Introduction
Chlamydia trachomatis (CT) is a clinically important pathogen. In 2–5% of cases, infection results in the development of reactive arthritis. We have previously shown that human dendritic cells (DC) can be readily infected with live CT following in vitro exposure [1]. Infected DC efficiently process chlamydia and present chlamydial antigens to both CD4+ [1] and CD8+ T cells [1, 2]. Infected DC also produce a number of cytokines including IL-12 and tumour necrosis factor alpha but not IL-10 [1]. The production of IL-12 following infection gives DC the ability to stimulate Th1 responses to chlamydia. Here we have investigated production of another two cytokines from the IL-12 family – IL-23 and IL-27 – by DC infected with live CT. The results were compared with those obtained following DC activation with other inflammatory stimuli.
IL-23 is a heterodimer composed of p19 and p40 subunits, where the p40 subunit is shared between IL-23 and IL-12. IL-27 is a heterodimer composed of p28 and Epstein–Barr virus-induced protein 3 (EBI3) subunits. The main function of both of these cytokines is to stimulate interferon gamma (IFN-γ) production in T cells. However, whereas IL-27 activity primarily affects naïve T cells, IL-23 stimulates both primed and memory cells.