The IL-23/IL-17 axis in inflammation.

By Y. Iwakura, H. Ishigame. Journal of Clinical Investigation, 2006

1,097 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/f72126ec7ab7ad8bda25b7c7295754332e1d1464

How researchers see this paper

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In Genetics

1. DM Mosser
2. X. Zhang

In Immunology

1. M. Collins
2. DM Mosser
3. X. Zhang

Citations in the corpus

• Macrophage activation by endogenous danger signals (2008, background): “Th17 T cells belong to a novel group of CD4+ T helper cells that are found highly up-regulated in the gut of IBD mice and which have been implicated in the pathology of IBD.”
• Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides (2006, background): “pneumoniae, supporting the idea that Th17 cells may have evolved to combat extracellular pathogens (11, 18).”
• Neutralization of Human Interleukin 23 by Multivalent Nanobodies Explained by the Structure of Cytokine–Nanobody Complex (2017, background): “Th17/ ThIL17 cells are likely to play critical roles in the development of autoimmunity and allergic reaction, and the IL23/IL17, but not IL12/IFN-γ, axis is critical for the development of autoimmune inflammatory diseases (7).”