自身免疫
免疫学
生殖系
自身抗体
PI3K/AKT/mTOR通路
免疫缺陷
生物
免疫系统
免疫耐受
信号转导
自身免疫性疾病
遗传学
基因
抗体
作者
Julia Bier,Elissa K. Deenick
摘要
Better treatment of autoimmune diseases requires an improved understanding of the cellular and molecular mechanisms that lead to the breakdown of immune tolerance. The discovery of individuals with germline mutations in PIK3CD (which encodes the p110δ catalytic subunit of PI3K) has revealed the importance of regulated PI3Kδ activity to maintain tolerance. These patients display a range of symptoms including both immunodeficiency and autoimmunity. Here, we discuss recent advances in our understanding of how dysregulated PI3Kδ signaling affects the activation and differentiation of multiple cell types leading to the production of autoantibodies in these patients. This has lessons, not only for the treatment of these patients, but also for the potential role of dysregulated PI3Kδ in other patients with autoimmune conditions.
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