Anti-Integrins, Anti-Interleukin 12/23p40, and JAK Inhibitors for the Inflammatory Bowel Disease Treatment

Author(s):  
Karine Mariane Steigleder ◽  
Fernando Lopes Ponte Neto ◽  
Cristiane Kibune Nagasako ◽  
Raquel Franco Leal
2021 ◽  
Vol 22 (21) ◽  
pp. 11322
Author(s):  
Jin-Woo Kim ◽  
Su-Young Kim

For a significant proportion of patients with inflammatory bowel disease (IBD), primary non-response and secondary loss of response to treatment remain significant issues. Anti-tumor necrosis factor therapies have been licensed for use in IBD. Other disease-related pathways have been targeted as well, including the interleukin 12/23 axis and lymphocyte tracking. However, the need for parenteral administration and the associated costs of dispensing and monitoring all biologics remain a burden on healthcare systems and patients. Janus kinase inhibitors are small-molecule drugs that can be administered orally and are relatively inexpensive, thus offering an additional option for treating IBD. They have been shown to be effective in patients with ulcerative colitis (UC), but they are less effective in those with Crohn’s disease (CD). Nonetheless, given the immune-system-based mechanism of these drugs, their safety profile remains a cause for concern. This article provides an overview of Janus kinase (JAK) inhibitors and new trends in the treatment of IBD.


2018 ◽  
Vol 30 (8) ◽  
pp. 854-860 ◽  
Author(s):  
Kamolyut Lapumnuaypol ◽  
Napatt Kanjanahattakij ◽  
David Pisarcik ◽  
Charat Thongprayoon ◽  
Karn Wijarnpreecha ◽  
...  

2021 ◽  
Vol 25 ◽  
pp. 101231
Author(s):  
Jingjing Gan ◽  
Yuxiao Liu ◽  
Lingyu Sun ◽  
Wenjuan Ma ◽  
Guopu Chen ◽  
...  

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.


Pathobiology ◽  
2002 ◽  
Vol 70 (3) ◽  
pp. 177-183 ◽  
Author(s):  
Carsten Schmidt ◽  
Thomas Marth ◽  
Bianca M. Wittig ◽  
Andreas Hombach ◽  
Hinrich Abken ◽  
...  

2016 ◽  
Vol 152 ◽  
pp. 370-381 ◽  
Author(s):  
Siti Hajar Md Ramli ◽  
Tin Wui Wong ◽  
Idanawati Naharudin ◽  
Anirbandeep Bose

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