1). It is remarkable that many aspects of systemic autoimmune diseases resemble those of chronic viral infections and that both type I IFNs and IL-17, which contribute to disease pathogenesis, have a crucial role in early innate defense mechanisms. This supports the long-existing idea of an environmental trigger such as infection for systemic autoimmune diseases to develop in genetically susceptible individuals,
who may either display increased immune responses to the initial trigger or lack the ability to abort such responses in time, or both. This, in turn, may explain why polymorphisms in genes involved in the control of innate inflammatory pathways — such as IRFs — are often associated with autoimmune diseases. Data generated in the past few years GSK3 inhibitor point to a role for IL-17 and IL-17-producing cells in the pathogenesis of systemic auto-immune diseases such as SLE. Such studies have, however, focused mainly only on IL-17 and Th17 cells, raising questions about Maraviroc the possible involvement of other immune cell subsets known to produce IL-17, as well as the contribution of other Th17-derived cytokines, in the pathogenic mechanisms and end organ damage. In particular, in light
of recent studies showing that Th17 cells do not represent one defined cell subset but rather a spectrum of cells with different cytokine expression profiles and degrees of pathogenicity, it will be interesting to further define the Th17 cells involved in systemic autoimmune diseases, as well as the cytokines they secrete in addition to IL-17. Financial
support was obtained from the Karolinska Institute, next the Swedish Research Council, the Göran Gustafsson Foundation, the Torsten and Ragnar Söderberg Foundation, the King Gustaf the Vth 80-year foundation, the Swedish Foundation for Strategic Research, the Heart-Lung Foundation, the Magn. Bergvall Foundation, the Lars Hiertas Minne Foundation, the Tore Nilsson Foundation, the Swedish Rheumatism Association, and the Jonas Söderqvist Foundation. The authors declare no financial or commercial conflict of interest. “
“Chlamydia trachomatis infections are a significant cause of reproductive tract pathology. Protective and pathological immune mediators must be differentiated to design a safe and effective vaccine. Wild-type mice and mice deficient in IL-22 and IL-23 were infected intravaginally with Chlamydia muridarum, and their course of infection and oviduct pathology were compared. Local genital tract and draining lymph node immune responses were also examined in IL-23-deficient mice. IL-22- and IL-23-deficient mice exhibited normal susceptibility to infection and oviduct pathology.