摘要
白细胞介素33(IL-33)是IL-1家族的一个新的细胞因子,并通过磺基转氨酶2受体介导它的生物学效应。动物实验表明,IL-33具有很强的促炎作用,且其致损伤作用有赖于肿瘤坏死因子受体1和干扰素γ的存在,IL-33在许多炎性疾病中大量表达,这里主要介绍类风湿关节炎。在类风湿关节炎患者的滑膜组织中大量表达IL-33,IL-33通过肥大细胞依赖途径促进疾病从急性到慢性的转化,从而导致疾病的迁延难愈。由于可溶性ST2有助于减轻IL-33引起的炎性效应,从而在类风湿关节炎治疗中看到了曙光。
Interleukin-33(IL-33)is a new cytokine of IL-1 family,and its biological effects are mediated through ST2 receptor.Animal experiments show that IL-33 has a strong pro-inflammatory role,and induces damages depending on the presence of tumor necrosis factor receptor2(TNFR1)and interferon γ(IFNγ).Excessive IL-33 is expressed in many inflammatory diseases,including rheumatoid arthritis.Synovial tissues in patients with rheumatoid arthritis overexpress IL-33,promoting disease from the acute to chronic conversion through mast cell-dependent pathway,leading to the prolongation of refractory disease.As sST2 helps to reduce IL-33-induced inflammatory effects,we can see a dawn in the treatment of rheumatoid arthritis.
出处
《医学综述》
2010年第11期1614-1617,共4页
Medical Recapitulate