轴向脊柱关节炎的骨髓侧。

The bone marrow side of axial spondyloarthritis.

机构信息

Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.

Unit of Rheumatology, San Giovanni Bosco Hospital, Naples, Italy.

出版信息

Nat Rev Rheumatol. 2023 Aug;19(8):519-532. doi: 10.1038/s41584-023-00986-6. Epub 2023 Jul 5.

Abstract

Spondyloarthritis (SpA) is characterized by the infiltration of innate and adaptive immune cells into entheses and bone marrow. Molecular, cellular and imaging evidence demonstrates the presence of bone marrow inflammation, a hallmark of SpA. In the spine and the peripheral joints, bone marrow is critically involved in the pathogenesis of SpA. Evidence suggests that bone marrow inflammation is associated with enthesitis and that there are roles for mechano-inflammation and intestinal inflammation in bone marrow involvement in SpA. Specific cell types (including mesenchymal stem cells, innate lymphoid cells and γδ T cells) and mediators (Toll-like receptors and cytokines such as TNF, IL-17A, IL-22, IL-23, GM-CSF and TGFβ) are involved in these processes. Using this evidence to demonstrate a bone marrow rather than an entheseal origin for SpA could change our understanding of the disease pathogenesis and the relevant therapeutic approach.

摘要

脊柱关节炎(SpA)的特征是先天和适应性免疫细胞浸润到附着点和骨髓。分子、细胞和影像学证据表明存在骨髓炎症,这是 SpA 的标志。在脊柱和外周关节中,骨髓在 SpA 的发病机制中起着关键作用。有证据表明骨髓炎症与附着点炎有关,机械炎症和肠道炎症在 SpA 的骨髓受累中起作用。特定的细胞类型(包括间充质干细胞、固有淋巴细胞和γδ T 细胞)和介质(Toll 样受体和细胞因子,如 TNF、IL-17A、IL-22、IL-23、GM-CSF 和 TGFβ)参与了这些过程。利用这些证据证明 SpA 起源于骨髓而不是附着点,可以改变我们对疾病发病机制和相关治疗方法的理解。

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