Understanding the IL-23-IL-17 immune pathway.

By Brent S. McKenzie, R. Kastelein, D. Cua. Trends in immunology, 2006

823 citations recorded by the source corpus.

Subfields: Dermatology, Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/4f97d85909feba37bb5b1bd9dd8a483ae8c7bb18

How researchers see this paper

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

In Dermatology

1. S. Rose‐John
2. Y. Iwakura
3. H. Ishigame
4. C. Weaver
5. Simon A. Jones
6. D. Cua
7. Henrietta Turner

In Immunology

1. J. O’Shea
2. D. Cua
3. S. Rose‐John
4. F. Powrie
5. J. Scheller
6. Y. Iwakura
7. K. Maloy
8. Simon A. Jones

In Pathology and Forensic Medicine

1. S. Rose‐John
2. Y. Iwakura
3. D. Cua
4. H. Ishigame
5. C. Tato
6. C. Weaver
7. F. Powrie
8. Simon A. Jones

Citations in the corpus

• Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation. (2007, background): “Importantly though, IL-17 has also been found to be overexpressed in a variety of autoimmune and autoinflammatory syndromes, both in mice and in humans (McKenzie et al., 2006).”
• Late Developmental Plasticity in the T Helper 17 Lineage (2009, background): “…that IL-23 and IL-12 shared the common IL-12p40 (IL-12b) subunit and their receptors used the common IL-12Rb1 subunit, gave rise to speculation that IL-17-producing effectors developed as a late branch of the Th1 lineage (Bettelli and Kuchroo, 2005; Mathur et al., 2006; McKenzie et al., 2006).”
• A crucial role for interleukin (IL)-1 in the induction of IL-17–producing T cells that mediate autoimmune encephalomyelitis (2006, background): “MS and the mouse model, experimental autoimmune encephalomyelitis (EAE), are chronic infl ammatory diseases of the central nervous system (1), which until recently were assumed to be mediated by Th1 cells (2).”
• Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation (2011, neutral): “Th17 cells specific for self-antigens and, possibly, for commensal microbiota have been also implicated in autoimmune diseases such as inflammatory bowel disease, arthritis, and psoriasis (Ahern et al., 2008; McKenzie et al., 2006).”
• Interleukin-23 drives innate and T cell–mediated intestinal inflammation (2006, background): “However, as bacteria-derived stimuli have been reported to induce secretion of both IL-12 and IL-23 by DCs and monocytes (16, 32), their relative roles in intestinal pathology remain undefi ned.”
• Specific microbiota direct the differentiation of Th17 cells in the mucosa of the small intestine (2008, neutral): “…to participate in inflammatory responses and to have critical functions in host defense against bacterial and fungal pathogens, particularly those encountered at mucosal surfaces (Aujla et al., 2007, 2008; Bettelli et al., 2007; Khader et al., 2007; McKenzie et al., 2006; Ouyang et al., 2008).”