Department of Immunology, School of Medicine and Dr. Jose Eleuterio Gonzalez University Hospital, Universidad Autónoma de Nuevo León, Monterrey, Mexico.
Front Immunol. 2024 Apr 4;15:1360296. doi: 10.3389/fimmu.2024.1360296. eCollection 2024.
Mast cells have long been recognized for their involvement in allergic pathology through the immunoglobulin E (IgE)-mediated degranulation mechanism. However, there is growing evidence of other "non-canonical" degranulation mechanisms activated by certain pathogen recognition receptors. Mast cells release several mediators, including histamine, cytokines, chemokines, prostaglandins, and leukotrienes, to initiate and enhance inflammation. The chemical nature of activating stimuli influences receptors, triggering mechanisms for the secretion of formed and new synthesized mediators. Mast cells have more than 30 known surface receptors that activate different pathways for direct and indirect activation by microbes. Different bacterial strains stimulate mast cells through various ligands, initiating the innate immune response, which aids in clearing the bacterial burden. Mast cell interactions with adaptative immune cells also play a crucial role in infections. Recent publications revealed another "non-canonical" degranulation mechanism present in tryptase and chymase mast cells in humans and connective tissue mast cells in mice, occurring through the activation of the Mas-related G protein-coupled receptor (MRGPRX2/b2). This receptor represents a new therapeutic target alongside antibiotic therapy. There is an urgent need to reconsider and redefine the biological role of these MASTer cells of innate immunity, extending beyond their involvement in allergic pathology.
肥大细胞长期以来一直因其在过敏病理中的作用而被认识，通过免疫球蛋白 E（IgE）介导的脱颗粒机制。然而，越来越多的证据表明，某些病原体识别受体激活了其他“非典型”的脱颗粒机制。肥大细胞释放几种介质，包括组胺、细胞因子、趋化因子、前列腺素和白三烯，以启动和增强炎症。激活刺激物的化学性质影响受体，触发形成和新合成介质分泌的机制。肥大细胞有超过 30 种已知的表面受体，这些受体通过微生物的直接和间接激活激活不同的途径。不同的细菌菌株通过各种配体刺激肥大细胞，启动先天免疫反应，有助于清除细菌负荷。肥大细胞与适应性免疫细胞的相互作用在感染中也起着至关重要的作用。最近的出版物揭示了人类的类胰蛋白酶和糜蛋白酶肥大细胞和小鼠的结缔组织肥大细胞中存在的另一种“非典型”脱颗粒机制，通过激活 Mas 相关 G 蛋白偶联受体（MRGPRX2/b2）发生。该受体是抗生素治疗之外的一个新的治疗靶点。迫切需要重新考虑和重新定义这些先天免疫的肥大细胞的生物学作用，超越其在过敏病理中的作用。
