摘要
Inflammasomes are large multipro- tein platforms that translate recog-nition of immune 'danger' into activation of pro-caspase- 1. Caspase- 1 in turn pro- teolytically activates the precursors of the pro-inflammatory cytokines IL-I~ and IL-18, which are secreted to support the inflammatory response. The recruit- ment of pro-caspase-1 to both NLRP3- and absent in melanoma 2 (MM2)- containing inflammasome complexes is mediated by the apoptosis-associated speck-like protein containing a caspase- recruitment domain (CARD) (ASC).
Inflammasomes are large multipro- tein platforms that translate recog-nition of immune 'danger' into activation of pro-caspase- 1. Caspase- 1 in turn pro- teolytically activates the precursors of the pro-inflammatory cytokines IL-I~ and IL-18, which are secreted to support the inflammatory response. The recruit- ment of pro-caspase-1 to both NLRP3- and absent in melanoma 2 (MM2)- containing inflammasome complexes is mediated by the apoptosis-associated speck-like protein containing a caspase- recruitment domain (CARD) (ASC).
