Tchen John, Charles Nicolas
Université Paris Cité, Centre de recherche sur l'inflammation, Inserm UMR1149, CNRS ERL8252, Faculté de médecine site Bichat, Paris, France - Université Paris Cité, Laboratoire d'excellence Inflamex, Paris, France.
Med Sci (Paris). 2022 Apr;38(4):366-373. doi: 10.1051/medsci/2022040. Epub 2022 Apr 29.
Understanding the pathophysiology of antibody-driven autoimmune diseases (AAID) represents a major challenge for the biomedical community to develop innovative therapeutic strategies that are still lacking to control these diseases. If the reason why AAID are developing still needs to be defined, loss of tolerance to self-antigens leads to the development of an autoimmune chain reaction in some individuals. However, autoreactive antibodies are present in a large proportion of the general population without any associated pathological condition. The amplification of autoantibody production, circulating immune complex formation and innate immune system activation leading to this amplification are some central phenomena in AAID pathophysiology. In this review, we summarize the contribution of type 2 immunity, basophils and IgE in the initiation of some amplification loops that are pathogenic in some AAID, including systemic lupus erythematosus and mixed connective tissue disease.
了解抗体驱动的自身免疫性疾病(AAID)的病理生理学是生物医学界面临的一项重大挑战,目前仍缺乏创新的治疗策略来控制这些疾病。虽然AAID的发病原因仍有待明确,但对自身抗原耐受性的丧失会导致部分个体发生自身免疫连锁反应。然而,在大部分普通人群中都存在自身反应性抗体,却没有任何相关的病理状况。自身抗体产生的放大、循环免疫复合物的形成以及导致这种放大的固有免疫系统激活是AAID病理生理学中的一些核心现象。在本综述中,我们总结了2型免疫、嗜碱性粒细胞和IgE在某些AAID(包括系统性红斑狼疮和混合性结缔组织病)发病过程中一些致病放大环路启动中的作用。