scholarly journals Anti-TNF antibody-induced psoriasiform skin lesions in patients with inflammatory bowel disease are characterised by interferon-γ-expressing Th1 cells and IL-17A/IL-22-expressing Th17 cells and respond to anti-IL-12/IL-23 antibody treatment

Gut ◽  
2013 ◽  
Vol 63 (4) ◽  
pp. 567-577 ◽  
Author(s):  
Cornelia Tillack ◽  
Laura Maximiliane Ehmann ◽  
Matthias Friedrich ◽  
Rüdiger P Laubender ◽  
Pavol Papay ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Th17 Cells ◽  
Skin Lesions ◽  
Interferon Γ ◽  
Th1 Cells ◽  
Antibody Treatment ◽  
Inflammatory Bowel

scholarly journals Th17 cells give rise to Th1 cells that are required for the pathogenesis of colitis

2015 ◽  
Vol 112 (22) ◽  
pp. 7061-7066 ◽  
Author(s):  
Stacey N. Harbour ◽  
Craig L. Maynard ◽  
Carlene L. Zindl ◽  
Trenton R. Schoeb ◽  
Casey T. Weaver
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Developmental Plasticity ◽  
Transfer Model ◽  
Th1 Cells ◽  
Inflammatory Bowel ◽  
Ifn Γ

Th17 cells reactive to the enteric microbiota are central to the pathogenesis of certain types of inflammatory bowel disease. However, Th17 cells display substantial developmental plasticity, such that some progeny of Th17 cell precursors retain a predominantly IL-17A+ phenotype, whereas others extinguish IL-17 expression and acquire expression of IFN-γ, giving rise to “Th1-like” cells. It remains unclear what role these subsets play in inflammatory bowel disease. Using a Th17 transfer model of colitis, we found that IFN-γ–deficient Th17 cells retained an IL-17A+ phenotype and were unable to induce colitis in recipients. Development of disease required the transition of a subset of Th17 precursors to Th1-like cells and was contingent on the expression of both Stat4 and T-bet, but not the IL-12 or IFN-γ receptors. Moreover, Th17 cells could provide “help” for the development of pathogenic Th1 cells from naïve precursors. These results indicate that Th17 cells are potent mediators of colitis pathogenesis by dual mechanisms: by directly transitioning to Th1-like cells and by supporting the development of classic Th1 cells.

scholarly journals P718 Risk of tuberculosis in patients with inflammatory bowel disease receiving biologics using two interferon-γ release assays as monitoring

2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S480-S481
Author(s):  
R de Francisco ◽  
M Arias-Guillén ◽  
A Castaño-García ◽  
I Pérez-Martínez ◽  
J J Palacios ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Interferon Γ ◽  
Inflammatory Bowel

scholarly journals Characterization of Human CD39+ Th17 Cells with Suppressor Activity and Modulation in Inflammatory Bowel Disease

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e87956 ◽  
Author(s):  
Maria Serena Longhi ◽  
Alan Moss ◽  
Aiping Bai ◽  
Yan Wu ◽  
Huang Huang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Th17 Cells ◽  
Suppressor Activity ◽  
Inflammatory Bowel
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