IL‐12 and IL‐23: master regulators of innate and adaptive immunity
By C. Langrish, Brent S. McKenzie, N. Wilson, R. de Waal Malefyt, R. Kastelein, D. Cua. Immunological Reviews, 2004
818 citations recorded by the source corpus.
Subfields: Dermatology, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/e5f50ec0b0796f9a18bb83b22e155aaf136bc136
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Citations in the corpus
- New IL-12-family members: IL-23 and IL-27, cytokines with divergent functions (2005, background): “These latter observations have led to the idea that IFN-γ is part of a regulatory system that counterbalances the effects of IL-23 (Ref”
- IL-23 plays a key role in Helicobacter hepaticus–induced T cell–dependent colitis (2006, background): “IL-23, which is produced by DCs and macrophages in response to Toll-like receptor stimuli (23), may contribute to intestinal pathology in multiple ways.”
- A protective function for interleukin 17A in T cell–mediated intestinal inflammation (2009, neutral): “The IL-12 cytokine family member IL-23 is secreted by 'professional' antigen-presenting cells during inflammatory responses to pathogenic as well as nonpathogenic stimul”
- Interleukin-23 drives innate and T cell–mediated intestinal inflammation (2006, background): “Although colon homogenates prepared from Hh+ 129SvEvRAG−/− mice contained markedly elevated levels of IL-6, monocyte chemoattractant protein–1 (MCP-1), IFN-γ, TNF-α, mouse chemokine CXCL1 (KCs), and IL-1β, samples isolated from Hh+ 129SvEvRAG−/− mice that had received anti–IL-23p19 expressed similar”
- Discovery and biology of IL-23 and IL-27: related but functionally distinct regulators of inflammation. (2007, background): “This is illustrated by the importance of p40 for the development of central nervous system (CNS) inflammation during EAE, but animals that lack IFN-γ-mediated signaling (ifn-, ifnr-, and stat1-deficient mice) remain susceptible to this condition and actually develop more severe pathology (13).”