Department of Biochemistry and Molecular Pharmacology, New York University (NYU) Grossman School of Medicine, New York, NY, United States.
Department of Medicine, New York University (NYU) Grossman School of Medicine, New York, NY, United States.
Front Immunol. 2022 Jan 28;13:812649. doi: 10.3389/fimmu.2022.812649. eCollection 2022.
Autoimmune diseases are often associated with autoantibodies that abnormally target self-antigens (autoantigens). An intuitive therapeutic strategy for diseases caused by aAbs is to design decoys, or soluble molecules that target the antigen combining site of these aAbs, thereby blocking binding of aAb to self-antigen and subsequent tissue damage. Here, we review the known decoy molecules of these types, discuss newer technological opportunities afforded by monoclonal antibody and structural biology advances, and discuss the challenges to this approach. Recent opportunities relevant to this approach for cardiac phenotypes, specifically Ro-associated long QT syndrome, are discussed.
自身免疫性疾病通常与异常针对自身抗原（自身抗原）的自身抗体（aAbs）有关。针对由 aAbs 引起的疾病的一种直观的治疗策略是设计诱饵，或针对这些 aAbs 的抗原结合位点的可溶性分子，从而阻断 aAb 与自身抗原的结合及其随后的组织损伤。在这里，我们回顾了这些类型的已知诱饵分子，讨论了单克隆抗体和结构生物学进步带来的新技术机会，并讨论了这种方法面临的挑战。还讨论了与这种方法相关的心脏表型（特别是 Ro 相关的长 QT 综合征）的最新机会。
