Whether T cells promote bone loss following immobilization after spinal cord injury (SCI) remains undetermined. Therefore, wild-type (WT) and T cell-deficient (Tcrb-/- ) male mice underwent sham or contusion SCI to cause hindlimb paralysis. Femurs were isolated and distal and midshaft regions were evaluated by microcomputed tomography scanning. Bone marrow (BM) levels of bone turnover markers, as well as receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG), were measured by ELISA. At 2 weeks post-SCI, immobilization resulted in marked reduction in trabecular fractional bone volume (55%), thickness (40%), connectivity, and cortical thickness only in the Tcrb-/- animals (interaction with P < 0.05). BM analysis revealed lower bone formation (procollagen type 1 intact N-terminal propeptide), higher bone resorption (tartrate-resistant acid phosphatase-5b), and a higher RANKL/OPG ratio in the Tcrb-/- SCI animals. At 5 weeks post-SCI, while both WT and Tcrb-/- paralyzed animals showed deterioration of all indices of bone structure, they were more severe in Tcrb-/- animals. In summary, unlike other skeletal disorders, loss of αβ T cells compromises, rather than preserves, skeletal integrity under conditions of immobilization.

中文翻译：

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缺乏αβT细胞会加速雄性小鼠脊髓损伤后的废用性骨丢失

T 细胞是否促进脊髓损伤 (SCI) 后固定后的骨丢失仍未确定。因此，野生型 (WT) 和 T 细胞缺陷型 (Tcrb-/- ) 雄性小鼠接受假性或挫伤性 SCI 导致后肢麻痹。分离股骨，通过微型计算机断层扫描评估远端和中轴区域。通过ELISA测量骨转换标志物的骨髓（BM）水平，以及核因子-κB配体（RANKL）和骨保护素（OPG）的受体激活剂。在 SCI 后 2 周，固定导致仅 Tcrb-/- 动物的小梁部分骨体积 (55%)、厚度 (40%)、连接性和皮质厚度显着减少（与 P < 0.05 的相互作用）。BM 分析显示骨形成较低（1 型前胶原完整的 N 末端前肽），Tcrb-/- SCI 动物中较高的骨吸收（抗酒石酸酸性磷酸酶 5b）和较高的 RANKL/OPG 比率。在 SCI 后 5 周，虽然 WT 和 Tcrb-/- 瘫痪动物的所有骨结构指标均出现恶化，但在 Tcrb-/- 动物中它们更为严重。总之，与其他骨骼疾病不同，αβ T 细胞的丢失会损害而不是保留固定条件下的骨骼完整性。