Articlenpj biomedical innovations2026
Controlled release of CD200 inhibits inflammatory macrophages and chondrocyte catabolism.
Article in npj biomedical innovations, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Encoded Cell-Material Interactions to Reroute Cytokine Signaling for Regenerative Medicine.Advanced healthcare materials · 2026Article
- Encoded cell-material interactions to reroute cytokine signaling for regenerative medicine.bioRxiv : the preprint server for biology · 2025Article
- Instructional materials that control cellular activity through synthetic Notch receptors.Biomaterials · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
In the osteoarthritic joint, activated macrophages release pro-inflammatory factors that promote cartilage degeneration. The CD200:CD200R immune checkpoint pathway is a promising therapeutic target that inhibits classical macrophage activation. We hypothesized that the presentation of CD200 to macrophages would shift their cytokine profile from pro-inflammatory to pro-regenerative, thereby reducing chondrocyte catabolism. CD200 encapsulated in poly(lactide-co-glycolide) microparticles (MPs) were incubated with murine bone marrow-derived macrophages. CD200 MP treatment reduced protein and gene expression of pro-inflammatory mediators in M1 macrophages and increased protein and gene expression of anti-inflammatory mediators in M2 and M1/2 macrophages. Conditioned media from CD200 MP-treated M1 macrophages reduced the expression of catabolic enzyme genes in chondrocytes. This study is the first to demonstrate that delivery of CD200 alters the inflammatory cascade and paracrine signaling to chondrocytes. There is significant potential for the CD200:CD200R inhibitory signaling pathway to be leveraged as an intra-articular treatment of OA.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.