Faculty Opinions recommendation of Commensal-Specific CD4(+) Cells From Patients With Crohn's Disease Have a T-Helper 17 Inflammatory Profile.

Author(s):  
Charles Elson
2016 ◽  
Vol 151 (3) ◽  
pp. 489-500.e3 ◽  
Author(s):  
Elisabeth Calderón-Gómez ◽  
Helena Bassolas-Molina ◽  
Rut Mora-Buch ◽  
Isabella Dotti ◽  
Núria Planell ◽  
...  

2017 ◽  
Vol 152 (5) ◽  
pp. S993 ◽  
Author(s):  
Kyohei Nishino ◽  
Hirotsugu Imaeda ◽  
Shigeki Sakai ◽  
Masashi Ohno ◽  
Atsushi Nishida ◽  
...  

Digestion ◽  
2021 ◽  
pp. 1-10
Author(s):  
Yutaro Ihara ◽  
Takehiro Torisu ◽  
Kohta Miyawaki ◽  
Junji Umeno ◽  
Keisuke Kawasaki ◽  
...  

<b><i>Background:</i></b> Ustekinumab (UST), an antibody targeting the p40 subunit of interleukin (IL)-12 and IL-23, is effective in treating Crohn’s disease (CD). To clarify the mechanism of UST, we investigated T-cell differentiation in CD patients treated with UST. <b><i>Methods:</i></b> Twenty-seven patients with active CD were enrolled in this study. Seventeen patients were treated with UST, and 10 patients were treated with anti-tumor necrosis factor (TNF)-alpha therapy. The changes in the proportions of T-cell subsets after these therapies were analyzed by flow cytometry. Comprehensive gene expression changes in the colonic mucosa were also evaluated. <b><i>Results:</i></b> The frequency of T helper (Th) 17 cells was significantly decreased in the peripheral blood of patients with active CD after UST therapy. Anti-TNF therapy had a minimal effect on Th17 cells but increased the proportion of regulatory T cells. Enrichment analysis showed the expression of genes involved in the Th17 differentiation pathway was downregulated in the colonic mucosa after UST but not anti-TNF therapy. There were no common differentially expressed genes between CD patients treated with UST and anti-TNF therapy, suggesting a clear difference in their mechanism of action. <b><i>Conclusion:</i></b> In patients with active CD, UST therapy suppressed Th17 cell differentiation both in the peripheral blood and colonic tissues.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Oswald Moling ◽  
Alfonsina Di Summa ◽  
Loredana Capone ◽  
Josef Stuefer ◽  
Andrea Piccin ◽  
...  

The immune system protects the organism from foreign invaders and foreign substances and is involved in physiological functions that range from tissue repair to neurocognition. However, an excessive or dysregulated immune response can cause immunopathology and disease. A 39-year-old man was affected by severe hepatosplenic schistosomiasismansoniand by amyotrophic lateral sclerosis. One question that arose was, whether there was a relation between the parasitic and the neurodegenerative disease. IL-17, a proinflammatory cytokine, is produced mainly by T helper-17 CD4 cells, a recently discovered new lineage of effector CD4 T cells. Experimental mouse models of schistosomiasis have shown that IL-17 is a key player in the immunopathology of schistosomiasis. There are also reports that suggest that IL-17 might have an important role in the pathogenesis of amyotrophic lateral sclerosis. It is hypothesized that the factors that might have led to increased IL-17 in the hepatosplenic schistosomiasismansonimight also have contributed to the development of amyotrophic lateral sclerosis in the described patient. A multitude of environmental factors, including infections, xenobiotic substances, intestinal microbiota, and vitamin D deficiency, that are able to induce a proinflammatory immune response polarization, might favor the development of amyotrophic lateral sclerosis in predisposed individuals.


2018 ◽  
Vol 154 (6) ◽  
pp. S-131-S-132
Author(s):  
Jose E. Aguirre ◽  
Ellen J Beswick ◽  
Carl Grim ◽  
Romain Villeger ◽  
Don W. Powell ◽  
...  

2005 ◽  
Vol 128 (3) ◽  
pp. 687-694 ◽  
Author(s):  
Giovanni Monteleone ◽  
Ivan Monteleone ◽  
Daniele Fina ◽  
Piero Vavassori ◽  
Giovanna Del Vecchio Blanco ◽  
...  

1999 ◽  
Vol 94 (8) ◽  
pp. 2149-2155 ◽  
Author(s):  
Tomomasa Kakazu ◽  
Junichi Hara ◽  
Takayuki Matsumoto ◽  
Shiro Nakamura ◽  
Nobuhide Oshitani ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (6) ◽  
pp. 577 ◽  
Author(s):  
Benoît Foligné ◽  
Coline Plé ◽  
Marie Titécat ◽  
Arnaud Dendooven ◽  
Aurélien Pagny ◽  
...  

An original immuno-regulatory strategy against inflammatory bowel diseases based on the use of 28 kDa glutathione S-transferase (P28GST), a unique schistosome protein, was recently proposed. Improvement of intestinal inflammation occurs through restoration of the immunological balance between pro-inflammatory T-helper 1 (Th1) responses and both T-helper 2 (Th2) and regulatory responses. However, detailed mechanisms explaining how P28GST prevents colitis and promotes gut homeostasis remain unknown. Considering the complex interplay between the adaptive and innate immune system and the intestinal microbiota, we raised the question of the possible role of the microbial ecosystem in the anti-inflammatory effects mediated by the helminth-derived P28GST protein. We first analyzed, by 16S rRNA sequencing, the bacterial profiles of mice fecal microbiota at several time points of the P28GST-immunomodulation period prior to trinitrobenzene sulfonic acid (TNBS)-colitis. The influence of gut microbiota in the P28GST-mediated anti-inflammatory effects was then assessed by fecal microbiota transplantation experiments from P28GST-immunized mice to either conventional or microbiota depleted naïve recipient mice. Finally, the experimental data were supplemented by the temporal fecal microbiota compositions of P28GST-treated Crohn’s disease patients from a pilot clinical study (NCT02281916). The P28GST administration slightly modulated the diversity and composition of mouse fecal microbiota while it significantly reduced experimental colitis in mice. Fecal microbiota transplantation experiments failed to restore the P28GST-induced anti-inflammatory effects. In Crohn’s disease patients, P28GST also induced slight changes in their overall fecal bacterial composition. Collectively, these results provide key elements in both the anti-inflammatory mechanisms and the safe therapeutic use of immunomodulation with such promising helminth-derived molecules.


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