Non‐bilayer phospholipids arrangements (NPAs) are transient molecular associations different from lipid bilayers. When they become stable, they can trigger a disease in mice resembling human lupus, which is mainly characterized by the production of anti‐NPA IgG antibodies. NPAs are stabilized on liposomes or cell bilayers by the drugs procainamide or chlorpromazine, which produce drug‐induced lupus in humans. Here, we evaluated the participation of the T_H2 response, through its hallmark cytokine IL‐4, on the development of the lupus‐like disease in mice. Wild‐type or IL‐4 knockout BALB/c mice received liposomes bearing drug‐induced NPAs, the drugs alone, or an anti‐NPA monoclonal antibody (H308) to induce the lupus‐like disease (the last two procedures stabilize NPAs on mice cells). IL‐4 KO mice showed minor disease manifestations, compared to wild‐type mice, with decreased production of anti‐NPA IgG antibodies, no anti‐cardiolipin, anti‐histones and anticoagulant antibodies, and no kidney or skin lesions. In these mice, H308 was the only inducer of anti‐NPA IgG antibodies. These findings indicate that IL‐4 has a central role in the development of the murine lupus‐like disease induced by NPA stabilization.

中文翻译：

---

白介素4缺乏症限制了非双层安排的磷脂触发的小鼠狼疮样疾病的发展

非双层磷脂排列（NPA）是不同于脂质双层的瞬时分子缔合。当它们变得稳定时，它们可以引发类似于人狼疮的小鼠疾病，其主要特征是产生抗-NPA IgG抗体。普鲁卡因酰胺或氯丙嗪可将NPA稳定在脂质体或细胞双层上，从而在人体中产生药源性狼疮。在这里，我们评估了T _H的参与通过其标志性细胞因子IL-4对小鼠狼疮样疾病的发展产生2种反应。野生型或IL-4基因敲除的BALB / c小鼠接受带有药物诱导的NPA的脂质体，单独使用药物或抗NPA单克隆抗体（H308）诱导狼疮样疾病（后两种方法可稳定小鼠的NPAs细胞）。与野生型小鼠相比，IL-4 KO小鼠表现出较小的疾病表现，其抗-NPA IgG抗体的产生减少，没有抗心磷脂，抗组蛋白和抗凝抗体，并且没有肾脏或皮肤病变。在这些小鼠中，H308是抗NPA IgG抗体的唯一诱导剂。这些发现表明，IL-4在由NPA稳定诱导的鼠类狼疮样疾病的发展中起着核心作用。