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We are analyzing https://www.nature.com/articles/s41467-023-36468-2.

Title:
Remodeling articular immune homeostasis with an efferocytosis-informed nanoimitator mitigates rheumatoid arthritis in mice | Nature Communications
Description:
Massive intra-articular infiltration of proinflammatory macrophages is a prominent feature of rheumatoid arthritis (RA) lesions, which are thought to underlie articular immune dysfunction, severe synovitis and ultimately joint erosion. Here we report an efferocytosis-informed nanoimitator (EINI) for in situ targeted reprogramming of synovial inflammatory macrophages (SIMs) that thwarts their autoimmune attack and reestablishes articular immune homeostasis, which mitigates RA. The EINI consists of a drug-based core with an oxidative stress-responsive phosphatidylserine (PtdSer) corona and a shell composed of a P-selectin-blocking motif, low molecular weight heparin (LMWH). When systemically administered, the LMWH on the EINI first binds to P-selectin overexpressed on the endothelium in subsynovial capillaries, which functions as an antagonist, disrupting neutrophil synovial trafficking. Due to the strong dysregulation of the synovial microvasculature, the EINI is subsequently enriched in the joint synovium where the shell is disassembled upon the reactive oxygen species stimulation, and PtdSer corona is then exposed. In an efferocytosis-like manner, the PtdSer-coroneted core is in turn phagocytosed by SIMs, which synergistically terminate SIM-initiated pathological cascades and serially reestablish intra-articular immune homeostasis, conferring a chondroprotective effect. These findings demonstrate that SIMs can be precisely remodeled via the efferocytosis-mimetic strategy, which holds potential for RA treatment. Proinflammatory macrophages are involved in rheumatoid arthritis (RA). Here the authors use an efferocytosis-mimetic self-deliverable nanoimitator to mitigate RA by targeted reprogramming of synovial inflammatory macrophages, reducing proinflammatory cytokines and reinstating articular immune homeostasis.
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fig, nanoimitator, macrophages, article, mice, pubmed, google, scholar, supplementary, cells, arthritis, data, immune, neutrophils, cas, siirfeini, irf, rheumatoid, synovial, treatment, group, joint, analysis, shandong, pbs, independent, inflammatory, cell, cia, ptdser, synovium, articular, joints, nature, sims, staining, experiments, fluorescence, homeostasis, shown, min, patients, mouse, images, bone, tnf, treated, nat, eini, results,

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nature portfolio reduce air-pollution-induced thrombosis blinded researcher based prostaglandin e2-ep2/ep4 signaling fitc-labeled anti-ly-6g antibody terminating sim-initiated cascades sim-initiated pathological cascades abort sim-initiated cascades human p-selectin/cd62p antibody peer review nature 434 nature data availability references sparks reprints fitc-conjugated anti-f4/80 antibodies thermo fisher scientific 10 mg/kg metformin-equivalent dose siirf5-laden efferocytosis-informed nanoimitator japan media regional low-ph-triggered structural disassembly innovation research groups anti-ly-6g antibody fundamental research funds siirf5-carrying efferocytosis-informed nanoimitator intra-articular blood vessels original author ros-responsive ptdser-nbc conjugate macrophage-derived chemokine cxcl1 accession code e-mtab-614152 m-csf-oriented cells present tartrate-resistant acid phosphatase supplementary information review board protocol biotinylated anti-rabbit igg technology research tissue-tek oct compound hyaluronic acid–bilirubin nanomedicine neutrophil attractants-chemokine cxcl114 successful lyso/endosome escape metformin-mediated metabolic reprogramming low-molecular-weight-heparin osteoclast-dependent cartilage destruction mouse collagen-induced arthritis peer reviewer reports macrophage-derived cxcl1 levels source data file time-dependent ros elimination

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Perspectives from masters in rheumatology and autoimmunity: can we get closer to a cure for rheumatoid arthritis?

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      headline:Remodeling articular immune homeostasis with an efferocytosis-informed nanoimitator mitigates rheumatoid arthritis in mice
      description:Massive intra-articular infiltration of proinflammatory macrophages is a prominent feature of rheumatoid arthritis (RA) lesions, which are thought to underlie articular immune dysfunction, severe synovitis and ultimately joint erosion. Here we report an efferocytosis-informed nanoimitator (EINI) for in situ targeted reprogramming of synovial inflammatory macrophages (SIMs) that thwarts their autoimmune attack and reestablishes articular immune homeostasis, which mitigates RA. The EINI consists of a drug-based core with an oxidative stress-responsive phosphatidylserine (PtdSer) corona and a shell composed of a P-selectin-blocking motif, low molecular weight heparin (LMWH). When systemically administered, the LMWH on the EINI first binds to P-selectin overexpressed on the endothelium in subsynovial capillaries, which functions as an antagonist, disrupting neutrophil synovial trafficking. Due to the strong dysregulation of the synovial microvasculature, the EINI is subsequently enriched in the joint synovium where the shell is disassembled upon the reactive oxygen species stimulation, and PtdSer corona is then exposed. In an efferocytosis-like manner, the PtdSer-coroneted core is in turn phagocytosed by SIMs, which synergistically terminate SIM-initiated pathological cascades and serially reestablish intra-articular immune homeostasis, conferring a chondroprotective effect. These findings demonstrate that SIMs can be precisely remodeled via the efferocytosis-mimetic strategy, which holds potential for RA treatment. Proinflammatory macrophages are involved in rheumatoid arthritis (RA). Here the authors use an efferocytosis-mimetic self-deliverable nanoimitator to mitigate RA by targeted reprogramming of synovial inflammatory macrophages, reducing proinflammatory cytokines and reinstating articular immune homeostasis.
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