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Blood, 1 November 2008, Vol. 112, No. 9, pp. 3696-3703.
Prepublished online as a Blood First Edition Paper on August 12, 2008; DOI 10.1182/blood-2008-05-155408.
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Submitted May 5, 2008
Accepted July 29, 2008
Prostaglandin E2 (PGE2) synergistically with interleukin-23 (IL-23) favors human Th17 expansion
Carlo Chizzolini*, Rachel Chicheportiche, Montserrat Alvarez, Casimir de Rham, Pascale Roux-Lombard, Sylvie Ferrari-Lacraz, and Jean-Michel Dayer
Immunology & Allergy, Internal Medicine, Geneva University Hospital and School of Medicine, Geneva, Switzerland
* Corresponding author; email: chizzolini{at}medecine.unige.ch.
Microenvironment molecular cues direct T helper (Th) cells differentiation, however Th17 fate determination is still imprecisely understood in humans. To assess the role of PGE2 in Th expansion we activated peripheral blood mononuclear cells (PBMC) by CD3 cross-linking. In the presence of exogenous PGE2, PBMC produced higher IL-17, CCL20/MIP-3alpha, CXCL8/IL-8 and lower IFN- and IL-22 levels than in control cultures. Exogenous PGE2 and IL-23 synergized in inducing IL-17, while indomethacin and IL-23 blockade drastically reduced IL-17 but not IFN-gamma production. Furthermore, IL-1 but not TNF was absolutely required for IL-17 production. PGE2 doubled the frequency of CD4+ T cells producing IL-17 and within the CD4+ subset enhanced CCR6 and CCR4, while decreasing CXCR3 expression. Furthermore, in CD4+ T cell lines the production of IL-17 segregated with the CCR6+ subset. In the presence of CCR6+ compared to CXCR3+ Th cells, monocytes/macrophages produced much higher levels of matrix metalloproteinase-1, -3, -9 but similar levels of CXCL10 and IL-1-beta. These results identify PGE2 and IL-23 in participating to the expansion of CD4+ T cells endowed with high IL-17 production capacity, which in turn favor monocyte production of mediators important for host defense and tissue destruction
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