Inflammasomes are crucial protein complexes in immunology that regulate host defense against pathogens and contribute to various diseases. They are activated by pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs), leading to the processing of pro-IL-1β and pro-IL-18 by caspase-1, which triggers pyroptosis. NLRs and ALRs are key receptors involved in inflammasome assembly, with NLRP1, NLRP3, NLRC4, and AIM2 being major components. Recent studies have shown that caspase-8, caspase-11, IRAK, and RIP kinases also play roles in inflammasome functions. Post-translational modifications, such as ubiquitination and phosphorylation, regulate inflammasome activities. Genetic mutations in these receptors are linked to autoinflammatory diseases, enterocolitis, and cancer. The inflammasome is tightly regulated by scaffolding proteins and modifications, ensuring controlled activation to prevent tissue damage. The NLRP1 inflammasome is activated by anthrax lethal toxin, while the NLRP3 inflammasome responds to a wide range of PAMPs and DAMPs. Caspase-11 is involved in the non-canonical NLRP3 inflammasome pathway, and the NLRC4 inflammasome is activated by bacterial flagellin and inner rod proteins. The AIM2 inflammasome recognizes double-stranded DNA and contributes to host defense against pathogens. ASC is a central component in inflammasome signaling, facilitating caspase-1 activation and pyroptosis. Other pattern-recognition receptors, such as Pyrin, NLRP6, and IFI16, also contribute to inflammasome assembly and function. The regulation of inflammasome activity is essential for maintaining homeostasis and preventing disease. Future research aims to understand the roles of new inflammasome receptors and develop therapies targeting inflammasome components for disease treatment.Inflammasomes are crucial protein complexes in immunology that regulate host defense against pathogens and contribute to various diseases. They are activated by pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs), leading to the processing of pro-IL-1β and pro-IL-18 by caspase-1, which triggers pyroptosis. NLRs and ALRs are key receptors involved in inflammasome assembly, with NLRP1, NLRP3, NLRC4, and AIM2 being major components. Recent studies have shown that caspase-8, caspase-11, IRAK, and RIP kinases also play roles in inflammasome functions. Post-translational modifications, such as ubiquitination and phosphorylation, regulate inflammasome activities. Genetic mutations in these receptors are linked to autoinflammatory diseases, enterocolitis, and cancer. The inflammasome is tightly regulated by scaffolding proteins and modifications, ensuring controlled activation to prevent tissue damage. The NLRP1 inflammasome is activated by anthrax lethal toxin, while the NLRP3 inflammasome responds to a wide range of PAMPs and DAMPs. Caspase-11 is involved in the non-canonical NLRP3 inflammasome pathway, and the NLRC4 inflammasome is activated by bacterial flagellin and inner rod proteins. The AIM2 inflammasome recognizes double-stranded DNA and contributes to host defense against pathogens. ASC is a central component in inflammasome signaling, facilitating caspase-1 activation and pyroptosis. Other pattern-recognition receptors, such as Pyrin, NLRP6, and IFI16, also contribute to inflammasome assembly and function. The regulation of inflammasome activity is essential for maintaining homeostasis and preventing disease. Future research aims to understand the roles of new inflammasome receptors and develop therapies targeting inflammasome components for disease treatment.