Crohn’s disease: Th1, Th17 or both? The change of a paradigm: new immunological and genetic insights implicate Th17 cells in the pathogenesis of Crohn’s disease

By S. Brand. Gut, 2009

687 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Immunology

View Paper: https://www.semanticscholar.org/paper/c628616a9959bfe071d65018c4005d8ff36c1960

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Q. Guan
2. Curtis Huttenhower
3. Bruce E. Sands
4. J. Emer
5. Xochitl C. Morgan
6. Dirk Gevers
7. Alexander Y. Rudensky
8. Nora Koutruba

In Hematology

1. Werner Müller
2. J. Emer
3. Q. Guan
4. Nora Koutruba
5. M. Lebwohl
6. T. Kanai
7. K. Matsuoka

In Immunology

1. Alexander Y. Rudensky
2. A. Chaudhry
3. P. Treuting
4. Robert Samstein
5. Yuqiong Liang
6. Werner Müller
7. Jens C. Brüning
8. J. Heinrich

Citations in the corpus

• New IBD genetics: common pathways with other diseases (2011, background): “Many components of the IL23 pathway (IL23R, IL12B, STAT3, JAK2 and TYK2) are true IBD susceptibility genes, suggesting a critical role for this pathway in maintaining intestinal immune homeostasis (figure 4).(30) Furthermore, IL10 signalling increasingly appears to play a central role in IBD pathoge”
• Review of ustekinumab, an interleukin-12 and interleukin-23 inhibitor used for the treatment of plaque psoriasis (2010, positive): “IL-12/23 has also been implicated in the pathophysiology of Crohn’s disease; however the complex relationship between Th1 and Th17 cells has not been completely analyzed.(45) It is thought that IL-23 may play important roles in controlling the differential of Th1/Th17 balance in both ulcerative coli”
• Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment (2012, background): “SFB are often abundant in the rodent terminal ileum and are responsible for the maturation of Th17 cells [84], which play an important role in CD-associated inflammation [85].”
• The Glucose Transporter Glut1 is Selectively Essential for CD4 T Cell Activation and Effector Function (2014, neutral): “Colitis is driven by Th1 and Th17 Teff cells and suppressed by Treg cells (Brand, 2009).”
• Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation (2011, positive): “Recent work has demonstrated that inflammatory Th1 and Th17 cell responses can facilitate both colitis development and progression (Brand, 2009).”
• A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease (2019, background): “Macrophages in Crohn’s disease patients produce high levels of IL-12 [155].”