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Both activation of the NLRP3 inflammasome and excessive generation of reactive oxygen species (ROS) act independently and synergistically to promote \u03b2\u2010cell apoptosis and accelerate disease progression. Therapeutic approaches that concurrently inhibit NLRP3 activation and oxidative stress may therefore hold promise for preventing or slowing type 1 diabetes development and\/or progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>This study developed a targeted nanotherapeutic consisting of M2 macrophage membrane\u2010coated, MCC950 (a selective NLRP3 inflammasome inhibitor)\u2010incorporated, BSA\u2010loaded cerium\u2010layered double hydroxide nanoparticles (CLMBM NPs), engineered for targeted delivery to inflamed tissues and controlled, ROS\u2010responsive drug release.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>CLMBM NPs effectively eliminated intracellular ROS and reduced apoptosis in MIN\u20106 cells. Macrophage membrane cloaking facilitated immune evasion and targeted accumulation in inflamed pancreatic tissue. In streptozocin (STZ) induced diabetic mice, CLMBM NPs demonstrated pancreas\u2010targeted accumulation and ROS\u2010responsive release of MCC950, enabling precise modulation of local inflammation and significant therapeutic effects on blood glucose homeostasis by down\u2010regulating pro\u2010inflammatory markers such as IL\u20101\u03b2 and IL\u20106.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>Findings reveal that pancreas\u2010targeted CLMBM NPs exert potent anti\u2010ROS, anti\u2010inflammatory and antiapoptotic effects, highlighting a promising therapeutic avenue for targeted immunomodulation in type 1 diabetes.<\/jats:p>\n                  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