Prostaglandin E2 induces IL-23 production in bone marrow-derived dendritic cells AMIR F. SHEIBANIE, IMAN TADMORI, HUIE JING, EVROS VASSILIOU and DOINA GANEA 1 Department of Biological Sciences, Rutgers University, Newark, New Jersey, USA 1 Correspondence: Rutgers University, Department Biological Sciences, 101 Warren St., Newark, NJ 07102, USA. E-mail: dganea@andromeda.rutgers.edu <h3>SPECIFIC AIMS</h3> Structurally related cytokines IL-12 and the recently discovered IL-23 and IL-27 have overlapping but distinct functions. IL-27, IL-12, and IL-23 act sequentially on CD4+ T cells, inducing the differentiation of Th0 into Th1 effectors, and subsequently into memory Th1. The responsiveness of Th0/effector Th1/memory Th1 cells to different members of the IL-12 family is due to differential expression of the specific receptors. IL-23 is a heterodimer consisting of the subunit p40 shared with IL-12 and the unique subunit p19, distantly related to the IL-12p35 subunit. IL-23 emerged recently as one of the most potent proinflammatory cytokines. Transgenic p19 overexpressing mice die before the age of 3 months after systemic inflammation, indicating a prominent proinflammatory role for IL-23. The proinflammatory effect of IL-23 has both beneficial and detrimental consequences. Through its effects on activated/memory T cells, IL-23 contributes to systemic immunity against pathogens and tumors. However, recent studies
/lp/fed-of-american-socs-for-experimental-biology/prostaglandin-e2-induces-il-23-production-in-bone-marrow-derived-XZajaaI5kv