Systemic lupus erythematosus (SLE) is a systemic and potentially fatal autoimmune disease. SLE pathophysiology is complex and involves the interplay between the innate and adaptive immune systems, with a particularly significant role for type I interferons. Recently, the participation of other actors such as platelets and IgE has been described in SLE. On the one hand, platelets activated by different stimuli (antiphospholipid antibodies, immune complexes…) participate in immune dysregulation through direct interactions with immune cells. On the other hand, autoreactive IgE can activate basophils, promoting a Th2 environment and subsequent antibody production by plasma cells. In synergy with IgG, IgE is also able to activate plasmacytoid DCs (pDCs) increasing interferon alpha production. Mirroring the IgG paradox, total nonautoreactive IgE is described as a potential regulator of IFNα production. This review summarizes recent and novel data on innate immunity in SLE pathophysiology with a focus on platelets and IgE, as they represent novel players in immune dysregulation and potential therapeutic targets.

中文翻译：

---

血小板和IgE：塑造系统性红斑狼疮的先天免疫反应。

系统性红斑狼疮（SLE）是一种系统性且可能致命的自身免疫性疾病。SLE病理生理学很复杂，涉及先天性免疫系统和适应性免疫系统之间的相互作用，对I型干扰素尤为重要。最近，SLE中描述了其他参与者（例如血小板和IgE）的参与。一方面，由不同刺激（抗磷脂抗体，免疫复合物……）激活的血小板通过与免疫细胞的直接相互作用而参与免疫失调。另一方面，自身反应性IgE可以激活嗜碱性粒细胞，从而促进Th2环境并随后由浆细胞产生抗体。与IgG协同作用，IgE还能够激活浆细胞样DC（pDC），从而增加干扰素α的产生。反映IgG悖论，总的非自身反应性IgE被描述为IFNα产生的潜在调节剂。这篇综述总结了关于SLE病理生理中先天免疫的最新和新颖数据，重点是血小板和IgE，因为它们代表了免疫失调和潜在治疗靶点的新角色。