A human interleukin-12/23 monoclonal antibody for the treatment of psoriasis.

By G. Krueger, R. Langley, C. Leonardi, N. Yeilding, C. Guzzo, Yuhua Wang, L. Dooley, M. Lebwohl. New England Journal of Medicine, 2007

812 citations recorded by the source corpus.

Subfields: Dermatology, Immunology, Rheumatology

View Paper: https://www.semanticscholar.org/paper/f443f9912afcfadf056e95baf8172026d8cf11ba

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. D. Cua
2. Dan R. Littman
3. Frank O. Nestle
4. M. Suárez‐Fariñas
5. T. Korn
6. E. Bettelli
7. M. Oukka
8. V. Kuchroo

In Immunology

1. D. Cua
2. Dan R. Littman
3. V. Kuchroo
4. K. Honda
5. T. Korn
6. J. O’Shea
7. M. Oukka
8. R. Kastelein

In Rheumatology

1. K. Honda
2. J. O’Shea
3. J. Krueger

Citations in the corpus

• The biological functions of T helper 17 cell effector cytokines in inflammation. (2008, neutral): “Recently, a critical role of IL-23 in the pathogenesis of psoriasis was indicated on the basis of both genetic-association study and human clinical data (Cargill et al., 2007; Kauffman et al., 2004; Krueger et al., 2007; Lee et al., 2004).”
• Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis. (2011, background): “Numerous clinical trials have now established that antagonism of the p40 subunit, shared between IL-12 and IL-23, can suppress psoriasis in 70–80% of patients (Krueger et al., 2007; Menter, 2009).”
• The IL-23/Th17 axis in the immunopathogenesis of psoriasis. (2009, background): “In humans, results from phase I (Kauffman et al., 2004) and phase II studies (Krueger et al., 2007; Kimball et al., 2008) have shown that both CNTO-1275 and ABT-874 can be appropriate treatments for moderate-to-severe psoriasis (Nestle and Conrad, 2004), being able to modulate IL-8, IL-18, IFN-g,…”
• The safety and side effects of monoclonal antibodies (2010, background): “An interleukin-12/23 (IL-12/23)-specific mAb has been shown to be effective in moderate-to-severe plaque psoriasi”
• Therapeutic targeting of the IL-12/23 pathways: generation and characterization of ustekinumab (2011, methodology): “allowed the development of a combined phase 2a/2b psoriasis adaptive design tria”
• Th17 cell differentiation: the long and winding road. (2008, positive): “Anti-p40 treatment—which inhibits both IL-12 and IL-23—was highly efficacious for treatment of psoriasis ( Krueger et al., 2007 ).”