Safety and Environmental Assurance Centre, Unilever, Colworth Science Park, Sharnbrook, Bedford MK44 1LQ, U.K.
MRC Centre for Drug Safety Science, Department of Molecular and Clinical Pharmacology, The University of Liverpool, Liverpool L69 3GE, U.K.
Chem Res Toxicol. 2024 Jun 17;37(6):850-872. doi: 10.1021/acs.chemrestox.4c00062. Epub 2024 Jun 4.
Humans are exposed to numerous electrophilic chemicals either as medicines, in the workplace, in nature, or through use of many common cosmetic and household products. Covalent modification of human proteins by such chemicals, or protein haptenation, is a common occurrence in cells and may result in generation of antigenic species, leading to development of hypersensitivity reactions. Ranging in severity of symptoms from local cutaneous reactions and rhinitis to potentially life-threatening anaphylaxis and severe hypersensitivity reactions such as Stephen-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), all these reactions have the same Molecular Initiating Event (MIE), i.e. haptenation. However, not all individuals who are exposed to electrophilic chemicals develop symptoms of hypersensitivity. In the present review, we examine common chemistry behind the haptenation reactions leading to formation of neoantigens. We explore simple reactions involving single molecule additions to a nucleophilic side chain of proteins and complex reactions involving multiple electrophilic centers on a single molecule or involving more than one electrophilic molecule as well as the generation of reactive molecules from the interaction with cellular detoxification mechanisms. Besides generation of antigenic species and enabling activation of the immune system, we explore additional events which result directly from the presence of electrophilic chemicals in cells, including activation of key defense mechanisms and immediate consequences of those reactions, and explore their potential effects. We discuss the factors that work in concert with haptenation leading to the development of hypersensitivity reactions and those that may act to prevent it from developing. We also review the potential harnessing of the specificity of haptenation in the design of potent covalent therapeutic inhibitors.
人类会接触到许多亲电子化学物质,无论是作为药物、在工作场所、在自然界中,还是通过使用许多常见的化妆品和家用产品。这些化学物质会使人类蛋白质发生共价修饰,即蛋白质半抗原化,这在细胞中很常见,可能会产生抗原性物质,导致过敏反应的发生。从局部皮肤反应和鼻炎到潜在的危及生命的过敏反应和严重的过敏反应,如史蒂文斯-约翰逊综合征(Stevens-Johnson syndrome,SJS)和中毒性表皮坏死松解症(toxic epidermal necrolysis,TEN),这些反应的严重程度不一,其共同的分子起始事件(Molecular Initiating Event,MIE)是半抗原化。然而,并非所有接触亲电子化学物质的人都会出现过敏症状。在本综述中,我们检查了导致新抗原形成的半抗原化反应背后的常见化学原理。我们探讨了涉及蛋白质亲核侧链单一分子加成的简单反应,以及涉及单个分子上多个亲电子中心或涉及多个亲电子分子的复杂反应,以及与细胞解毒机制相互作用产生的反应性分子。除了产生抗原性物质和激活免疫系统外,我们还探讨了直接来自细胞中亲电子化学物质存在的其他事件,包括关键防御机制的激活及其反应的直接后果,并探讨了它们的潜在影响。我们讨论了与半抗原化协同作用导致过敏反应发展的因素,以及可能防止其发展的因素。我们还回顾了在设计有效的共价治疗抑制剂时利用半抗原化特异性的潜力。