TY - CHAP
T1 - In Vitro Study of TLR4-NLRP3-Inflammasome Activation in Innate Immune Response
AU - Mezzasoma, Letizia
AU - Schmidt-Weber, Carsten B.
AU - Fallarino, Francesca
N1 - Publisher Copyright:
© 2023, The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2023
Y1 - 2023
N2 - Toll-like receptors (TLRs) are pivotal players in mediating immune responses. TLR4 is the main receptor for LPS, a strong activator of immune cells. LPS/TLR4-dependent pathway, by inducing NF-κB activation, is responsible for the release of several mediators, including IL-1β, one of the most powerful cytokines deeply involved in inflammatory and immune responses. The same pathway is also involved in NLRP3-inflammasome activation, essential for IL-1β maturation. NLRP3 is a major component of innate immune responses, being a crucial player of host immune defense against virus, bacterial, or fungal infections. NLRP3-inflammasome and IL-1β hyperactivation have been associated to the pathogenesis of a wide range of disorders and represent therapeutic targets for the development of new treatments of inflammasome-driven inflammatory and autoimmune diseases. Here, we describe an in vitro protocol to induce LPS/TLR4-dependent NLRP3-inflammasome/IL-1β activation in immune cells, in order to provide a useful assay to study the efficacy of different anti-inflammatory/immune-modulatory agents.
AB - Toll-like receptors (TLRs) are pivotal players in mediating immune responses. TLR4 is the main receptor for LPS, a strong activator of immune cells. LPS/TLR4-dependent pathway, by inducing NF-κB activation, is responsible for the release of several mediators, including IL-1β, one of the most powerful cytokines deeply involved in inflammatory and immune responses. The same pathway is also involved in NLRP3-inflammasome activation, essential for IL-1β maturation. NLRP3 is a major component of innate immune responses, being a crucial player of host immune defense against virus, bacterial, or fungal infections. NLRP3-inflammasome and IL-1β hyperactivation have been associated to the pathogenesis of a wide range of disorders and represent therapeutic targets for the development of new treatments of inflammasome-driven inflammatory and autoimmune diseases. Here, we describe an in vitro protocol to induce LPS/TLR4-dependent NLRP3-inflammasome/IL-1β activation in immune cells, in order to provide a useful assay to study the efficacy of different anti-inflammatory/immune-modulatory agents.
KW - Autoimmune diseases
KW - IL-1β
KW - Inflammatory diseases
KW - LPS
KW - NF-κB
KW - NLRP3-inflammasome
KW - Toll-like receptor 4
UR - http://www.scopus.com/inward/record.url?scp=85168428828&partnerID=8YFLogxK
U2 - 10.1007/978-1-0716-3366-3_9
DO - 10.1007/978-1-0716-3366-3_9
M3 - Chapter
C2 - 37603180
AN - SCOPUS:85168428828
T3 - Methods in Molecular Biology
SP - 163
EP - 176
BT - Methods in Molecular Biology
PB - Humana Press Inc.
ER -