期刊文献+

多发性骨髓瘤骨病患者白细胞介素-17的表达及其意义 被引量:1

Expression and significance of IL-17 in multiple myeloma bone disease
原文传递
导出
摘要 目的研究多发性骨髓瘤(MM)骨病患者骨髓中自细胞介素17(IL-17)的表达水平及其与骨髓单个核细胞核因子.(B受体活化因子配体(RANKL)表达的关系,探讨IL-17在MM骨病发病机制中的作用及其临床意义。方法采用双抗体夹心酶联免疫吸附(ELISA)法检测33例MM骨病患者及20例对照者骨髓上清中IL-17水平,采用荧光定量PCR检测上述两组骨髓单个核细胞RANKLmRNA的表达。结果MM骨病组及对照组的骨髓上清均表达IL-17,骨髓单个核细胞均表达RANKLmRNA。MM骨病组骨髓上清中IL-17的含量[(52.69±4.55)pg/ml]高于对照组[(14.35±1.25)Pg/m1],MM骨病组骨髓单个核细胞RANKLmRNA的表达[(0.96±0.12)Pg/ml]高于对照组[(0.42±0.03)Pg/m1],差异均有统计学意义(P〈0.05)。活动期MM骨病患者骨髓IL-17[(76.71±7.06)pg/m1]水平显著高于稳定期MM骨病患者[(40.67±3.84)Pg/ml],差异有统计学意义(P〈0.05),活动期MM骨病患者骨髓单个核细胞RANKL mRNA的表达水平(1.22±0.27)显著高于稳定期MM骨病患者(0,83±O.12),差异有统计学意义(P〈0.05)。MM骨病组骨髓IL-17与RANKL的表达呈显著正相关(r=0.690,P〈0.05)。结论MM骨病患者骨髓IL-17的表达显著增高,骨髓IL-17水平与MM活动期和(或)稳定期相关,骨髓IL-17与RANKI.的表达呈正相关,I-17可能在MM骨病的发病机制中起重要的作用。 Objective To detect IL-17 level of bone marrow in patients with muhiple myeloma bone disease,and to investigate its clinical significance. Methods The bone marrow IL-17 levelswere quantified in 33 cases of multiple myeloma patients and 20 normal control by ELISA assay. RANKL mRNA expression were detected by using RT-PCR. Results In bone marrow supematant, IL-17 was detected in both groups, and RANKL mRNA were detected in both groups too. IL-17 and RANKL mRNA levels in bone marrow of patients with MM were significantly higher than those in the control group (P〈0.05). The bone marrow concentrations of IL-17 and bone marrow mononuclear ceils' RANKL mRNA expression in active stage were significantly higher than those in stable stage (P〈0.05). The bone marrow IL-17 and RANKL were significantly correlated (r = 690, P〈0.05). Conclusion IL-17 may play an important role in the pathogenesis of MM.
出处 《白血病.淋巴瘤》 CAS 2012年第5期282-284,共3页 Journal of Leukemia & Lymphoma
关键词 多发性骨髓瘤骨病 白细胞介素-17 核因子kB受体活化因子配体 Multiple myeloma bone disease Interleukin-17 Receptor activator of nuclear factor- kappaB
  • 相关文献

参考文献18

  • 1Walsh MC, Kim N, Kadono Y, et al. Osteoimmunology:interplay between the immune system and bone metabolism. Annu Rev Immunol, 2006, 24:33-63.
  • 2Takayanagi H. Inflammatory bone destruction and osteoimmunology. J Periodontal Res, 2005, 40:287-293.
  • 3Sato K, Takayanagi H. Osteoclasts, rheumatoid arthritis, and osteoimmunology. Curr Opin Rheumatol, 2006, 18:419-426.
  • 4Theill LE, Boyle WJ, Penninger JM. RANK-L and RANK:T cells, bone loss, and mammalian evolution. Annu Rev Immunol, 2002, 20: 795-823.
  • 5Teitelbaum SL, Ross FP. Genetic regulation of osteoclast development and function. Nat Rev Genet, 2003,4:638-649.
  • 6Boyle WJ, Simonet WS, Lacey DL. Osteoclast differentiation and activation. Nature, 2003, 423:337-342.
  • 7Suda T, Takahashi N, Udagawa N, et al. Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families. Endocr Rev, 1999, 20:345-357.
  • 8Dong C. Diversification of T-helper-cell lineages:finding the family root of IL-17-producing cells. Nat Rev Immunol, 2006, 6:329-333.
  • 9Weaver CT, Harrington LE, Mangan PR, et al. Thl7:an effector CD4T cell lineage w~th regulatory T cell ties. Immunity, 2006, 24:677-688.
  • 10Sezer 0, Heider U, Zavrski I, et al. RANK ligand and ostooprotegerin in myeloma bone disease. Blood, 2003,101:2094-2098.

同被引文献6

引证文献1

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部