为了阐明炎性细胞因子是否可能影响椎间盘和黄韧带源祖细胞向成骨或脂肪生成的承诺，特别是白细胞介素-1β（IL-1β）、IL-19和IL-20，该研究纳入了60例椎间盘退变性滑脱和腰椎或腰骶椎管狭窄患者。排除了脊柱损伤、感染以及良性或恶性肿瘤。从9个患者样本中经过原代培养分离出椎间盘和黄韧带源细胞，由于感染了支原体，排除了两个临床样本。在 vitro 中研究了IL-1β、IL-19以及IL-20在调节成骨和脂肪生成方面的影响。 发现原发椎间盘/黄韧带细胞具有与胎盘来源间充质干细胞（MSCs）相似的细胞形态和表面标记物（CD44、CD90和CD105）配置。原发椎间盘/黄韧带细胞具有高度分化为成骨细胞和脂肪细胞的能力。IL-19倾向于促进脂肪生成。IL-20抑制成骨形成并促进脂肪生成；IL-1β促进成骨形成但抑制脂肪生成。 IL-1β、IL-19和IL-20影响椎间盘和黄韧带源细胞的脂肪生成和骨生成分化。调控IL-1β、IL-19和IL-20的表达为控制椎间盘和黄韧带源细胞的分化提供了一个潜在途径，这可能对于退变性滑脱和脊柱狭窄具有益处。© 2023. 作者，独家授权给德国斯普林格维尔根出版社，斯普林格自然出版集团的一部分。

To elucidate whether pro-inflammatory cytokines might influence the commitment of intervertebral disc (IVD)- and ligamentum flavum (LF)-derived progenitor cells toward either osteogenesis or adipogenesis, specifically Interleukin-1β (IL-1β), IL-19, and IL-20.Sixty patients with degenerative spondylolisthesis and lumbar or lumbosacral spinal stenosis were included in the study. Injuries to the spine, infections, and benign or malignant tumors were excluded. From nine patient samples, IVD- and LF-derived cells were isolated after primary culture, and two clinical samples were excluded due to mycoplasma infection. The effects of IL-1β, IL-19, as well as IL-20 in regulating osteogenic and adipogenic differentiation in vitro were investigated.Primary IVD- and LF-derived cells were found to have a similar cell morphology and profile of surface markers (CD44, CD90, and CD105) as placenta-derived mesenchymal stem cells (MSCs). Primary IVD/LF cells have a high capacity to differentiate into osteocytes and adipocytes. IL-19 had a tendency to promote adipogenesis. IL-20 inhibited osteogenesis and promoted adipogenesis; IL-1β promoted osteogenesis but inhibited adipogenesis.IL-1β, IL-19, and IL-20 impact the adipogenic and osteogenic differentiation of IVD-derived and LF-derived cells. Modulating the expression of IL-1β, IL-19, and IL-20 provides a potential avenue for controlling cell differentiation of IVD- and LF-derived cells, which might have beneficial effect for degenerative spondylolisthesis and spinal stenosis.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.