Dobrican Carmen-Teodora, Muntean Ioana Adriana, Pintea Irena, Petricău Carina, Deleanu Diana-Mihaela, Filip Gabriela Adriana
Discipline of Allergology and Immunology, Department of Functional Sciences, Iuliu Hatieganu University of Medicine and Pharmacy, 400162 Cluj-Napoca, Romania.
Discipline of Physiology, Department of Functional Sciences, Iuliu Hatieganu University of Medicine and Pharmacy, 400162 Cluj-Napoca, Romania.
Exp Ther Med. 2022 Jun;23(6):381. doi: 10.3892/etm.2022.11309. Epub 2022 Apr 8.
Chronic urticaria (CU) is a condition characterized by intensely pruritic, edematous, erythematous papules lasting for more than 6 weeks. Over half of the cases have concomitant swelling of deeper tissues, known as angioedema. The socio-economic burden of the disease is significant. Unfortunately, patients with severe CU, refractory to conventional treatment, have limited and expensive therapeutic options. The pathogenesis of CU is not yet completely understood. Therefore, elucidating the pathophysiological mechanisms involved would potentially identify new therapeutic targets. It has been accepted in recent years that mast cells and their activation, followed by excessive degranulation represent the key pathophysiological events in chronic spontaneous urticaria (CSU). The triggering events and the complexity of the effector mechanisms, however, remain intensely debated topics with conflicting studies. One pathogenetic mechanism incriminated in chronic spontaneous urticaria is the response mediated by the high-affinity receptor for IgE (FcεRI) expressed on mast cells. Increasing recognition of chronic spontaneous urticaria as an autoimmune disease linked to the cytokine-chemokine network imbalance resulting from alteration of innate immune response is another pathogenetic explanation. It is likely that these different pathological mechanisms are more interconnected, both acting synergistically, rather than separately, to produce the clinical expression of CU. The discovery and understanding of pathogenic mechanisms represent the premise for the development of safe and effective immunomodulators and targeted biological treatment for severe, refractory CU.
慢性荨麻疹（CU）是一种以剧烈瘙痒、水肿性红斑丘疹持续超过6周为特征的疾病。超过半数的病例伴有深部组织肿胀，即血管性水肿。该疾病的社会经济负担较重。不幸的是，重度CU患者对传统治疗无效，治疗选择有限且费用高昂。CU的发病机制尚未完全明确。因此，阐明其中涉及的病理生理机制可能会确定新的治疗靶点。近年来，人们已经认识到肥大细胞及其激活，随后过度脱颗粒是慢性自发性荨麻疹（CSU）的关键病理生理事件。然而，触发事件和效应机制的复杂性仍是存在相互矛盾研究的激烈争论话题。慢性自发性荨麻疹中涉及的一种发病机制是肥大细胞上表达的IgE高亲和力受体（FcεRI）介导的反应。越来越多的人认识到慢性自发性荨麻疹是一种自身免疫性疾病，与先天免疫反应改变导致的细胞因子 - 趋化因子网络失衡有关，这是另一种发病学解释。这些不同的病理机制可能相互关联更强，协同而非单独作用以产生CU的临床表型。致病机制的发现和理解是开发针对重度、难治性CU的安全有效免疫调节剂和靶向生物治疗的前提。
