Nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) is the most widely investigated inflammasome member whose overactivation can be a driver of several carcinomas. It is activated in response to different signals and plays an important role in metabolic disorders and inflammatory and autoimmune diseases. NLRP3 belongs to the pattern recognition receptors (PRRs) family, expressed in numerous immune cells, and it plays its primary function in myeloid cells. NLRP3 has a crucial role in myeloproliferative neoplasms (MPNs), considered to be the diseases best studied in the inflammasome context. The investigation of the NLRP3 inflammasome complex is a new horizon to explore, and inhibiting IL-1 beta or NLRP3 could be a helpful cancer-related therapeutic strategy to improve the existing protocols.

The Role of NLRP3, a Star of Excellence in Myeloproliferative Neoplasms

Parciante, Elisa;Cumbo, Cosimo;Anelli, Luisa;Zagaria, Antonella;Redavid, Immacolata;Minervini, Angela;Conserva, Maria Rosa;Tota, Giuseppina;Coccaro, Nicoletta;Tarantini, Francesco;Minervini, Crescenzio Francesco;Macchia, Maria Giovanna;Specchia, Giorgina;Musto, Pellegrino;Albano, Francesco
2023-01-01

Abstract

Nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) is the most widely investigated inflammasome member whose overactivation can be a driver of several carcinomas. It is activated in response to different signals and plays an important role in metabolic disorders and inflammatory and autoimmune diseases. NLRP3 belongs to the pattern recognition receptors (PRRs) family, expressed in numerous immune cells, and it plays its primary function in myeloid cells. NLRP3 has a crucial role in myeloproliferative neoplasms (MPNs), considered to be the diseases best studied in the inflammasome context. The investigation of the NLRP3 inflammasome complex is a new horizon to explore, and inhibiting IL-1 beta or NLRP3 could be a helpful cancer-related therapeutic strategy to improve the existing protocols.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/434880
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