Sigalov Alexander B
Department of Pathology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester 01655, Massachusetts, USA.
Adv Exp Med Biol. 2008;640:268-311. doi: 10.1007/978-0-387-09789-3_20.
Protein-protein interactions play a central role in biological processes and thus are an appealing target for innovative drug design a nd development. They can be targeted bysmall molecule inhibitors, peptides and peptidomimetics, which represent an alternative to protein therapeutics that carry many disadvantages. In this chapter, I describe specific protein-protein interactions suggested by a novel model of immune signaling, the Signaling Chain HOmoOLigomerization (SCHOOL) model, to be critical for cell activation mediated by multichain immune recognition receptors (MIRRs) expressed on different cells of the hematopoietic system. Unraveling a long-standing mystery of MIRR triggering and transmembrane signaling, the SCHOOL model reveals the intrareceptor transmembrane interactions and interreceptor cytoplasmic homointeractions as universal therapeutic targets for a diverse variety of disorders mediated by immune cells. Further, assuming that the general principles underlying MIRR-mediated transmembrane signaling mechanisms are similar, the SCHOOL model can be applied to any particular receptor of the MIRR family. Thus, an important application of the SCHOOL model is that global therapeutic strategies targeting key protein-protein interactions involved in MIRR triggering and transmembrane signal transduction may be used to treat a diverse set of immune-mediated diseases. This assumes that clinical knowledge and therapeutic strategies can be transferred between seemingly disparate disorders, such as T-cell-mediated skin diseases and platelet disorders, or combined to develop novel pharmacological approaches. Intriguingly, the SCHOOL model unravels the molecular mechanisms underlying ability of different human viruses such as human immunodeficiency virus, cytomegalovirus and severe acute respiratory syndrome coronavirus to modulate and/or escape the host immune response. It also demonstrates how the lessons learned from viral pathogenesis can be used practically for rational drug design. Application of this model to platelet collagen receptor signaling has already led to the development of a novel concept of platelet inhibition and the invention of new platelet inhibitors, thus proving the suggested hypothesis and highlighting the importance and broad perspectives of the SCHOOL model in the development of new targeting strategies.
蛋白质-蛋白质相互作用在生物过程中起着核心作用,因此是创新药物设计与开发的一个有吸引力的靶点。它们可被小分子抑制剂、肽和肽模拟物靶向,这些代表了携带许多缺点的蛋白质疗法的一种替代方案。在本章中,我描述了一种新的免疫信号模型——信号链同源寡聚化(SCHOOL)模型所提示的特定蛋白质-蛋白质相互作用,这些相互作用对于造血系统不同细胞上表达的多链免疫识别受体(MIRR)介导的细胞活化至关重要。SCHOOL模型解开了MIRR触发和跨膜信号传导这一长期存在的谜团,揭示了受体内跨膜相互作用和受体间细胞质同源相互作用是由免疫细胞介导的多种疾病的通用治疗靶点。此外,假设MIRR介导的跨膜信号传导机制的一般原则相似,SCHOOL模型可应用于MIRR家族的任何特定受体。因此,SCHOOL模型的一个重要应用是,针对MIRR触发和跨膜信号转导中涉及的关键蛋白质-蛋白质相互作用的全球治疗策略可用于治疗多种免疫介导的疾病。这假定临床知识和治疗策略可以在看似不同的疾病之间转移,例如T细胞介导的皮肤病和血小板疾病,或者可以结合起来开发新的药理学方法。有趣的是,SCHOOL模型揭示了不同人类病毒(如人类免疫缺陷病毒、巨细胞病毒和严重急性呼吸综合征冠状病毒)调节和/或逃避宿主免疫反应能力的分子机制。它还展示了从病毒发病机制中学到的经验教训如何实际用于合理的药物设计。将该模型应用于血小板胶原受体信号传导已经导致了血小板抑制新概念的发展和新血小板抑制剂的发明,从而证明了所提出的假设,并突出了SCHOOL模型在新靶向策略开发中的重要性和广阔前景。