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Prevalence of HLA-DQ*02 and HLA-DQ*08 in Patients with Celiac Disease in Eastern Anatolia and the Diagnostic Role of HLA-DQ*02 and HLA-DQ*08 Genotyping 东安纳托利亚地区乳糜泻患者HLA-DQ*02和HLA-DQ*08的患病率及HLA-DQ*02和HLA-DQ*08基因分型的诊断作用
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/TJI.2019.862
E. Balkan, A. Islek, E. Yaşar, H. Doğan
Introducton: Celiac disease (CD) is diagnosed with serological tests and small bowel biopsy. There is a strong link between CD and human leukocyte antigens (HLA). In this study, we aimed to determine the role of HLA alleles DQ*02 and DQ*08 in the diagnosis of pediatric CD patients and to determine the prevalence of these alleles in the population. Materials and Methods: The study included 72 school-aged celiac patients diagnosed according to serology and small bowel biopsy results, and a control group consisting of 70 unrelated individuals with no systemic disease. HLA-DQ*02 and HLA-DQ*08 typing was done using the sequence-specific primer (PCR-SSP) method. Results: The mean age of the CD patients included in the study was 10.06±2.10 years. HLA-DQ*02 frequency was significantly higher in the CD group (67%) compared to the control group (17%) (p<0.001). HLA-DQ*08 frequencies did not differ significantly between the patient and control groups (26% and 24%, respectively; p>0.05). Conclusions: Genetic risk profiles in CD are helpful for predicting susceptibility to disease and disease progression. The results of our study showed that the prevalence of HLA-DQ*02 was higher among CD patients than healthy individuals, and it was higher than the prevalence of HLA-DQ*08. Our study further supports the link between HLADQ*02 and increased risk of disease.
简介:乳糜泻(CD)是通过血清学检查和小肠活检诊断的。在乳糜泻和人类白细胞抗原(HLA)之间有很强的联系。在本研究中,我们旨在确定HLA等位基因DQ*02和DQ*08在儿科CD患者诊断中的作用,并确定这些等位基因在人群中的患病率。材料与方法:本研究纳入72例经血清学和小肠活检结果诊断的学龄期乳糜泻患者,以及70例无全身性疾病的非相关个体作为对照组。HLA-DQ*02和HLA-DQ*08分型采用序列特异性引物(PCR-SSP)法。结果:纳入研究的CD患者平均年龄为10.06±2.10岁。CD组HLA-DQ*02频率(67%)显著高于对照组(17%),差异有统计学意义(p0.05)。结论:CD的遗传风险谱有助于预测疾病易感性和疾病进展。我们的研究结果显示,HLA-DQ*02在CD患者中的患病率高于健康人群,并且高于HLA-DQ*08的患病率。我们的研究进一步支持HLADQ*02与疾病风险增加之间的联系。
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引用次数: 0
Immune-mediated Sensorineural Hearing Loss: Patho-Mechanisms and Therapeutic Strategies 免疫介导的感音神经性听力损失:病理机制和治疗策略
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/tji.2019.1015
S. ParidhyVanniya., K. Ramkumar, C. Srisailapathy
The immune system protects the inner ear from various infections. However, the fragile audiological and vestibular structures are damaged due to immune-related and inflammatory responses, thus resulting in sensorineural hearing loss. Immune-mediated sensorineural hearing loss (ISNHL) can either be of autoimmune or autoinflammatory origin, and studies have shown that ISNHL ultimately results from inflammatory responses in both the cases. Several disorders have been identified that either primarily cause hearing loss due to localized inflammation (such as Meniere’s disease) or as an additional manifestation resulting from systemic inflammation (as seen in Muckle-Well syndrome). Immune molecularand patho-mechanisms have been proposed to explain ISNHL, yet it has been an enigma. A crucial mechanism leading to immune activation and inflammation involves the increased levels of NLRP3 inflammasome-associated IL-1β and TNF-α, in resident macrophages of the inner ear. The presence of autoantibodies to inner ear antigens have been reported as a causative ISNHL and these antibodies also serve as diagnostic markers. Genetic-susceptibility to ISNHL in some individuals has been reported. ISNHL is reversible, where hearing and vestibular functions can be restored. Several studies have put forward therapeutic strategies to alleviate hearing impairment, by usage of immunosuppressive drugs, monoclonal antibodies, IL-1β and TNF-α antagonists, and NLRP3 inflammasome-inhibitors. Emerging approaches for treating autoimmune disease include altering gut microbiota, stem cell therapy and precision medicine. The present report reviews the various molecularand patho-mechanisms associated with ISNHL. It further focuses on possible therapeutic targets and the relevance in application of emerging therapeutic strategies to alleviate hearing loss.
免疫系统保护内耳免受各种感染。然而,脆弱的听力学和前庭结构由于免疫相关反应和炎症反应而受损,从而导致感音神经性听力损失。免疫介导的感音神经性听力损失(ISNHL)既可以是自身免疫性的,也可以是自身炎症性的,研究表明,这两种情况下的ISNHL最终都是由炎症反应引起的。已经确定了几种疾病,它们要么主要是由于局部炎症(如梅尼埃病)引起的听力损失,要么是由全身炎症引起的附加表现(如Muckle-Well综合征)。免疫分子和病理机制已被提出来解释ISNHL,但它一直是一个谜。导致免疫激活和炎症的一个关键机制涉及内耳巨噬细胞中NLRP3炎症小体相关IL-1β和TNF-α水平的升高。内耳抗原自身抗体的存在已被报道为ISNHL的病因,这些抗体也可作为诊断标志物。一些个体对ISNHL有遗传易感性的报道。ISNHL是可逆的,听力和前庭功能可以恢复。一些研究提出了使用免疫抑制药物、单克隆抗体、IL-1β和TNF-α拮抗剂以及NLRP3炎性小体抑制剂来减轻听力障碍的治疗策略。治疗自身免疫性疾病的新方法包括改变肠道微生物群、干细胞疗法和精准医学。本报告综述了与ISNHL相关的各种分子和病理机制。它进一步侧重于可能的治疗靶点和应用新兴的治疗策略,以减轻听力损失的相关性。
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引用次数: 0
Anti-inflammatory and Anti-atherogenic Effects of Lactobacillus plantarum in Hypercholesterolemic Mice 植物乳杆菌对高胆固醇血症小鼠的抗炎和抗动脉粥样硬化作用
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/TJI.2019.955
M. Selli, A. Bermúdez-Fajardo, E. Oviedo-Orta
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引用次数: 0
Neem Leaf Glycoprotein Facilitates Lung Carcinoma- Associated Antigen-Specific Anti-Cancer Immune Response Utilizing Macrophage-Mediated Antigen Presentation and Induction of Type 1 Cytokines Coupled with Nitric Oxide Production 印度楝叶糖蛋白利用巨噬细胞介导的抗原呈递和诱导1型细胞因子偶联一氧化氮产生促进肺癌相关抗原特异性抗癌免疫反应
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/tji.2019.1012
A. Rai, Akshaya Mahalakshmi Surendran, K. Nandakumar, S. Bose, Shairee Sanyal, Sumantra Mondal, Sayantanee Mukherjee, Koustav Sarkar
Introduction: Based on earlier observations on unique immunomodulatory and adjuvant functions of neem leaf glycoprotein (NLGP), investigations of this work were designed. NLGP was attempted to be used as an adjuvant for lung carcinoma-associated antigen (LCA) which not only activated macrophages but also induced macrophages to release nitric oxide (NO), a key tumoricidal agent known to regulate T-cell proliferation, cytokine production, cell signaling, and apoptosis. Materials and Methods: Macrophages, generated from peripheral blood mononuclear cells (PBMCs), were pulsed with LCA isolated from lung carcinoma cell line A549, in presence or absence of NLGP for antigen presentation. Intramacrophageal NO was estimated based on Griess reaction. Cytokine levels were estimated by ELISA. Lymphocytic proliferation was checked by MTT assay. Cytotoxic T lymphocytes (CTLs) generated cytotoxicity was tested by LDH assay. Results: NLGP potentiates immune responses during pulsation with LCA by specific lymphocytic proliferation (p<0.001) and generation of CTLs (p<0.001). LCA+NLGP treatment creates a type-1 immune environment by increasing secretion of type-1 cytokines IFN-g and IL-12 (p<0.001) and decrease in type-2 cytokines IL-4 and IL-10 (p<0.001). LCA+NLGP treatment increased the release of type-1 cytokine-dependent NO. In vitro neutralization of IFN-g/IL-12 results into drastic decrease in NO release from macrophages. Conclusion: Obtained results demonstrated the interdependence of three anti-tumor immune functions, namely, NO production, CTL generation and production of a type-1 immune response mediated through NLGP. NLGP-generated anti-LCA immune response would be an effective strategy to treat lung carcinomas.
基于前期对印楝叶糖蛋白(NLGP)独特的免疫调节和佐剂功能的观察,本研究进行了设计。NLGP被用作肺癌相关抗原(LCA)的佐剂,它不仅能激活巨噬细胞,还能诱导巨噬细胞释放一氧化氮(NO),一氧化氮是一种关键的杀瘤剂,已知可调节t细胞增殖、细胞因子产生、细胞信号传导和细胞凋亡。材料和方法:将外周血单核细胞(PBMCs)生成的巨噬细胞用肺癌细胞系A549分离的LCA脉冲,在NLGP存在或不存在的情况下进行抗原呈递。根据Griess反应估计巨噬细胞内NO。ELISA法检测细胞因子水平。MTT法检测淋巴细胞增殖。LDH法检测细胞毒性T淋巴细胞(ctl)产生的细胞毒性。结果:NLGP通过特异性淋巴细胞增殖(p<0.001)和ctl的产生(p<0.001)增强LCA搏动期间的免疫反应。LCA+NLGP治疗通过增加1型细胞因子IFN-g和IL-12的分泌(p<0.001)和降低2型细胞因子IL-4和IL-10的分泌(p<0.001)创造1型免疫环境。LCA+NLGP治疗增加了1型细胞因子依赖性NO的释放。体外中和IFN-g/IL-12导致巨噬细胞释放NO急剧减少。结论:所得结果证明了三种抗肿瘤免疫功能的相互依赖性,即NO的产生、CTL的产生和NLGP介导的1型免疫应答的产生。lngp产生的抗lca免疫应答可能是治疗肺癌的有效策略。
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引用次数: 0
İmmünomodülatör ve Antioksidan Bir Molekül Olarak D Vitamini: D Vitamini Eksikliği ve Sistemik Skleroz İlişkisi
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/tji.2019.945
Nazlı Ecem Dal, H. Işlekel
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引用次数: 0
Increased Expression of Lymphocyte Activation Gene-3 by Regulatory T Cells in Multiple Sclerosis Patients with Fingolimod Treatment 经芬戈莫治疗的多发性硬化症患者调节性T细胞淋巴细胞活化基因-3的表达增加
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/TJI.2019.1035
N. Sedaghat, H. Motedayyen, F. Alsahebfosoul, M. Etemadifar, Vajiheh Ostadi, F. Kianpour, M. Akbari, Elettra Vestri, Seyed Hamid Zarkesh Esfahani
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引用次数: 4
Regulation of Immunity by Estrogen Through Sympathetic Nervous System in Aging 雌激素通过交感神经系统对衰老免疫的调节作用
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/TJI.2019.1013
Ramasamy Vasantharekha, L. Hima, P. Thandapani, Sanjana Kumaraguru, R. Priya, P. Ananthasubramanian, S. Thyagarajan
Women are more prone to autoimmune diseases, hormone-dependent cancers, osteoporosis, and neurodegenerative diseases with advancing age. The age-associated increase in the incidence and development of diseases and cancer is the result of a decline in immunocompetence facilitated by dysfunctions of nervous system and endocrine system. Reciprocal interactions between the brain and primary (bone marrow and thymus) and secondary (spleen and lymph nodes) lymphoid organs, via neurotransmitters and immune molecules determine an individual’s health or disease status. One of the major contributing factors for this imbalance in homeostatic functioning of the neuroendocrineimmune system is estradiol (E2) that exerts its effects through alterations in the production of neurochemicals and immune mediators. Estrogen’s reported beneficial effects such as anti-inflammatory and neuroprotective functions and deleterious effects of cancer progression are dependent upon age of women, type of cells and receptors, and the intracellular pathways and signaling molecules involved in mediating its effects. It is imperative that the diverse effects of estrogen on organ systems should be investigated via a longitudinal study beginning with early middle-aged rats to understand the long-term of exposure of estrogen on health and development of diseases. In this review, we present evidence for the biphasic effects of E2 on neural-immune interactions in the thymus, spleen, and lymph nodes and brain areas of early middle-aged female rats. These effects were dependent on pro/antioxidant status, and expression of growth factors and intracellular signaling molecules that are crucial to the neuronal plasticity influencing neuroprotection and inflammatory processes causing neurodegeneration.
随着年龄的增长,女性更容易患自身免疫性疾病、激素依赖性癌症、骨质疏松症和神经退行性疾病。与年龄相关的疾病和癌症的发病率和发展增加是神经系统和内分泌系统功能障碍导致免疫能力下降的结果。大脑与原发性(骨髓和胸腺)和继发性(脾脏和淋巴结)淋巴器官之间通过神经递质和免疫分子的相互作用决定了个体的健康或疾病状态。造成神经内分泌免疫系统稳态功能失衡的主要因素之一是雌二醇(E2),它通过改变神经化学物质和免疫介质的产生来发挥作用。据报道,雌激素的有益作用,如抗炎和神经保护功能,以及癌症进展的有害作用,取决于女性的年龄、细胞和受体的类型,以及介导其作用的细胞内途径和信号分子。为了了解雌激素长期暴露对健康和疾病发展的影响,迫切需要通过一项从中年早期大鼠开始的纵向研究来调查雌激素对器官系统的多种影响。在这篇综述中,我们提供了E2对早期中年雌性大鼠胸腺、脾脏、淋巴结和大脑区域的神经免疫相互作用的双相效应的证据。这些作用依赖于前/抗氧化状态,以及生长因子和细胞内信号分子的表达,这些对影响神经保护和炎症过程导致神经退行性变的神经元可塑性至关重要。
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引用次数: 0
Immunoregulatory Effects of Human Amnion Epithelial Cells on Natural Killer and T Cells in Women with Recurrent Spontaneous Abortion (RSA) 人羊膜上皮细胞对复发性自然流产妇女自然杀伤细胞和T细胞的免疫调节作用
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/TJI.2019.991
Fahimeh Khadem, N. Esmaeil, A. Rezaei, Hossein Motadayen, B. Khani
Introduction: Unexplained Recurrent Spontaneous Abortion (URSA) is the most common immunological complication during pregnancy. It has been found that the cells such as human amnion epithelial cells (hAECs) have the potency to modulate immune responses in vitro and in vivo. In the present study, we assessed the immunomodulatory effect of hAECs on NK cells and T cells in women with URSA. Materials and Methods: Peripheral Blood mononuclear cells (PBMC) were obtained from 14 URSA patients and co-cultured with isolated hAECs. NK cells and T cells were identified using anti-CD56 and anti-CD3 monoclonal antibodies (mAb). The expression of the activating receptor CD69 and the degranulation marker CD107a on NK cells and T cells were detected using specific mAb and analyzed by flow cytometry. Results: We found that CD69 activating receptor expression on NK cells and T cells was significantly decreased by incubation with hAECs in a dose-dependent manner (p=0.049). Also, the degranulation marker CD107a was significantly downregulated on NK cells and T cells following incubation with hAEC (p=0.003). Conclusion: Our results suggest hAECs have immune regulatory effects on activation and cytotoxicity of NK and T cells. Potential therapeutic application of hAECs for dysregulated NK and T cells immunity should be investigated in the future.
不明原因复发性自然流产(URSA)是妊娠期最常见的免疫并发症。人羊膜上皮细胞(hAECs)等细胞在体内体外均具有调节免疫应答的作用。在本研究中,我们评估了haec对URSA女性NK细胞和T细胞的免疫调节作用。材料与方法:取14例URSA患者外周血单个核细胞(PBMC),与分离的haec共培养。NK细胞和T细胞用抗cd56和抗cd3单克隆抗体(mAb)进行鉴定。用特异性单抗检测NK细胞和T细胞上活化受体CD69和脱颗粒标志物CD107a的表达,并用流式细胞术分析。结果:我们发现,与hAECs孵育后,NK细胞和T细胞上CD69激活受体的表达呈剂量依赖性显著降低(p=0.049)。此外,与hAEC孵育后,NK细胞和T细胞上的脱颗粒标志物CD107a显著下调(p=0.003)。结论:hAECs对NK细胞和T细胞的活化和细胞毒性具有免疫调节作用。heec在治疗NK和T细胞免疫失调方面的潜在应用有待进一步研究。
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引用次数: 6
Primer İmmün Yetersizliklerde Western Blot Yönteminin Önemi: İki Aile Olgusundan Örnekler
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/tji.2019.1178
Sevil Oskay Halacli, Deniz Çağdaş, F. Tezcan
{"title":"Primer İmmün Yetersizliklerde Western Blot Yönteminin Önemi: İki Aile Olgusundan Örnekler","authors":"Sevil Oskay Halacli, Deniz Çağdaş, F. Tezcan","doi":"10.25002/tji.2019.1178","DOIUrl":"https://doi.org/10.25002/tji.2019.1178","url":null,"abstract":"","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":"30 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80721750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Oxidative Biomarkers of Immuno-Oncology 免疫肿瘤学的氧化生物标志物
IF 1.2 Q4 IMMUNOLOGY Pub Date : 2019-01-01 DOI: 10.25002/tji.2019.1137
S. Ekmekcioglu
{"title":"Oxidative Biomarkers of Immuno-Oncology","authors":"S. Ekmekcioglu","doi":"10.25002/tji.2019.1137","DOIUrl":"https://doi.org/10.25002/tji.2019.1137","url":null,"abstract":"","PeriodicalId":41088,"journal":{"name":"Turkish Journal of Immunology","volume":"12 1","pages":""},"PeriodicalIF":1.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86854490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Turkish Journal of Immunology
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