CRCINA, INSERM, Université de Nantes, Université d'Angers, LabEx IGO, 49000 Angers, France; Service de Néphrologie-Dialyse-Transplantation, CHU Angers, 49000 Angers, France.
ImmunoConcEpT, CNRS-UMR 5164 and Université de Bordeaux, 146 rue Léo Saignat, 33076 Bordeaux, France; Centre Hospitalier Universitaire de Bordeaux, FHU ACRONIM, Place Amélie Raba Léon, 33076 Bordeaux, France.
Autoimmun Rev. 2018 Apr;17(4):361-365. doi: 10.1016/j.autrev.2017.11.027. Epub 2018 Feb 7.
Systemic lupus erythematosus (SLE) is a complex autoimmune disease involving multiple immunological pathways. Recently, several studies have suggested an implication of Immunoglobulin E (IgE) in the pathophysiology of SLE. In the Lyn and FcγIIB.Yaa lupus mouse models, autoreactive IgE activate basophils, and promote a Th2 environment with, subsequently, production of autoantibodies by plasma cells. Autoreactive IgE has been also shown to play a role in the activation of human plasmacytoid dendritic cells (pDCs), in synergy with IgG, which results in an increase of interferon-alpha (IFN-α) production. In contrast, a protective effect of total non-autoreactive IgE has also been suggested, through a decreased ability of FcεRI-triggered pDCs to secrete IFN-α. This review summarizes in a comprehensive manner the emerging recent literature in the field, and propose new concepts to reconcile the observations.
系统性红斑狼疮（SLE）是一种复杂的自身免疫性疾病，涉及多种免疫途径。最近，几项研究表明免疫球蛋白 E（IgE）在 SLE 的病理生理学中起作用。在 Lyn 和 FcγIIB.Yaa 狼疮小鼠模型中，自身反应性 IgE 激活嗜碱性粒细胞，并促进 Th2 环境，随后浆细胞产生自身抗体。自身反应性 IgE 也被证明在与 IgG 协同作用下，在人类浆细胞样树突状细胞（pDC）的激活中起作用，导致干扰素-α（IFN-α）的产生增加。相比之下，通过降低 FcεRI 触发的 pDC 分泌 IFN-α的能力，总非自身反应性 IgE 也显示出保护作用。本综述全面总结了该领域新出现的文献，并提出了新的概念来协调这些观察结果。
