Jeanine D. Mattson

TL;DR: Using passive transfer studies, it is confirmed that these IL-23–dependent CD4+ T cells are highly pathogenic and essential for the establishment of organ-specific inflammation associated with central nervous system autoimmunity.

TL;DR: It is demonstrated that IL-23 and IL-1β induced the development of human and mouse TH-17 cells expressing IL-17A,IL-17F, IL-22, Il-26, interferon-γ, the chemokine CCL20 and transcription factor RORγt, and that human TH- 17 cells may regulate innate immunity in epithelial cells.

TL;DR: This study shows that in these models, IL-23 is essential for manifestation of chronic intestinal inflammation, whereas IL-12 is not, and a critical target of IL- 23 is a unique subset of tissue-homing memory T cells, which are specifically activated by IL-21 to produce the proinflammatory mediators IL-17 and IL-6.

TL;DR: A new heterodimeric cytokine termed IL-27 is described that consists of EBI3, an IL-12p40-related protein, and p28, a newly discovered IL- 12p35-related polypeptide and drives rapid clonal expansion of naive but not memory CD4(+) T cells.

TL;DR: It is shown that IL-23 is an important molecular link between tumour-promoting pro-inflammatory processes and the failure of the adaptive immune surveillance to infiltrate tumours.