Inflammasomes are intracellular multiprotein signaling complexes, mainly present in myeloid cells. They commonly assemble around a cytoplasmic receptor of the nucleotide-binding leucine-rich repeat containing receptor (NLR) family, although other cytoplasmic receptors like pyrin have been shown to form inflammasomes. The nucleation of the multiprotein scaffolding platform occurs upon detection of a microbial, a danger or a homeostasis pattern by the receptor that will, most commonly, associate with the adaptor protein ASC (apoptosis-associated speck-like protein containing a CARD) through homotypic domain interactions resulting in recruitment of procaspase-1. This will lead to the autoproteolytic activation of caspase-1, which regulates the secretion of proinflammatory IL1β and IL18 cytokines and pyroptosis, a caspase-1-mediated form of cell death. Pyroptosis occurs through cleavage of Gasdermin D, a membrane pore forming protein. Recently, non-canonical inflammasomes have been described, which directly sense intracellular pathogens through caspase-4 and -5 in humans, leading to pyroptosis.

Inflammasomes are important in host defense; however, a deregulated activity is associated with a number of inflammatory, immune and metabolic disorders. Furthermore, mutations in inflammasome receptor coding genes are causal for an increasing number of rare autoinflammatory diseases. Biotherapies targeting the products of inflammasome activation as well as molecules that directly or indirectly inhibit inflammasome nucleation and activation are promising therapeutic areas. This review discusses recent advances in inflammasome biology, the molecular pathology of several inflammasomes, and current therapeutic approaches in autoinflammatory diseases and in selected common multifactorial inflammasome-mediated disorders.

炎性小体是细胞内多蛋白信号传导复合物，主要存在于髓样细胞中。它们通常在核苷酸结合的富含亮氨酸的重复序列包含受体（NLR）家族的细胞质受体周围组装，尽管已经显示出其他细胞质受体（如吡喃）会形成炎症小体。多蛋白支架平台的成核发生在受体检测到微生物，危险或体内稳态模式时发生，该模式通常会通过同型域与衔接蛋白ASC（与CARD凋亡相关的斑点样蛋白）缔合。相互作用导致procaspase-1的募集。这将导致caspase-1的自蛋白水解激活，从而调节促炎性IL1β和IL18细胞因子的分泌和焦磷酸化（一种由caspase-1介导的细胞死亡形式）。细胞凋亡是通过裂解形成膜孔的蛋白质Gasdermin D发生的。近来，已经描述了非规范的炎性体，其通过人中的胱天蛋白酶-4和-5直接感测细胞内病原体，从而导致细胞凋亡。

炎症小体在宿主防御中很重要。然而，活性失调与许多炎症，免疫和代谢疾病有关。此外，炎性体受体编码基因的突变是导致越来越多的罕见自身炎性疾病的原因。针对炎性体活化产物以及直接或间接抑制炎性体成核和活化的分子的生物疗法是有前途的治疗领域。这篇综述讨论了炎症小体生物学，几种炎症小体的分子病理学以及自体炎症和某些常见的多因素炎症小体介导的疾病的当前治疗方法的最新进展。