Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma

Objective: Airway inflammation and airway hyper-responsiveness (AHR) are principle pathological manifestations of asthma. Cluster of differentiation 69 (CD69) is a well-known co-stimulatory factor associated with the activation, proliferation as well as apoptosis of immune cells. This study aims to examine the effect of anti-CD69 monoclonal antibody (mAb) on the pathophysiology of a mouse model of asthma. Methods: A murine model of ovalbumin (OVA)-induced allergic airway inflammation was used in this study. Briefly, mice were injected with 20 μg chicken OVA intraperitoneally on Days 0 and 14, followed by aerosol provocation with 1% (0.01 g/ml) OVA on Days 24, 25, and 26. Anti-CD69 mAb or isotype IgG was injected intraperitoneally after OVA challenge; dexamethasone (DXM) was administrated either before or after OVA challenge. AHR, mucus production, and eosinophil infiltration in the peribronchial area were examined. The levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-5 (IL-5) in bronchoalveolar lavage fluid (BALF) were also assayed as indices of airway inflammation on Day 28 following OVA injection. Results: Pretreatment with DXM together with anti-CD69 mAb treatment after OVA provocation completely inhibited AHR, eosinophil infiltration and mucus overproduction, and significantly reduced BALF IL-5. However, treatment with DXM alone after OVA challenge only partially inhibited AHR, eosinophil infiltration and mucus overproduction, and did not diminish BALF IL-5. Treatment with either DXM or anti-CD69 mAb did not alter the concentration of BALF GM-CSF. Conclusions: Anti-CD69 mAb treatment inhibits established airway inflammation as effectively as DXM pretreatment. This study provides a potential alternative therapeutic opportunity for the clinical management of asthma and its exacerbation.     

前列腺素及其受体对相关炎症细胞调控功能研究进展

随着前列腺素D2(PGD2)和其受体系统研究的深入，目前认为它在哮喘的慢性气道炎症中起关键作用，PGD2可通过在炎症细胞上DP／CRTh2受体(前列腺素D2受体／Th2细胞上表达的化学趋向性受体同种分子)对其发生调控作用，尤其是对嗜酸性粒细胞的浸润，募集的趋化等方面，本文就此有关方面的近年研究进展进行综述。     

Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells

Background

Epithelial-mesenchymal transition (EMT) is believed to be the critical process in malignant tumor invasion and metastases, and has a great influence on improving the survival rate in non-small-cell lung cancer (NSCLC) patients. Recent studies suggested that eukaryotic initiation factor 5A-2 (eIF5A-2) might serve as an adverse prognostic marker of survival. We detected eIF5A-2 in NSCLC A549 cells, and found that the invasive capability correlates with the eIF5A-2 expression.

Methods

Transforming growth factor (TGF)-β1 was used to induce EMT in A549 cells. Western blotting, immunofluorescence, wound healing assay, and transwell-matrigel invasion chambers were used to identify phenotype changes. Western blotting was also used to observe changes of the expression of eIF5A-2. We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence. We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.

Results

After stimulating with TGF-β1, almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities. These cells also had higher eIF5A-2 protein expression. Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.

Conclusions

The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells, which correlated with enhanced tumor invasion and metastatic capabilities. Furthermore, in the A549 cell line, the process of EMT phenotype change could be reversed by eIF5A-2 siRNA, with a consequent weakening of both invasive and metastatic capabilities.     

银杏叶提取物对哮喘大鼠气道嗜酸性粒细胞浸润的影响

目的：观察银杏叶提取物（Egb）对哮喘大鼠气道嗜酸性粒细胞趋化因子（Eotaxin）的表达及嗜酸性粒细胞（EOS）在气道局部浸润的影响。方法：复制哮喘大鼠模型,用免疫组化检测肺组织NF-κBp65亚基及Eotaxin蛋白活性;细胞分类计数法检测支气管肺泡灌洗液（BALF）中EOS的绝对计数和百分比;病理学方法观察气道炎症程度。结果：哮喘组肺组织NF-κBp65（0.256±0.063）及Eotaxin（0.197±0.055）表达量均显著高于正常组（分别为0.015±0.006,0.034±0.008）（均为P〈0.01）。Egb组肺组织NF-κBp65（0.104±0.056）及Eotaxin（0.115±0.010）的表达均显著低于哮喘组（均为P〈0.01）;Egb组BALF中EOS的绝对计数和百分比均低于哮喘组（均为P〈0.01）;光镜下观察Egb组气道炎症较哮喘组显著减轻。结论：哮喘组肺组织NF-κBp65及Eotaxin表达显著增强,Egb能有效抑制哮喘大鼠肺组织NF-κBp65的活性从而抑制Eotaxin的转录合成,减少EOS在局部的浸润,减轻气道炎症。     

益肾活血平喘合剂对哮喘大鼠气道TGFβ1表达的影响

目的：探讨益肾活血平喘合剂对哮喘大鼠气道TGFβ1表达的影响。方法：健康雌性SD大鼠60只。随机分为4组,即正常组、模型组、地塞米松阳性对照组、益肾活血平喘合剂组,每组15只大鼠。除正常组外,其余3组均利用哮喘模型。各组于造模后14d开始每天给药及雾化吸入。造模后28d处死动物,取同一部位肺叶,包埋,切片,HE染色及免疫组化检测气道TGFβ1的表达。结果：益肾活血平喘合剂组气道TGFβ1的表达明显少于模型组（P〈0．01）及阳性对照组（P〈0．05）。结论：益肾活血平喘合剂通过抑制气道TGFβ1的表达,减轻哮喘气道炎症及重塑的发生。     

Science Letters: A synthetic Toll-like receptor 2 ligand decreases allergic immune responses in a mouse rhinitis model sensitized to mite allergen

It has been proposed that activation of Toll-like receptors (TLRs) plays crucial roles in the polarization of adaptive immune responses. A synthetic Toll-like receptor 2 (TLR2) ligand, Pam3CSK4, has been reported to modulate the balance of Thl/Tn2 responses. We evaluated the modulation effect of Pam3CSK4 on allergic immune response in a mouse rhinitis model sensitized to house dust mite allergen (HDM). Mice were sensitized and challenged with Dermatophagoides farinae allergen (Der f), and then the allergic mice were treated by Pam3CSK4. Nasal allergic symptoms and eosinophils were scored. Der f-specific cytokine responses were examined in the splenocytes and bronchoalveolar lavage fluid (BALF). Serum level of total IgE was also detected. After establishing a mouse allergic rhinitis model with HDM, we have showed that Pam3CSK4 treatment not only ameliorated the nasal allergic symptoms remarkably but also decreased the eosinophils and total inflammation cells in BALF significantly. Analysis of cytokine profile found that' IFN-γ released from either BALF or stimulated splenocytes increased markedly in Pam3CSK4-treated mice, while IL-13 decreased significantly. Moreover, serum level of total IgE was significantly lower in Pam3CSK4-treated mice than in the untreated. Thus, in an allergic rhinitis mouse model developed with HDM, Pam3CSK4 was shown to exhibit an antiallergic effect, indicating its potential application in allergic diseases.     

Science Letters： A synthetic Toll-like receptor 2 ligand decreases allergic immune responses in a mouse rhinitis model sensitized to mite allergen

It has been proposed that activation of Toll-like receptors (TLRs) plays crucial roles in the polarization of adaptive immune responses. A synthetic Toll-like receptor 2 (TLR2) ligand, Pam3CSK4, has been reported to modulate the balance of Thl/Tn2 responses. We evaluated the modulation effect of Pam3CSK4 on allergic immune response in a mouse rhinitis model sensitized to house dust mite allergen (HDM). Mice were sensitized and challenged with Dermatophagoides farinae allergen (Der f), and then the allergic mice were treated by Pam3CSK4. Nasal allergic symptoms and eosinophils were scored. Der f-specific cytokine responses were examined in the splenocytes and bronchoalveolar lavage fluid (BALF). Serum level of total IgE was also detected. After establishing a mouse allergic rhinitis model with HDM, we have showed that Pam3CSK4 treatment not only ameliorated the nasal allergic symptoms remarkably but also decreased the eosinophils and total inflammation cells in BALF significantly. Analysis of cytokine profile found that' IFN-γ released from either BALF or stimulated splenocytes increased markedly in Pam3CSK4-treated mice, while IL-13 decreased significantly. Moreover, serum level of total IgE was significantly lower in Pam3CSK4-treated mice than in the untreated. Thus, in an allergic rhinitis mouse model developed with HDM, Pam3CSK4 was shown to exhibit an antiallergic effect, indicating its potential application in allergic diseases.     

Written emotional expression as an intervention for asthma

This investigation employed a multiple baseline design across five participants to examine written emotional expression as an intervention to improve lung function in high school‐aged students, college students, and adults with asthma. The predicted forced expiratory volume in 1 second (FEV₁ measure of large airway functioning) and forced expiratory flow (FEF_25–75 measure of small airway functioning) were evaluated using spirometry. In addition, anxiety was measured using state and trait anxiety self‐report scales. Generally, results were effective. Individuals with asthma are at higher risk for increased hospitalization and death. For the school‐aged population, asthma is associated with increased absenteeism, restriction of various class activities such as physical education, and poor relationships with peers. Therefore, adults and children with asthma are in need of services and school psychologists appear uniquely qualified to intervene. More recently, the role of the school psychologist is diversifying with corresponding training (e.g., wellness, consultation, prevention, assessment and treatment of health issues) in the areas of health‐related disorders that involve a psychological component. © 2003 Wiley Periodicals, Inc. Psychol Schs 40: 193–207, 2003.     

Science Letters：IGFBP7 plays a potential tumor suppressor role against colorectal carcinogenesis with its expression associated with DNA hypomethylation of exon 1

Insulin-like growth factor binding-protein-7 （IGFBP7） was obtained from our previous colonic adenocarcinoma （CRC） and normal mucosa suppression subtraction hybridization （SSH） cDNA libraries. By RT-PCR and immunohistochemistry, we found that IGFBP7 was overexpressed in CRC tissue compared to normal tissue. However, our in vitro experiments performed in 10 CRC cell lines showed that IGFBP7 expressed only in SW480 and Caco2 cell lines, which implied an underlying reversible regulatory mechanism. Using methylation-specific PCR （MSP） and bisulfite sodium PCR （BSP）, we found that its expression was associated with DNA hypomethylation of exonl. This was further supported by the in vitro study which showed restored IGFBP7 expression after demethylation agent 5-aza-2＇-deoxycytidine treatment. Correlation analysis between IGFBP7 expression and prognosis indicated that overexpression of IGFBP7 in CRC tissue correlated with favourable survival. Investigation of the functional role of IGFBP7 through transfection studies showed that IGFBP7 protein could inhibit growth rate, decrease colony formation activity, and induce apoptosis in RKO and SW620 cells, suggesting it a potential tumor suppressor protein in colorectal carcinogenesis. In conclusion, our study clearly demonstrated that IGFBP7 plays a potential tumor suppressor role against colorectal carcinogenesis and its expression is associated with DNA hypomethylation of exon 1.     

Effect of Palrnatine on lipopolysaccharide-induced acute lung injury by inhibiting activation of the Akt/NF‍-κB pathway

Inflammation plays an important role in the development of acute lung injury (ALI). Severe pulmonary inflammation can cause acute respiratory distress syndrome (ARDS) or even death. Expression of proinflammatory interleukin-‍1β (IL-‍1β) and inducible nitric oxide synthase (iNOS) in the process of pulmonary inflammation will further exacerbate the severity of ALI. The purpose of this study was to explore the effect of Palrnatine (Pa) on lipopolysaccharide (LPS)-induced mouse ALI and its underlying mechanism. Pa, a natural product, has a wide range of pharmacological activities with the potential to protect against lung injury. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) assays were performed to detect the expression and translation of inflammatory genes and proteins in vitro and in vivo. Immunoprecipitation was used to detect the degree of P65 translocation into the nucleus. We also used molecular modeling to further clarify the mechanism of action. The results showed that Pa pretreatment could significantly inhibit the expression and secretion of the inflammatory cytokine IL-1β, and significantly reduce the protein level of the proinflammatory protease iNOS, in both in vivo and in vitro models induced by LPS. Further mechanism studies showed that Pa could significantly inhibit the activation of the protein kinase B (Akt)/nuclear factor-κB (NF-κB) signaling pathway in the LPS-induced ALI mode and in LPS-induced RAW264.7 cells. Through molecular dynamics simulation, we observed that Pa was bound to the catalytic pocket of Akt and effectively inhibited the biological activity of Akt. These results indicated that Pa significantly relieves LPS-induced ALI by activating the Akt/NF-κB signaling pathway.     

孟鲁司特对哮喘大鼠骨髓CD34^＋细胞IL-4 mRNA和IL-4蛋白表达的影响

目的：研究IL-4mRNA和IL-4蛋白在哮喘大鼠CD34^＋细胞中的转录表达及孟鲁司特（montelukast,MK）对其表达的影响。方法：将SD大鼠随机分为3组：哮喘组、MK组和正常对照组。用卵白蛋白制备大鼠哮喘模型。应用双抗体夹心酶联免疫吸附试验测定血浆中IL-4和γ-干扰素（IFN-γ）浓度;用MiniMACS磁珠分选系统分离骨髓CD34^＋细胞;采用SYBRGREEN I荧光实时定量PCR法测定CD34^＋细胞中IL-4mRNA的相对表达量。采用免疫组化技术测定CD34＋细胞中IL-4蛋白的表达量。结果：哮喘组骨髓CD34＋细胞中IL-4mR．NA和IL-4蛋白的表达量高于其它各组（p〈0．01）;哮喘组除了IFN-1水平低外,IL-4浓度和嗜酸性粒细胞（EOS）绝对值都是三组中最高的（P〈0．01）;除哮喘组外,其余组的各项指标相近（P〉0．05）。IL-4mRNA表达量与IL-4浓度、Eos绝对值呈正相关（P〈0．01）,与IFN-γ浓度呈负相关（P〈0．01）。结论：哮喘大鼠骨髓CD34^＋细胞中IL-4 mKNA的表达增强;孟鲁司特可以下调IL-4mRNA的表达。可能成为其抑制哮喘气道炎症形成的重要机制之一。     

Potential immunomodulation effect of the extract of Nigella sativa on ovalbumin sensitized guinea pigs

Several different pharmacological effects have been described for Nigella sativa (Siah-Daneh), including an anti-inflammatory effect. In the present study, the effect of the extract of N. sativa on lung pathology and blood interleukin-4 (IL-4) and interferon-γ (IFN-γ) of sensitized guinea pigs was examined. Three groups (n=8 for each group) of guinea pigs sensitized to ovalbumin (OA) were given drinking water alone, and drinking water containing low and high concentrations of the plant extract, respectively. The animals of the control group (n=8) were treated with saline instead of OA and were given drinking water. The pathological changes of the lung, including infiltration of eosinophils and lymphocytes, local epithelial necrosis, the presence of oedema, thickening of the basement membrane, smooth muscle layer hypertrophy, mucosal secretion, and the presence of mucosal plug, and blood IL-4 and IFN-γ of sensitized guinea pigs were evaluated. The lungs of the sensitized group showed significant pathological changes (P<0.001). Blood IL-4 and IFN-γ were increased in sensitized animals compared to the controls (P<0.01 and P<0.001, respectively). Treatment of sensitized animals with the extract led to a significant decrease in pathological changes of the lung (P<0.01 to P<0.001), except for the oedema in the sensitized group treated with low concentration of the extract, but an increased IFN-γ. These results confirm a preventive effect of N. sativa extract on lung inflammation of sensitized guinea pigs.     

Serum macrophage migration inhibitory factor as a potential biomarker to evaluate therapeutic response in patients with allergic asthma: an exploratory study

Background: Previous studies have shown that macrophage migration inhibitory factor(MIF) is involved in the pathogenesis of asthma. This study aimed to investigate whether serum MIF reflects a therapeutic response in allergic asthma.Methods: We enrolled 30 asthmatic patients with mild-to-moderate exacerbations and 20 healthy controls, analyzing the parameter levels of serum MIF, serum total immunoglobulin E(tIgE), peripheral blood eosinophil percentage(EOS%), and fractional exhaled nitric oxide(FeNO). Lung function indices were used to identify disease severity and therapeutic response.Results: Our study showed that all measured parameters in patients were at higher levels than those of controls. After one week of treatment, most parameter levels decreased significantly except for serum tIgE. Furthermore, we found that serum MIF positively correlated with EOS% as well as FeNO, but negatively correlated with lung function indices. Receiver operator characteristic(ROC) curve analysis indicated that among the parameters, serum MIF exhibited a higher capacity to evaluate therapeutic response. The area under the curve(AUC) of MIF was 0.931, with a sensitivity of 0.967 and a specificity of 0.800.Conclusions: Our results suggested that serum MIF may serve as a potential biomarker for evaluating therapeutic response in allergic asthma with mild-to-moderate exacerbations.     

脂多糖诱导内脏器官白细胞介素15mRNA的表达

目的白细胞介素15（interleukin-15,IL-15）与炎症反应的关系。方法在含兔IL-15全长编码cDNA的质粒上缺失了部份片段．构建成竞争性RT—PCR的竞争子（competitor）。研究炎症反应后IL-15基因的转录情况。结果竞争性RT-PCR结果显示,IL-15与炎症反应密切相关,且脂多糖（LPS）增加了兔子内脏器官（心脏,肺,肾脏,脾脏和肝脏）中IL-15mRNA的表达。结论LPS可以增强IL-15的免疫反应。     

Albumin resuscitation protects against traumatic/hemorrhagic shock-induced lung apoptosis in rats

Objective: To determine the effects of albumin administration on lung injury and apoptosis in traumatic/hemorrhagic shock (T/HS) rats. Methods: Studies were performed on an in vivo model of spontaneously breathing rats with induced T/HS; the rats were subjected to femur fracture, ischemia for 30 min, and reperfusion for 20 min with Ringer’s lactate solution (RS) or 5% (w/v) albumin (ALB), and the left lower lobes of the lungs were resected. Results: Albumin administered during reperfusion markedly attenuate...     

Is there a role of TNFR1 in acute lung injury cases associated with extracorporeal circulation?

The signaling pathway for tumor necrosis factor-α (TNF-α) and its receptors is up-regulated during extracorporeal circulation (ECC), and recruits blood neutrophil into the lung tissue, which results in acute lung injury (ALI). In this study, we evaluated the role of tumor necrosis factor receptor 1 (TNFR1) in ECC-induced ALI by blocking TNF-α binding to TNFR1 with CAY10500. Anesthetized Sprague-Dawley (SD) rats were pretreated intravenously with phosphate buffered saline (PBS) or vehicle (0.3 ml ethanol IV) or CAY10500, and then underwent ECC for 2 h. The oxygenation index (OI) and pulmonary inflammation were assessed after ECC. OI was significantly decreased, while TNF-α and neutrophil in bronchoalveolar lavage fluid (BALF) and plasma TNF-α increased after ECC. Pretreatment of CAY10500 decreased plasma TNF-α level, but did not decrease TNF-α levels and neutrophil counts in BALF or improve OI. Lung histopathology showed significant alveolar congestion, infiltration of the leukocytes in the airspace, and increased thickness of the alveolar wall in all ECC-treated groups. CAY10500 pretreatment slightly reduced leukocyte infiltration in lungs, but did not change the wet/dry ratio in the lung tissue. Blocking TNF-α binding to TNFR1 by CAY10500 intravenously slightly mitigates pulmonary inflammation, but cannot improve the pulmonary function, indicating the limited role of TNFR1 pathway in circulating inflammatory cell in ECC-induced ALI.     

Application of a recombinant replicase to localize the Trionyx sinensis hemorrhagic syndrome virus and evaluate its effects on antiviral genes of T. sinensis

Trionyx sinensis Hemorrhagic Syndrome Virus(TSHSV) is an arterivirus newly discovered in Chinese softshell turtles. Little is known about the effect of antibodies against the virus or the distribution of the virus in different organs of infected turtles. In this study, a partial protein of TSHSV-HP4 was produced using a prokaryotic expression system, and its polyclonal antibody was generated. The polyclonal antibody was confirmed by western blot and dot enzyme-linked immunosorbent assay(dot-ELISA). The distribution of TSHSV in different organs of T. sinensis was examined by immunohistochemistry(IHC) and the expression of immune-related genes was analyzed using quantitative real-time polymerase chain reaction(qRT-PCR). The results indicated that the recombinant TSHSV-HP4 protein was successfully expressed, and the generated polyclonal antibody showed specific binding to viral particles in the lung tissues of infected turtles. The IHC assay indicated that the virus was highly localized in various cells, including intestinal lymphocytes,enterocytes, kidney epithelial cells, spleen cells, lung macrophages, and cardiomyocytes. The qRT-PCR analysis revealed that TSHSV was detected in all organs tested, including the lungs, liver, kidneys, spleen, and heart. The numbers of viral mRNA copies in lung and heart tissues were significantly higher in the virus-antibody group than in the virus group. The interferonstimulated genes(ISGs), myxovirus resistance protein 2(MX2) and radical S-adenosyl methionine domain containing 2(RSAD2) were highly upregulated in all groups of infected turtles. Antibody-dependent enhancement(ADE) seemed to occur after stimulation by the polyclonal antibody, because significantly greater expression of the two genes was detected in the virus-antibody group than in the virus group. Overall, these results are important in understanding the cell localization of TSHSV and the immune response of infected turtles.     

鼻息肉患者嗜酸性粒细胞及肥大细胞脱颗粒电镜观察

目的:为了解活化的嗜酸性粒细胞及肥大细胞的脱颗粒情况,应用透射电镜观察嗜酸性粒细胞及肥大细胞的形态变化、颗粒情况及脱颗粒类型,借此探讨嗜酸性粒细胞及肥大细胞在鼻息肉发病机制中的作用,找到一种预防鼻息肉的好方法.方法:鼻息肉组10例,鼻息肉组织来自2001年我科住院做鼻内窥镜手术的多发性鼻息肉病人,男6例,女4例.正常对照组5例,选取同期因鼻外伤住院病人,男4例,女1例.所有组织均在鼻内窥镜下采取,病变组取息肉组织,对照组取下鼻甲组织,标本迅速放入10%甲醛液及4%戊二醛液固定,分别供光镜及电镜检查备检,HE染色及常规电镜制片.结果:光镜下可见大量炎性细胞浸润,以嗜酸性粒细胞为主,主要位于黏膜下,小血管周围;正常对照组炎细胞较少,统计学分析鼻息肉组嗜酸性粒细胞数目明显高于正常对照组,且有显著性差异(P＜0.05).肥大细胞的超微结构特点:正常对照组多为正常肥大细胞,大小基本一致,胞浆内多为高电子密度颗粒,表面可见微绒毛,无空泡形成;鼻息肉组:绝大多数为脱颗粒肥大细胞,表现为颗粒变大、电子密度减低、颗粒间相互融合、颗粒与胞膜融合、空泡形成.另外在息肉组织内可见浆细胞存在,有一较大的核,核内异染色质呈斑块状,分布在核周围,胞浆内充满膨大的粗面内质网,说明蛋白合成旺盛.结论:经研究我们发现鼻息肉组织中有大量的炎性细胞浸润,其中以嗜酸性粒细胞最多,而且大部分是活化状态,嗜酸性粒细胞及肥大细胞脱颗粒后释放炎性介质、细胞毒性蛋白及细胞因子等生物活性物质,引起上皮脱落、组织水肿、血管增生,最终导致鼻息肉的发生和发展,鼻腔局部应用皮质类固醇激素可以抑制炎性细胞的聚集和活化,减轻组织中的炎性反应,从而达到控制鼻息肉的目的.     

Regulatory T cells and asthma

Asthma is a chronic disease of airway inflammation due to excessive T helper cell type 2 (Th2) response. Present treatment based on inhalation of synthetic glucocorticoids can only control Th2-driven chronic eosinophilic inflammation, but cannot change the immune tolerance of the body to external allergens. Regulatory T cells (Tregs) are the main negative regulatory cells of the immune response. Tregs play a great role in regulating allergic, autoimmune, graft-versus-host responses, and other immune responses. In this review, we will discuss the classification and biological characteristics, the established immunomodulatory mechanisms, and the characteristics of induced differentiation of Tregs. We will also discuss the progress of Tregs in the field of asthma. We believe that further studies on the regulatory mechanisms of Tregs will provide better treatments and control strategies for asthma.