Data availability 数据可用性
文章中描述的研究没有使用任何数据。
Table 1. Animal and In vivo studies of IL-21 in Allergic diseases.
表1。IL-21在过敏性疾病中的动物和体内研究。
Model of study 学习模式 | Effect on immune responses 对免疫反应的影响 | Ref 编号 |
---|---|---|
Nasal administration of rmIL-21 in AHR 经鼻给予rmIL-21治疗急性肾衰竭 |
| [143] |
IL21r-deficient mice model of asthma and OVA-induced asthma using Il21r-deficient mice IL21r缺陷小鼠哮喘和OVA诱导哮喘模型 |
| [87], [144] |
Intranasal use of mouse rIL‑21 in OVA‑induced mouse model of AR 小鼠rIL-21在OVA诱导的AR小鼠模型中的鼻内应用 |
| [89], [129] |
IL-21 in a mouse with cutaneous immediate hypersensitivity reaction (IHR). IL-21在患有皮肤即刻超敏反应(IHR)的小鼠中的作用。 |
| [90] |
IL-21 in a mouse model of asthma induced by house dust mites (HDMs) 屋尘螨哮喘小鼠模型中IL-21的表达 |
| [48] |
Roles of IL-21 and IL-21R in AD IL-21和IL-21R在阿尔茨海默病中的作用 |
| [117] |
Gene expression profile in animal models of food allergy 食物过敏动物模型中的基因表达谱 |
| [145] |
OVA-induced allergic asthma mouse model OVA诱导的过敏性哮喘小鼠模型 |
| [133] |
IL-21R deficiency in OVA-induced model and HDM -induced allergic mouse model OVA诱导模型和HDM诱导的过敏小鼠模型中IL-21R缺乏 |
| [87], [89], [144] |
In vivo using of IL-21 in the peanut allergy model IL-21在花生过敏模型中的体内应用 |
| [85] |
Airway inflammation in IL-21R KO mice model IL-21R基因敲除小鼠模型气道炎症 |
| [87] |
local airway challenge with HDM in wild type BALB/c and Il21r-deficient mice HDM对野生型BALB/c和Il21r缺陷小鼠的局部气道攻击 |
| [146] |
Table 2. Human studies of IL-21 in Allergic diseases.
表2。IL-21在过敏性疾病中的人体研究。
Model of study 学习模式 | Effect on immune responses 对免疫反应的影响 | Ref 编号 |
---|---|---|
Nucleotide polymorphisms (SNP; C1455T, G1472T, C5250T and C8381T), In asthmatics patients 哮喘患者的核苷酸多态性(SNP;C1455T、G1472T、C5250T和C8381T) |
| [129] |
Expression levels of IL-6, IL-18, IL-21, IL-23, and TGF-β in nasal biopsies in AR patients AR患者鼻活检中IL-6、IL-18、IL-21、IL-23和TGF-β的表达水平 |
| [147] |
Signaling lymphocytic activation molecules (SLAMs) in the regulation of Tfh cells in Allergic rhinitis 信号淋巴细胞活化分子(SLAM)在变应性鼻炎Tfh细胞调节中的作用 |
| [148] |
Role of IL-21/IL-21 receptor (IL-21R) in patients with allergic rhinitis. IL-21/IL-21受体(IL-21R)在变应性鼻炎患者中的作用。 |
| [149] |
Single nucleotide polymorphism (T-83C) in the IL-21R IL-21R的单核苷酸多态性(T-83C) |
| [150], [151] |
Fig. 1. Sources and its cellular targets of IL-21. Interleukin‑21 (IL‑21) is produced by CD4+ T cell populations, with the highest production by T follicular helper (Tfh) cells and Th17 cells, Natural killer T (NKT) cells and also CD8+ T cells. IL‑21 exerts actions on multiple lymphoid and myeloid populations as well as on epithelial cells. Treg, regulatory; DC, dendritic cell; MQ, macrophage; Th17, T helper 17 [41], [47], [48], [52], [59].
图1。IL-21的来源及其细胞靶点。白细胞介素-21(IL-21)由CD4+T细胞群产生,其中T滤泡辅助细胞(Tfh)和Th17细胞、自然杀伤T细胞(NKT)以及CD8+T细胞的产量最高。IL-21对多种淋巴样和髓样细胞群以及上皮细胞具有作用。Treg,监管;DC,树突状细胞;MQ,巨噬细胞;Th17,T辅助细胞17[41],[47],[48],[52],[59]。
Fig. 2. Mechanisms of allergic diseases. Fig. 2: Mechanisms of allergic sensitization. When allergen uptake by DCs. Then, DCs migrate to draining lymph nodes where they present allergen- derived peptides on MHC class II molecules to naive T cells. With the presence of several co– stimulatory and cytokine signals, those T cells are differentiated to Th2 cells. Type 2 cytokines involving allergic inflammation including IL- 4, IL- 5, IL- 13, are predominantly secreted by Th2 cells. Whereas, IL- 21, IL- 4, and IL- 13 are secreted by TFH cells and initiate the B- cell class– switching to IgE, plasma cell differentiation and allergen- specific IgE production. The secreted allergen- specific IgE antibodies from plasma cells bind to FcεRI molecules on mast cells and basophils. Subsequent exposure to allergen induces mast cell and basophil degranulation. IL-21 induces selective apoptosis of IgE-committed B cells, leading to reduced production of IgE in the presence of IL-21. DC, dendritic cell; FcεRI, Fc epsilon receptor I; Ig, immunoglobulin; IL, interleukin; MHC, major histocompatibility complex; Th, T helper cell; Tfh, T follicular helper cell [42], [84], [85], [86], [91].
图2。过敏性疾病的机制。图2:过敏致敏机制。当DC摄取过敏原时。然后,DC迁移到引流淋巴结,在那里它们将MHC II类分子上的过敏原衍生肽呈递给幼稚T细胞。在几种共刺激和细胞因子信号的存在下,这些T细胞分化为Th2细胞。涉及过敏性炎症的2型细胞因子,包括IL-4、IL-5、IL-13,主要由Th2细胞分泌。然而,IL-21、IL-4和IL-13由TFH细胞分泌,并启动B细胞类转化为IgE、浆细胞分化和过敏原特异性IgE的产生。浆细胞分泌的过敏原特异性IgE抗体与肥大细胞和嗜碱性粒细胞上的FcεRI分子结合。随后接触过敏原会诱导肥大细胞和嗜碱性粒细胞脱颗粒。IL-21诱导IgE导向的B细胞选择性凋亡,导致在IL-21存在的情况下IgE的产生减少。DC,树突状细胞;FcεRI、Fcε受体I;Ig,免疫球蛋白;IL、白细胞介素;MHC,主要组织相容性复合体;Th、T辅助细胞;Tfh,T卵泡辅助细胞[42],[84],[85],[86],[91]。