetic pathways, and therapy. Key Messages: Microbiome seems relevant in both conditions: a reduction of beneficial bacteria has been observed. IBD and PS have in common some comorbidities like cardiovascular disease, similar risk of cancer and psychiatric problems. Many biological therapies such as anti-tumour necrosis factor (TNF) and anti-interleukin 23 are effective in both conditions, underlining the common immunological mechanisms. Paradoxical PS has been mainly observed after anti-TNF therapies, but preliminary reports show that it can also occur with other biologics. Genetic predisposition to this phenomenon has been reported.


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