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<p>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.</p>

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Controlled release of CD200 inhibits inflammatory macrophages and chondrocyte catabolism

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月29日

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  • Shreedevi Kumar,
  • Folly M. Patterson,
  • Tiffany Conklin,
  • Ssu-Chieh J. Hsu,
  • Vijaykumar Meli,
  • Kiara Chan,
  • Kyle D. Allen,
  • Wendy F. Liu,
  • Blanka Sharma

摘要

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.