May act as the sensor component of the Nlrp1b inflammasome, which mediates inflammasome activation in response to various pathogen-associated signals, leading to subsequent pyroptosis (By similarity). Inflammasomes are supramolecular complexes that assemble in the cytosol in response to pathogens and other damage-associated signals and play critical roles in innate immunity and inflammation (By similarity). May act as a recognition receptor (PRR), which recognizes specific pathogens and other damage-associated signals and forms an inflammasome complex: the inflammasome directly recruits pro-caspase-1 (proCASP1) independently of PYCARD/ASC and promotes caspase-1 (CASP1) activation, which subsequently cleaves and activates inflammatory cytokines IL1B and IL18 and gasdermin-D (GSDMD), leading to pyroptosis (By. similarity). Contrary to Nlrp1b allele 1, allele 3 is not activated by Bacillus anthracis lethal toxin (PubMed:16429160, PubMed:19651869, PubMed:23230290). The absence of autocatalytic cleavage within the FIIND domain, which regulates activation in other alleles, suggests that allele 3 may be non-functional (PubMed:31383852). In contrast to allele 1, does not undergo autocatalytic cleavage within the FIIND domain and its mode of activation remains unclear (PubMed:32558991). In contrast to alleles 1 and 2, allele 3 is not activated by Val-boroPro (Talabostat, PT-100) (PubMed:31383852). Not activated by cleavage by B.anthracis lethal toxin (LT) endopeptidase (PubMed:16429160, PubMed:23230290, PubMed:31383852). Not activated by metabolic inhibitors, such as 2-deoxy-D-glucose and sodium azide (PubMed:23230290). Expressed in macrophages. The FIIND (domain with function to find) region may be involved in homomerization, but not in CASP1-binding. Contrary to allele 1, allele 3 does not undergo autocatalytic cleavage in this region. In contrast to allele 1 and 2, not able to mediate autocatalytic cleavage. Nlrp1b gene is extremely polymorphic. 5 alleles have been described in 18 inbred strains: 1 (AC Q2LKW6), 2 (AC A1Z198), 3 (this entry), 4 (AC Q2LKV2) and 5 (AC Q0GKD5). These alleles define susceptibility to B.anthracis lethal toxin (LT). Alleles 2 (carried by A/J, C57BL/6J and I/LnJ), 3 (AKR/J, NOD/LtJ and SJL/J) or 4 (DBA/2J, P/J and SM/J) are not activated by LT. Alleles 1 (carried by 129S1/SvImJ, BALB/cJ, C3H/HeJ, CBA/J, FVB/NJ, NON/ShiLtJ, NZO (NZO/HlLtJ) and SWR/J strains) and 5 (CAST/EiJ) confer macrophage susceptibility to LT. In susceptible strains, infection by Bacillus anthracis leads to IL1B release, neutrophil recruitment and macrophage pyroptosis. This early inflammatory response confers increased resistance to infection (PubMed:16429160). The sequence shown in this entry is that of allele 3 (PubMed:16429160). Three tandem Nrlp1 paralogs, Nrlp1a, Nrlp1b and Nrlp1c, have been identified. Nlrp1c is predicted to be a pseudogene. In macrophages and dendritic cells, NLRP1 inflammasome activation of CASP1 and IL1B maturation can be dampened by direct contact with activated effector and memory T-cells. This effect may be mediated by hexameric TNF ligands, such as CD40LG. Belongs to the NLRP family.