The neonatal fragment crystallizable (Fc) receptor (FcRn) functions as a recycling mechanism to prevent degradation and extend the half-life of IgG and albumin in the circulation. Several FcRn inhibitors selectively targeting IgG recycling are now moving rapidly toward clinical practice in neurology and hematology. These molecules accelerate the destruction of IgG, reducing pathogenic IgG and IgG immune complexes, with no anticipated effects on IgA, IgM, IgE, complement, plasma cells, B cells, or other cells of the innate or adaptive immune systems. FcRn inhibitors have potential for future use in a much wider variety of antibody-mediated autoimmune diseases. Given the imminent clinical use, potential for broader utility, and novel mechanism of action of FcRn inhibitors, here we review data from 4 main sources: (a) currently available activity, safety, and mechanism-of-action data from clinical trials of FcRn inhibitors; (b) other procedures and treatments that also remove IgG (plasma donation, plasma exchange, immunoadsorption); (c) diseases resulting in loss of IgG; and (d) primary immunodeficiencies with potential mechanistic similarities to those induced by FcRn inhibitors. These data have been evaluated to provide practical considerations for the assessment, monitoring, and reduction of any potential infection risk associated with FcRn inhibition, in addition to highlighting areas for future research.

新生儿片段可结晶 (Fc) 受体 (FcRn) 作为一种回收机制，可防止降解并延长 IgG 和白蛋白在循环中的半衰期。几种选择性靶向 IgG 回收的 FcRn 抑制剂目前正在迅速走向神经病学和血液学的临床实践。这些分子加速 IgG 的破坏，减少致病性 IgG 和 IgG 免疫复合物，但对 IgA、IgM、IgE、补体、浆细胞、B 细胞或先天或适应性免疫系统的其他细胞没有预期影响。FcRn 抑制剂未来有望用于更广泛的抗体介导的自身免疫性疾病。鉴于 FcRn 抑制剂迫在眉睫的临床应用、更广泛应用的潜力以及新颖的作用机制，我们在此回顾 4 个主要来源的数据：(a) 来自 FcRn 临床试验的当前可用的活性、安全性和作用机制数据抑制剂；(b) 也可去除 IgG 的其他程序和治疗（血浆捐赠、血浆置换、免疫吸附）；(c) 导致 IgG 丧失的疾病；(d) 与 FcRn 抑制剂诱导的原发性免疫缺陷具有潜在机制相似性。除了强调未来研究的领域外，这些数据还经过评估，为评估、监测和减少与 FcRn 抑制相关的任何潜在感染风险提供实际考虑。