Department of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis Medical Center, Sacramento, CA, USA.
Department of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Clin Immunol. 2023 Jun;251:109327. doi: 10.1016/j.clim.2023.109327. Epub 2023 Apr 8.
Interleukin 27 has both pro-inflammatory and anti-inflammatory properties in autoimmunity. The anti-inflammatory effects of IL-27 are linked with inhibition of Th17 differentiation but the IL-27 effect on myeloid cells is less studied. Herein we demonstrate that IL-27 inhibits IL-23-induced inflammation associated not only with Th17 cells but also with myeloid cell infiltration in the joints and splenic myeloid populations of CD11b GR1 and CD3CD11bCD11cGR1 cells. The IL-27 anti-inflammatory response was associated with reduced levels of myeloid cells in the spleen and bone marrow. Overall, our data demonstrate that IL-27 has an immunosuppressive role that affects IL-23-dependent myelopoiesis in the bone marrow and its progression to inflammatory arthritis and plays a crucial role in controlling IL-23 driven joint inflammation by negatively regulating the expansion of myeloid cell subsets.
白细胞介素 27 在自身免疫中具有促炎和抗炎特性。IL-27 的抗炎作用与抑制 Th17 分化有关,但 IL-27 对髓样细胞的作用研究较少。本文中我们证明,IL-27 抑制 IL-23 诱导的炎症,不仅与 Th17 细胞有关,而且与关节和脾髓样细胞浸润以及 CD11b GR1 和 CD3CD11bCD11cGR1 细胞的脾髓样细胞群有关。IL-27 的抗炎反应与骨髓中髓样细胞水平降低有关。总的来说,我们的数据表明,IL-27 具有免疫抑制作用,影响骨髓中依赖 IL-23 的髓样细胞生成及其向炎症性关节炎的进展,并通过负调控髓样细胞亚群的扩增在控制 IL-23 驱动的关节炎症中发挥关键作用。