These findings advance our understanding of inflammasome activity, recognising that this immune response occurs in concordance with a ZBTB16-dependent SUMOylation of ASC. A growing recognition of the impact of SUMO on the immune response has led to the proposition that inhibitors of the E1 or E2 enzymes or, alternatively, SUMO proteases can constitute immune therapies. However, the quantity and diversity of SUMO substrates suggest it will be difficult to achieve a coherent outcome with such an indiscriminate approach. Greater specificity could be achieved by targeting enzymes with more restricted activity. In this way, autoinflammatory disorders might be suppressed by inhibiting ZBTB16 or, on the other hand, anti-tumour immunity might be advanced by pharmacologically promoting ZBTB16 activity55–57. Accordingly, our findings identify a potential drug-targeting strategy for immune therapy by controlling inflammasome activity.
