%0 Generic %A M., Ballbach %A T., Hall %A A., Brand %A D., Neri %A A., Singh %A I., Schaefer %A E., Herrmann %A S., Hansmann %A R., Handgretinger %A J., Kuemmerle-Deschner %A D., Hartl %A N., Rieber %D 2016 %T Supplementary Material for: Induction of Myeloid-Derived Suppressor Cells in Cryopyrin-Associated Periodic Syndromes %U https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Induction_of_Myeloid-Derived_Suppressor_Cells_in_Cryopyrin-Associated_Periodic_Syndromes/3465473 %R 10.6084/m9.figshare.3465473.v1 %2 https://ndownloader.figshare.com/files/5455289 %2 https://ndownloader.figshare.com/files/5455388 %K •Myeloid-derived suppressor cells %K •Neutrophils %K •Autoinflammation %K •NLRP3 %K •Cryopyrin-associated periodic syndrome %K •IL-1β %K •Chemokines %K •Growth factors %X Cryopyrin-associated periodic syndromes (CAPS) are caused by mutations in the NLRP3 gene leading to overproduction of IL-1β and other NLRP3 inflammasome products. Myeloid-derived suppressor cells (MDSCs) represent a novel innate immune cell subset capable of suppressing T-cell responses. As inflammasome products were previously found to induce MDSCs, we hypothesized that NLRP3 inflammasome-dependent factors induce the generation of MDSCs in CAPS. We studied neutrophilic MDSCs, their clinical relevance, and MDSC-inducing factors in a unique cohort of CAPS patients under anti-IL-1 therapy. Despite anti-IL-1 therapy and low clinical disease activity, CAPS patients showed significantly elevated MDSCs compared to healthy controls. MDSCs were functionally competent, as they suppressed polyclonal T-cell proliferation, as well as Th1 and Th17 responses. In addition, MDSCs decreased monocytic IL-1β secretion. Multiplex assays revealed a distinct pattern of MDSC-inducing cytokines, chemokines, and growth factors. Experimental analyses demonstrated that IL-1 cytokine family members and autoinflammation-associated alarmins differentially induced human MDSCs. Increased MDSCs might represent a novel autologous anti-inflammatory mechanism in autoinflammatory conditions and may serve as a future therapeutic target. %I Karger Publishers