Immunology Division, Postgraduate Medical School, University of Chieti-Pescara, Viale Unità dell'Italia 73, 66013, Chieti, Italy.
Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Immunol Res. 2017 Oct;65(5):982-986. doi: 10.1007/s12026-017-8938-7.
The host response to either exogenous or endogenous insults produces a series of changes, characterized by alterations in immunological functions and generation of mediators called cytokines which include the interleukin-1 (IL-1) family members. IL-1 acts as a hormone mediating the host responses to infection and inflammation. Blocking inflammatory IL-1 family members can be effective against inflammatory disorders, including allergies. IL-37, (formerly IL-1 family member 7), emerges as an inhibitor of innate and adaptive immunity by reducing circulating and organ cytokine levels. IL-37, mainly expressed in dendritic cells, monocytes, and plasma cells after TIR ligand activation, inhibits inflammatory cytokines and augments the level of anti-inflammatory IL-10. IL-37 is involved in allergic reaction and its expression in dendritic cells causes tollerogenicity and inhibits inflammatory response. Mast cells (MCs) are ubiquitous in the body, reside in numerous mucosal tissues, and are mediators of allergic reaction, and innate and adaptive immunity. MCs are important regulators of cytokine generation in the course of inflammatory responses and allergy, and are implicated in the pathophysiology of allergic asthma. Cysteine protease caspase-1 activation leads to the cleavage of pro-form of IL-1 into active mature IL-1 which is present in stimulated and unstimulated inflammatory MCs. Inflammatory cytokine inhibition, along with the augmentation of anti-inflammatory IL-10 by IL-37, is certainly beneficial and improves the pathogenesis of allergic disorders. However, in these studies, the exact mechanism(s) of IL-37-induced anti-inflammatory and anti-allergic activity along with its side effect(s) remain to be determined.
宿主对外源或内源性损伤的反应会产生一系列变化，其特征是免疫功能的改变和细胞因子的产生，细胞因子包括白细胞介素-1（IL-1）家族成员。IL-1 作为一种激素，介导宿主对感染和炎症的反应。阻断炎症性的 IL-1 家族成员可以有效对抗炎症性疾病，包括过敏。IL-37（以前称为 IL-1 家族成员 7）通过降低循环和器官细胞因子水平，作为先天和适应性免疫的抑制剂出现。IL-37 主要在树突状细胞、单核细胞和浆细胞中表达，在 TIR 配体激活后，抑制炎症细胞因子并增加抗炎性细胞因子 IL-10 的水平。IL-37 参与过敏反应，其在树突状细胞中的表达导致耐受性，并抑制炎症反应。肥大细胞（MCs）在体内无处不在，存在于许多黏膜组织中，是过敏反应、先天和适应性免疫的介质。MCs 是炎症反应和过敏过程中细胞因子产生的重要调节剂，与过敏性哮喘的病理生理学有关。半胱氨酸蛋白酶 caspase-1 的激活导致前体形式的 IL-1 切割成活性成熟的 IL-1，存在于刺激和未刺激的炎症性 MCs 中。IL-37 抑制炎症性细胞因子，并增加抗炎性细胞因子 IL-10，这肯定是有益的，并改善过敏疾病的发病机制。然而，在这些研究中，IL-37 诱导的抗炎和抗过敏活性的确切机制及其副作用仍有待确定。
