ArticleBone & joint research2026
Targeting the neuropilin 1/interferon γ axis restores glucocorticoid-suppressed T cell function and rescues bone formation to prevent steroid-induced osteonecrosis.
Article in Bone & joint research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aims: Immune cells exert influence on skeletal homeostasis, and re-establishing metabolic equilibrium is central to the management of steroid-induced osteonecrosis of the femoral head (SIONFH). However, the osteoimmune mechanisms underpinning this pathology remain largely under-researched. This study aimed to delineate these mechanisms, thereby informing early therapeutic strategies to restore bone homeostasis. Methods: We identified the key immune cell subsets associated with SIONFH, and investigated their upstream regulatory factors and downstream effector molecules by integrating multiomics analyses (samples derived from human peripheral blood, femoral head tissues, and rat peripheral blood), mining of the GSE123568 dataset, and performing in vivo and in vitro experiments. Results: Clinical transcriptomics revealed enrichment of immune-related pathways, with ssGSEA consistently highlighting activated CD8 Conclusion: Glucocorticoids suppress T cell-derived IFNγ via NRP1 upregulation, thereby impairing Runx2 nuclear translocation and BMSC osteogenesis. Sec2 counteracts this cascade through antigen-presenting cell modulation, restoring the NRP1/IFNγ axis to preserve femoral head integrity.
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