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NLRP3 Inflammasome Inhibition by the Novel Bispecific Antibody InflamAb Attenuates Atherosclerosis in Apolipoprotein E–Deficient Mice

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Bibliographic Details
Title: NLRP3 Inflammasome Inhibition by the Novel Bispecific Antibody InflamAb Attenuates Atherosclerosis in Apolipoprotein E–Deficient Mice
Authors: Delfos, L., Depuydt, M.A.C., Chemaly, M., Coyle, S., Schaftenaar, F.H., Santbrink, P.J. van, Lindenbergh, P.P., Bernabé Kleijn, M.N.A., Costello, C., Power, C.A., Coll, R., Peace, A., Gregory-Ksander, M., Foks, A.C., Kuiper, J., McGilligan, V., Bot, I.
Source: JACC Basic Transl Sci
Publisher Information: Elsevier BV, 2025.
Publication Year: 2025
Subject Terms: Bispecific, Interleukin-1 receptor type 1, Atherosclerosis, Interleukin-1b, Antibody, NLRP3 inflammasome, Original Research - Preclinical
Description: The NLRP3 inflammasome contributes to the inflammatory process in atherosclerosis by producing IL-1β. Components of the intracellular NLRP3 inflammasome have been shown to be expressed by macrophages in the atherosclerotic plaque and are a potential therapeutic target. We aimed to determine the efficacy of the novel bispecific antibody InflamAb, designed to target the interleukin-1 receptor type 1 and the NLRP3 inflammasome, in inhibiting atherosclerosis. InflamAb effectively inhibited IL-1β secretion from bone marrow–derived macrophages and reduced circulating IL-1β levels in vivo. Furthermore, InflamAb treatment significantly inhibited atherosclerotic plaque development, accompanied by a reduction in relative macrophage and necrotic core content. InflamAb treatment did not affect the size of established atherosclerotic lesions; however, InflamAb significantly reduced relative macrophage and necrotic core content in these plaques. To conclude, inhibition of the NLRP3 inflammasome by the bispecific antibody InflamAb shows promising efficacy in inhibiting atherosclerotic plaque development and destabilization in Apoe(-/-) mice.
Document Type: Article
Other literature type
File Description: application/pdf
Language: English
ISSN: 2452-302X
DOI: 10.1016/j.jacbts.2024.12.012
Access URL: https://hdl.handle.net/1887/4212171
Rights: CC BY NC ND
Accession Number: edsair.doi.dedup.....d0e9efaa7eb9bca5ba8ef9cf6b31ed9c
Database: OpenAIRE
Description
Abstract:The NLRP3 inflammasome contributes to the inflammatory process in atherosclerosis by producing IL-1β. Components of the intracellular NLRP3 inflammasome have been shown to be expressed by macrophages in the atherosclerotic plaque and are a potential therapeutic target. We aimed to determine the efficacy of the novel bispecific antibody InflamAb, designed to target the interleukin-1 receptor type 1 and the NLRP3 inflammasome, in inhibiting atherosclerosis. InflamAb effectively inhibited IL-1β secretion from bone marrow–derived macrophages and reduced circulating IL-1β levels in vivo. Furthermore, InflamAb treatment significantly inhibited atherosclerotic plaque development, accompanied by a reduction in relative macrophage and necrotic core content. InflamAb treatment did not affect the size of established atherosclerotic lesions; however, InflamAb significantly reduced relative macrophage and necrotic core content in these plaques. To conclude, inhibition of the NLRP3 inflammasome by the bispecific antibody InflamAb shows promising efficacy in inhibiting atherosclerotic plaque development and destabilization in Apoe(-/-) mice.
ISSN:2452302X
DOI:10.1016/j.jacbts.2024.12.012