So far, three other inflammasome prototypes have been described: the NALP1

inflammasome, the IL-1β converting enzyme protease-activating factor (IPAF) inflammasome and recently the absent in melanoma 2 (AIM2) inflammasome.6 To date, much attention has focused around the inflammatory properties of ASC; however, recent evidence has highlighted the importance of ASC in adaptive immune responses. Studies using ASC−/− mice have Fostamatinib chemical structure revealed its significance in adaptive immunity in several physiological and pathological situations. It seems that ASC is essential to mount protective T-cell and B-cell immunity against influenza virus infection.7 Expression of ASC on dendritic cells (DCs) has also been described as being critical in T-cell priming and the subsequent induction of both antigen-specific cellular and humoral immunity and on the onset of collagen-induced arthritis.8 Furthermore, ASC has also been strongly linked to modulating joint inflammation

in antigen-induced arthritis by affecting the induction of antigen-specific cellular immunity.9 Finally, ASC has been shown to contribute to disease progression in experimental autoimmune encephalomyelitis.10 However, the cellular and molecular basis behind the importance of ASC in adaptive immunity remains largely unexplored. We have previously described how ASC−/− T cells exhibit impaired proliferative capacity in response to both antigen-specific and non-specific (anti-CD3/CD28) stimulation ex Talazoparib solubility dmso vivo.9 In this study we explored the cellular basis for the influence of ASC on T-cell proliferation and subsequent Rebamipide effector function. ASC−/− mice1 and NALP3−/− mice11 were backcrossed into the C57BL/6 background for at least nine generations and were compared with wild-type (WT) littermates in this study. Mice were bred under conventional, non-specific pathogen-free conditions. Mice between 8 and

12 weeks of age were used for experiments. All experiments were carried out in agreement with Institutional and Swiss regulations. CD3+ T cells were enriched from splenocyte suspensions by negative selection using the EasySep mouse T-cell enrichment kit (StemCell Technologies, Grenoble, France). Splenic CD4+ and CD8+ T-cell fractions were purified using magnetic antibody cell sorting CD4+ and CD8+ MicroBeads, respectively (> 95%) (Miltenyi Biotec, Bergisch Glaabach, Germany). T cells (2 × 105/200 μl per well) were cultured in 96-well plates previously coated with anti-mouse CD3 (2 μg/ml, clone 145-2C11; eBioscience, San Diego, CA) and anti-CD28 (2 μg/ml, clone 37-51; eBioscience). For co-culture experiments, different isolated T-cell fractions were plated in 96-well plates at a 1 : 1 ratio (1 × 105 T cells per fraction in 200 μl).