Failure to thrive: A severe manifestation of interleukin 10 receptor A mutation in adult inflammatory bowel disease

Author(s):  
Nicole C. Ruiz ◽  
Amir Y. Kamel ◽  
Xiuli Liu ◽  
Angela Pham ◽  
Christopher Forsmark ◽  
...  
2014 ◽  
Vol 41 (3) ◽  
pp. 1299-1310 ◽  
Author(s):  
Hongchao Lv ◽  
Yongshuai Jiang ◽  
Jin Li ◽  
Mingming Zhang ◽  
Zhenwei Shang ◽  
...  

2015 ◽  
Vol 21 (1) ◽  
pp. 051-061 ◽  
Author(s):  
Jae Hyung Park ◽  
Joong Goo Kwon ◽  
Sun Joo Kim ◽  
Dae Kyu Song ◽  
Seok Guen Lee ◽  
...  

2014 ◽  
Vol 8 (2) ◽  
pp. 147-160 ◽  
Author(s):  
Kristine Holgersen ◽  
Peter Helding Kvist ◽  
Helle Markholst ◽  
Axel Kornerup Hansen ◽  
Thomas Lindebo Holm

2012 ◽  
Vol 12 (5) ◽  
pp. 373-379 ◽  
Author(s):  
Neil Shah ◽  
Jochen Kammermeier ◽  
Mamoun Elawad ◽  
Erik-Oliver Glocker

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 397 ◽  
Author(s):  
Paolo Giuffrida ◽  
Sara Cococcia ◽  
Mariangela Delliponti ◽  
Marco Vincenzo Lenti ◽  
Antonio Di Sabatino

Inflammatory bowel disease (IBD) is caused by a dysregulated immune response against normal components of the intestinal microflora combined with defective functioning of anti-inflammatory pathways. Currently, all therapies approved for IBD manipulate the immune system by inhibiting pro-inflammatory mechanisms, such as tumor necrosis factor-α, gut-homing α4β7 integrin, interleukin-12/interleukin-23, and Janus kinases. However, some IBD patients are non-responders to these drugs, which are also associated with serious side effects. Thus, it has been hypothesized that therapies aimed at restoring anti-inflammatory signals, by exploiting the tolerogenic potential of cytokines (interleukin-10, transforming growth factor-β, granulocyte macrophage colony-stimulating factor), immune cells (regulatory T cells, tolerogenic dendritic cells), or mesenchymal stem cells, might offer promising results in terms of clinical efficacy with fewer side effects. In this review, we provide new insights into putative novel treatments aimed at restoring anti-inflammatory signaling pathways in IBD.


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