Institut National de la Santé et de la Recherche Médicale (INSERM) UMR_S699, Université Paris Diderot, Faculté de Médecine site Bichat, Labex Inflamex, DHU Fire - 16 rue Henri Huchard, 75870 Paris cedex 18, France.
Curr Opin Immunol. 2013 Dec;25(6):704-11. doi: 10.1016/j.coi.2013.10.003. Epub 2013 Oct 24.
Systemic lupus erythematosus is a complex autoimmune disease of multifactorial origins. All compartments of the immune system appear to be affected, at least in some way, and to contribute to disease pathogenesis. Because of an escape from negative selection autoreactive T and B cells accumulate in SLE patients leading to the production of autoantibodies mainly raised against nuclear components and their subsequent deposition into target organs. We recently showed that basophils, in an IgE and IL-4 dependent manner, contribute to SLE pathogenesis by amplifying autoantibody production. Here, we summarize what we have learned about the deleterious role of basophils in lupus both in a mouse model and in SLE patients. We discuss which possible pathways could be involved in basophil activation and recruitment to secondary lymphoid organs during SLE, and how basophils may amplify autoantibody production.
系统性红斑狼疮是一种复杂的自身免疫性疾病，具有多因素起源。免疫系统的所有部分似乎都受到影响，至少在某种程度上，并且有助于疾病的发病机制。由于逃避负选择，自身反应性 T 和 B 细胞在 SLE 患者中积累，导致主要针对核成分产生自身抗体，随后沉积到靶器官中。我们最近表明，嗜碱性粒细胞以 IgE 和 IL-4 依赖的方式通过放大自身抗体产生来促进 SLE 的发病机制。在这里，我们总结了我们在狼疮小鼠模型和 SLE 患者中了解到的嗜碱性粒细胞在狼疮中的有害作用。我们讨论了在 SLE 期间可能涉及嗜碱性粒细胞激活和募集到次级淋巴器官的哪些可能途径，以及嗜碱性粒细胞如何放大自身抗体的产生。
