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The interleukin (IL)‐1 family of cytokines plays a pivotal role in immune responses. Among the members of IL‐1 family, IL‐1β is synthesized as an inactive precursor (pro‐IL‐1β) and becomes active upon cleavage, which is typically facilitated by inflammasomes through caspase‐1. In our research, we explored the potential role of caspase‐3 in the cleavage of pro‐IL‐1β and found that caspase‐3 cleaves pro‐IL‐1β, specifically at Asp26. Moreover, we found that in the absence of caspase‐3 cleavage, the release of active IL‐1β via the inflammasome is increased. Our study introduces pro‐IL‐1β as a new substrate for caspase‐3 and suggests that caspase‐3‐mediated cleavage has the potential to suppress IL‐1β‐mediated inflammatory responses.
Kim et al. (Sat,) studied this question.