Institut National de la Santé et de la Recherche Médicale UMR699-Université Paris Diderot, Faculté de Médecine Xavier Bichat, 16 rue Henri Huchard, 75870 Paris, Cedex 18, France.
Curr Allergy Asthma Rep. 2011 Oct;11(5):378-87. doi: 10.1007/s11882-011-0216-5.
Systemic lupus erythematosus (SLE) is a heterogeneous disease that can affect multiple organs. A hallmark of this disease, as is the case for other autoimmune diseases, is the presence of large numbers of autoantibodies. As such, SLE is considered to be a B-cell disease perpetuated by the expansion of autoreactive T and B cells. The T cells involved have long been considered to be T-helper type 1 (Th1) and Th17 cells, as these potent proinflammatory cells can be found in the tissues of SLE patients. Recent advances point to a role for the Th2 environment in contributing to SLE through promotion of autoantibody production. Here we describe the recent work focusing on autoreactive IgE and the activation of basophils as promoting the production of autoantibodies in SLE. The findings, both in a murine model of SLE and in humans with SLE, support the concept that the activation of the basophil by autoreactive IgE-containing immune complexes serves to amplify the production of autoantibodies and contributes to the pathogenesis of disease. We propose that therapeutic targeting of this amplification loop by reducing the levels of circulating autoreactive IgE may have benefit in SLE.
系统性红斑狼疮（SLE）是一种异质性疾病，可影响多个器官。这种疾病的一个标志是存在大量的自身抗体。因此，SLE 被认为是一种由自身反应性 T 和 B 细胞扩增引起的 B 细胞疾病。长期以来，人们一直认为涉及的 T 细胞是辅助性 T 细胞 1（Th1）和 Th17 细胞，因为这些强效的促炎细胞可以在 SLE 患者的组织中找到。最近的进展表明，Th2 环境通过促进自身抗体的产生而在 SLE 中起作用。在这里，我们描述了最近的工作，重点是自身反应性 IgE 和嗜碱性粒细胞的激活，作为促进 SLE 中自身抗体产生的机制。在 SLE 的小鼠模型和 SLE 患者中的发现支持这样一种观点，即含有自身反应性 IgE 的免疫复合物激活嗜碱性粒细胞可放大自身抗体的产生，并有助于疾病的发病机制。我们提出，通过降低循环中自身反应性 IgE 的水平来靶向这种放大环可能对 SLE 有益。
