Su1835 Impact of Tumour Necrosis Factor Antagonists on Avoiding Surgery in Stricturing Crohn's Disease: A Tertiary Center Real-Life Experience

2016 ◽  
Vol 150 (4) ◽  
pp. S566
Author(s):  
Mariangela Allocca ◽  
Gionata Fiorino ◽  
Cristiana Bonifacio ◽  
Antonino Spinelli ◽  
Alessandro Repici ◽  
...  
2017 ◽  
Vol 49 (8) ◽  
pp. 872-877 ◽  
Author(s):  
Mariangela Allocca ◽  
Cristiana Bonifacio ◽  
Gionata Fiorino ◽  
Antonino Spinelli ◽  
Federica Furfaro ◽  
...  

Digestion ◽  
2017 ◽  
Vol 96 (3) ◽  
pp. 166-172 ◽  
Author(s):  
Mariangela Allocca ◽  
Rosario Landi ◽  
Stefanos Bonovas ◽  
Gionata Fiorino ◽  
Alfredo Papa ◽  
...  

2019 ◽  
Vol 13 (7) ◽  
pp. 905-915 ◽  
Author(s):  
Shrinivas Bishu ◽  
Mohammed El Zaatari ◽  
Atsushi Hayashi ◽  
Guoqing Hou ◽  
Nicole Bowers ◽  
...  

Abstract Background and Aims Tumour necrosis factor [TNF]α- and IL-17A-producing T cells are implicated in Crohn’s disease [CD]. Tissue-resident memory T [TRM] cells are tissue-restricted T cells that are regulated by PR zinc finger domain 1 [PRDM1], which has been implicated in pathogenic Th17 cell responses. TRM cells provide host defence but their role in CD is unknown. We thus examined CD4+ TRM cells in CD. Methods Colon samples were prospectively collected at endoscopy or surgery in CD and control subjects. Flow cytometry and ex vivo assays were performed to characterise CD4+ TRM cells. Results CD4+ TRM cells are the most abundant memory T cell population and are the major T cell source of mucosal TNFα in CD. CD4+ TRM cells are expanded in CD and more avidly produce IL-17A and TNFα relative to control cells. There was a unique population of TNFα+IL-17A+ CD4+ TRM cells in CD which are largely absent in controls. PRDM1 was highly expressed by CD4+ TRM cells but not by other effector T cells. Suppression of PRDM1 was associated with impaired induction of IL17A and TNFA by CD4+ TRM cells Conclusions CD4+ TRM cells are expanded in CD and are a major source of TNFα, suggesting that they are important in CD. PRDM1 is expressed by TRM cells and may regulate their function. Collectively, this argues for prospective studies tracking CD4+ TRM cells over the disease course.


2020 ◽  
Author(s):  
Judith Pichler ◽  
Nima Memaran ◽  
Wolf Dietrich Huber ◽  
Christoph Aufricht ◽  
Bettina Bidmon‐Fliegenschnee

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