Altered Expression of Interferon-γ and Interleukin-4 in Inflammatory Bowel Disease

1998 ◽  
Vol 4 (4) ◽  
pp. 285-290 ◽  
Author(s):  
Luisa Camoglio ◽  
Anje A. Te Velde ◽  
Albert J. Tigges ◽  
Pranab K. Das ◽  
Sander J. H. Van Deventer
2008 ◽  
Vol 94 (2) ◽  
pp. 341-347 ◽  
Author(s):  
G. M. SCHUERMANN ◽  
A. E. ABER-BISHOP ◽  
P. FACER ◽  
J. C. LEE ◽  
D. S. RAMPTON ◽  
...  

1999 ◽  
Vol 190 (5) ◽  
pp. 607-616 ◽  
Author(s):  
Hideki Iijima ◽  
Ichiro Takahashi ◽  
Daisuke Kishi ◽  
Jin-Kyung Kim ◽  
Sunao Kawano ◽  
...  

T cell receptor α chain–deficient (TCR-α−/−) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4+TCR-ββ (CD4+ββ) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4+ββ T cells, we treated TCR-α−/− mice with anti–IL-4 monoclonal antibody (mAb). Approximately 60% of TCR-α−/− mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti–IL-4 mAb–treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab–treated mice. Although TCR-α−/− mice treated with either specific or mock Ab developed CD4+ββ T cells, only those treated with anti–IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon γ–specific expression. These findings suggest that IL-4–producing Th2-type CD4+ββ T cells play a major immunopathological role in the induction of IBD in TCR-α−/− mice, a role that anti–IL-4 mAb inhibits by causing Th2-type CD4+ββ T cells to shift to the Th1 type.


2001 ◽  
Vol 120 (5) ◽  
pp. A525
Author(s):  
Keith Leiper ◽  
Sameena Javeed ◽  
Yamini Krishna ◽  
Jonathan M. Rhodes ◽  
Barry J. Campbell

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 ◽  
...  

2020 ◽  
Vol 26 (7) ◽  
pp. 985-993 ◽  
Author(s):  
Petr Jabandziev ◽  
Julia Bohosova ◽  
Tereza Pinkasova ◽  
Lumir Kunovsky ◽  
Ondrej Slaby ◽  
...  

Abstract Prevalence of inflammatory bowel disease (IBD), a chronic inflammatory disorder of the gut, has been on the rise in recent years—not only in the adult population but also especially in pediatric patients. Despite the absence of curative treatments, current therapeutic options are able to achieve long-term remission in a significant proportion of cases. To this end, however, there is a need for biomarkers enabling accurate diagnosis, prognosis, and prediction of response to therapies to facilitate a more individualized approach to pediatric IBD patients. In recent years, evidence has continued to evolve concerning noncoding RNAs (ncRNAs) and their roles as integral factors in key immune-related cellular pathways. Specific deregulation patterns of ncRNAs have been linked to pathogenesis of various diseases, including pediatric IBD. In this article, we provide an overview of current knowledge on ncRNAs, their altered expression profiles in pediatric IBD patients, and how these are emerging as potentially valuable clinical biomarkers as we enter an era of personalized medicine.


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