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From agammaglobulinemia to neutropenia: 'The TCF-3 has different clinical presentations'. 从激动球蛋白血症到中性粒细胞减少症:"TCF-3 具有不同的临床表现"。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-10 DOI: 10.1111/sji.13423
Hulya Kose, Akcahan Akalin, Sara Sebnem Kilic

The clinical picture of the TCF3 deficiency may manifest differently from neutropenia to antibody production defects.

TCF3 缺乏症的临床表现各不相同,有的表现为中性粒细胞减少,有的则表现为抗体生成缺陷。
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引用次数: 0
Adropin regulates macrophage phenotype via PPARγ signalling: A preliminary study of adropin and Crohn's disease. 阿托品通过 PPARγ 信号调节巨噬细胞表型:阿托品与克罗恩病的初步研究。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-01 DOI: 10.1111/sji.13415
Lingli Zeng, Jintong Chen, Hongchai Xie, Wenming Liu, Chengdang Wang

Macrophage polarization is increasingly recognized as a vital pathogenetic factor in Crohn's disease (CD). Adropin is a secreted protein implicated in energy homeostasis, chiefly linked to glucose and lipid metabolism. However, the significance of adropin in CD is not clear. The objective of this study was to detect the expression of adropin in CD patients and investigate the effect of adropin on macrophage polarization induced by lipopolysaccharide (LPS) and its potential mechanism. Our study showed that serum adropin levels were markedly lower in patients with CD in active (CDA) than patients with CD in remission (CDR) and control groups (p < 0.01), however, there was no significant difference between in remission CD and healthy controls (p > 0.05). The colon mucous adropin levels in CDA were distinctly higher than CDR and controls (p < 0.01), while a significant difference between in remission CD and in healthy controls was not observed (p > 0.05). Exploration of the specific mechanism of action indicated that adropin promoted LPS-induced RAW264.7 macrophage polarization to M2 phenotype by modulating the expression and nuclear translocation of peroxisome proliferator receptor gamma (PPARγ), which may help weaken the intestinal inflammatory response. PPARγ inhibitor GW9662 reversed adropin-induced M2 macrophage polarization. Knockdown of GPR19, an adropin receptor, abrogated the M2 macrophage polarization caused by PPARγ. These findings suggest that adropin in colonic mucosa is a protective response in patients with active Crohn's disease.

人们日益认识到,巨噬细胞极化是克罗恩病(CD)的一个重要致病因素。阿托品是一种分泌蛋白,与能量平衡有关,主要与葡萄糖和脂质代谢相关。然而,阿多巴蛋白在克罗恩病中的意义尚不明确。本研究的目的是检测 CD 患者体内阿托品的表达,并探讨阿托品对脂多糖(LPS)诱导的巨噬细胞极化的影响及其潜在机制。我们的研究表明,CD活动期(CDA)患者的血清阿托品水平明显低于CD缓解期(CDR)患者和对照组(P 0.05)。CDA 患者的结肠粘液阿拖品水平明显高于 CDR 和对照组(P 0.05)。具体作用机制的探索表明,阿托品通过调节过氧化物酶体增殖受体γ(PPARγ)的表达和核转位,促进 LPS 诱导的 RAW264.7 巨噬细胞极化为 M2 表型,这可能有助于削弱肠道炎症反应。PPARγ 抑制剂 GW9662 逆转了阿托品诱导的 M2 巨噬细胞极化。敲除阿拖品受体 GPR19 可抑制 PPARγ 引起的 M2 巨噬细胞极化。这些研究结果表明,结肠粘膜中的阿多平素是活动性克罗恩病患者的一种保护性反应。
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引用次数: 0
Unravelling T-cell dynamics and immune responses in initial and recurrent uveitis. 揭示初次和复发性葡萄膜炎的 T 细胞动态和免疫反应。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-07 DOI: 10.1111/sji.13417
Zhiruo Wang, Yuanyuan Yang, Guochun Chen, Gong Chen, Jing Luo, Yunping Li, Jingming Shi, Huihui Chen

This study aimed to identify novel serological targets and investigate immune responses in patients with non-infectious uveitis, focusing on differences between initial onset and recurrent episodes. Differential gene expression analysis, immunocyte typing and T-cell receptor (TCR) gene analysis were conducted on RNA-sequenced peripheral blood samples from healthy individuals (n = 6) and non-infectious uveitis patients (n = 12), divided into 6 patients each at initial onset and recurrent stages. Peripheral blood T-cell types were analysed using flow cytometry. Bioinformatics methods included tools for RNA sequencing data processing, CIBERSORT for immune cell type prediction and specialized software for TCR repertoire analysis. Findings indicated that individuals with recurrent uveitis demonstrated a stronger adaptive immune response and a more pronounced immune imbalance compared to those with initial onset. Memory T cells were predominant in recurrent episodes, suggesting their potential role as biomarkers for disease progression. Significant differences in TCR diversity and V(D)J gene usage were observed between the various uveitis groups and healthy controls. Importantly, 38 uveitis-specific TCR sequences showed substantial expansion in the uveitis patients compared to controls. An elevated expansion of these specific TCR sequences was associated with an increased risk of uveitis development. The study highlights the critical role of adaptive immune responses and specific immune cell types in the pathogenesis of recurrent uveitis. Identification of the uveitis-specific TCR repertoire set could provide deeper insights into the disease and facilitate the development of targeted therapies for uveitis patients.

本研究旨在确定新的血清学靶点,并调查非感染性葡萄膜炎患者的免疫反应,重点关注初次发病与复发之间的差异。研究人员对健康人(6 人)和非感染性葡萄膜炎患者(12 人)的 RNA 序列外周血样本进行了差异基因表达分析、免疫细胞分型和 T 细胞受体(TCR)基因分析,将初发期和复发期患者各分为 6 人。使用流式细胞术分析外周血 T 细胞类型。生物信息学方法包括 RNA 测序数据处理工具、用于免疫细胞类型预测的 CIBERSORT 和用于 TCR 重排分析的专用软件。研究结果表明,与初次发病者相比,复发性葡萄膜炎患者表现出更强的适应性免疫反应和更明显的免疫失衡。记忆T细胞在复发性葡萄膜炎患者中占主导地位,这表明它们有可能成为疾病进展的生物标志物。不同葡萄膜炎组别与健康对照组在TCR多样性和V(D)J基因使用方面存在显著差异。重要的是,与对照组相比,38 个葡萄膜炎特异性 TCR 序列在葡萄膜炎患者中出现了大幅扩增。这些特异性 TCR 序列的扩增与葡萄膜炎发病风险的增加有关。这项研究强调了适应性免疫反应和特异性免疫细胞类型在复发性葡萄膜炎发病机制中的关键作用。对葡萄膜炎特异性 TCR 重排集的鉴定可加深人们对该疾病的了解,并促进针对葡萄膜炎患者的靶向疗法的开发。
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引用次数: 0
Serum integrin accumulation during asthma exacerbation: The role of matrix metalloproteinases. 哮喘恶化期间血清整合素的积累:基质金属蛋白酶的作用
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-11-07 DOI: 10.1111/sji.13420
Tellez-Jimenez Olivia, Trejo-Jasso Christian, Ramos-Ramirez Patricia, Chapela Rocío, Miguel-Reyes José Luis, López-Estrada Erika Del Carmen, Bazán-Perkins Blanca

The inflammation caused by asthma exacerbation can lead to permanent changes in the airways and loss of lung function. Integrins are membrane receptors that interact with components of the extracellular matrix and cell adhesion molecules. It is known that these receptors can be found in soluble form in some conditions such as asthma, but it is unknown if exacerbation during asthma leads to soluble integrins. Our results indicated that asthma patients showed higher levels of soluble α1, α2, and β2 integrin subunits in their serum compared to controls, as confirmed by both ELISA and western blot. During asthma exacerbation, the levels of α2 and β2 integrin subunits increased even more compared to non-exacerbation and controls, while the α1 integrin subunit decreased. Western blot analysis identified two β2 integrin subunits, one at 75 kDa and another at 120 kDa; the 120 kDa subunit increased during asthma exacerbation. The activity of matrix metalloproteinase 9 (MMP9) increased during exacerbation, while MMP2 remained unchanged. Lower forced expiratory volume in 1 second (FEV1) values were associated with higher expression levels of α2, β1, and β2 integrin subunits. Active and latent MMP9 were correlated with the levels of the β2 integrin subunit, which means that at low levels of active and latent MMP9, there are lower levels of β2 integrin subunit. In conclusion, asthma exacerbation leads to the presence of soluble integrins, particularly the β2 subunit, most likely due to MMP9-induced proteolytic cleavage.

哮喘恶化引起的炎症可导致气道永久性病变和肺功能丧失。整合素是与细胞外基质成分和细胞粘附分子相互作用的膜受体。众所周知,这些受体在某些情况下(如哮喘)会以可溶性形式存在,但哮喘加重是否会导致可溶性整合素的出现尚不清楚。我们的研究结果表明,与对照组相比,哮喘患者血清中可溶性α1、α2和β2整合素亚基的含量更高,这一点已通过ELISA和Western印迹法得到证实。在哮喘加重期,α2 和 β2整合素亚基的水平比未加重期和对照组更高,而α1整合素亚基则有所下降。Western 印迹分析确定了两种 β2 整合素亚基,一种为 75 kDa,另一种为 120 kDa;120 kDa 亚基在哮喘加重期间有所增加。基质金属蛋白酶 9(MMP9)的活性在哮喘加重期间增加,而 MMP2 保持不变。较低的一秒用力呼气容积(FEV1)值与较高的α2、β1和β2整合素亚基表达水平有关。活性和潜伏的MMP9与β2整合素亚基的水平相关,这意味着在活性和潜伏的MMP9水平较低时,β2整合素亚基的水平也较低。总之,哮喘恶化会导致可溶性整合素的存在,尤其是β2亚基,这很可能是由于MMP9诱导的蛋白水解作用造成的。
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引用次数: 0
Probiotics as adjuvants to mitigate adverse reactions and enhance effectiveness in Food Allergy Immunotherapy. 益生菌作为佐剂,可减轻食物过敏免疫疗法的不良反应并提高疗效。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-10-15 DOI: 10.1111/sji.13405
Ingrid Lamminpää, Elena Niccolai, Amedeo Amedei

In the past decades, food allergies became increasingly dominant since early childhood, leading to a lower quality of life and to increasing costs addressed by the health care system. Beside standard avoidance of specific allergens and drug treatments following allergen exposure, a great deal of research has lately focused on Food Allergy Allergen Immunotherapy (FA-AIT). SCIT and EPIT (Subcutaneous and Epicutaneous Immunotherapy), OIT (Oral Immunotherapy), and SLIT (Sublingual Immunotherapy) consist in gradual exposure to allergens to desensitize and achieve tolerance once therapy has ended. Although promising, FA-AIT may bring acute local and systemic adverse reactions. To enhance efficacy, safety and convenience of AIT, the quest of potential adjuvants to mitigate the adverse reactions becomes crucial. Immunomodulatory activities, such as that of increasing the regulatory T cells and decreasing the IgE, have been observed in specific probiotics' strains and multiple studies elucidated the role of gut microbiota as a major interplayer among the host and its immune system. In this review, the microbiome modulation is shown as potential AIT adjuvant, nevertheless the need of more clinical studies in the near future is pivotal to assess the efficacy of targeted bacterial therapies and faecal microbiota transplantation.

在过去的几十年里,食物过敏在儿童早期就已日益普遍,导致生活质量下降,医疗保健系统的费用不断增加。除了标准的避免接触特定过敏原和接触过敏原后的药物治疗外,大量研究最近集中在食物过敏原免疫疗法(FA-AIT)上。SCIT和EPIT(皮下和表皮免疫疗法)、OIT(口服免疫疗法)和SLIT(舌下免疫疗法)都是通过逐渐接触过敏原来脱敏,并在治疗结束后达到耐受。FA-AIT虽然前景广阔,但可能会带来急性局部和全身不良反应。为了提高口服免疫疗法的疗效、安全性和便利性,寻找潜在的佐剂来减轻不良反应变得至关重要。在特定益生菌菌株中观察到了免疫调节活性,如增加调节性 T 细胞和降低 IgE,多项研究阐明了肠道微生物群在宿主及其免疫系统中的重要作用。在这篇综述中,微生物组调节被认为是潜在的 AIT 佐剂,然而在不久的将来,需要更多的临床研究来评估靶向细菌疗法和粪便微生物组移植的疗效。
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引用次数: 0
Dysregulation of T cell response in the pathogenesis of inflammatory bowel disease. 炎症性肠病发病机制中的 T 细胞反应失调。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-12-01 Epub Date: 2024-10-12 DOI: 10.1111/sji.13412
Rucha Chandwaskar, Rajdeep Dalal, Saurabh Gupta, Aishwarya Sharma, Deepak Parashar, Vivek K Kashyap, Jagdip Singh Sohal, Subhash K Tripathi

Inflammatory bowel disease (IBD), comprised of Crohn's disease (CD) and ulcerative colitis (UC), are gut inflammatory diseases that were earlier prevalent in the Western Hemisphere but now are on the rise in the East, with India standing second highest in the incidence rate in the world. Inflammation in IBD is a cause of dysregulated immune response, wherein helper T (Th) cell subsets and their cytokines play a major role in the pathogenesis of IBD. In addition, gut microbiota, environmental factors such as dietary factors and host genetics influence the outcome and severity of IBD. Dysregulation between effector and regulatory T cells drives gut inflammation, as effector T cells like Th1, Th17 and Th9 subsets Th cell lineages were found to be increased in IBD patients. In this review, we attempted to discuss the role of different Th cell subsets together with other T cells like CD8+ T cells, NKT and γδT cells in the outcome of gut inflammation in IBD. We also highlighted the potential therapeutic candidates for IBD.

炎症性肠病(IBD)包括克罗恩病(CD)和溃疡性结肠炎(UC),是一种肠道炎症性疾病,早先在西半球流行,但现在在东方呈上升趋势,印度的发病率位居世界第二。IBD 中的炎症是免疫反应失调的一个原因,其中辅助性 T(Th)细胞亚群及其细胞因子在 IBD 的发病机制中起着重要作用。此外,肠道微生物群、环境因素(如饮食因素)和宿主遗传也会影响 IBD 的结果和严重程度。效应T细胞和调节T细胞之间的失调是肠道炎症的诱因,因为在IBD患者中,Th1、Th17和Th9亚群Th细胞系等效应T细胞增多。在这篇综述中,我们试图讨论不同 Th 细胞亚群与其他 T 细胞(如 CD8+ T 细胞、NKT 和 γδT 细胞)在 IBD 肠道炎症中的作用。我们还强调了 IBD 的潜在候选疗法。
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引用次数: 0
Specific antibody responses to Qβ-displayed Plasmodium falciparum-derived UB05 and MSP3 proteins in mother-neonate couples. 母亲-新生儿夫妇对 Qβ 显示的恶性疟原虫衍生 UB05 和 MSP3 蛋白的特异性抗体反应。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-19 DOI: 10.1111/sji.13404
Abel Lissom, Rosette Megnekou, Thibau Flaurant Tchouangueu, Loveline Ngu, Jean Claude Djontu, Herve Fotso Ouambo, Carrie Sanders, Jules Colince Tchadji, Carole Stephanie Sake, Salomon Bonsi Tchuandom, Swapnil Bawage, Arinze Stanley Okoli, Chae Gyu Park, Alain Bopda Waffo, Nchinda Wapimewah Godwin

Malaria blood-stage parasite is a critical pathogenic stage responsible for serious adverse outcomes in pregnant women and their neonates. Immunoglobulin G (IgG) antibody responses specific to various asexual blood-stage antigens were well reported in non-pregnant individuals. However, little is still known during placental malaria. To assess the antibody responses specific to Plasmodium falciparum-derived MSP3 and UB05 malaria vaccine candidates in mother-neonate couples, mother's peripheral blood and neonate's cord blood samples were collected at delivery. After malaria diagnostic, plasma levels of IgG and IgG subclass responses specific to UB05, MSP3 and UB05-MSP3 were determined using ELISA. As outcomes, both mothers and neonates had significantly higher IgG responses to UB05 and UB05-MSP3 compared to anti-MSP3 IgG (p < 0.05), irrespective of malaria status. Significant negative correlations were observed between IgG levels specific to the three antigens and parasitaemia (p < 0.01). Anti-UB05 and anti-UB05-MSP3 IgG levels in neonates showed a significant positive correlation with the corresponding mothers' antibodies (rs = 0.25 with p = 0.04; rs = 0.31 with p = 0.01, respectively). UB05MSP3-specific IgG3 and IgG1 subclass responses were significantly higher than the IgG4 subclass (p < 0.01). The neonates IgG1 and IgG3 levels positively correlated with the corresponding antibody subclasses of mothers. These findings suggest an association between UB05 and UB05-MSP3-specific antibody responses and malaria control during pregnancy. Maternal-foetal transfer of MSP3 and UB05-specific IgG occurs during pregnancy, suggesting the interest in the future malaria vaccination strategies in pregnant women to generate early protective immunity in baby against malaria.

疟疾血期寄生虫是导致孕妇及其新生儿严重不良后果的关键致病阶段。据报道,非孕妇对各种无性血期抗原具有特异性免疫球蛋白 G(IgG)抗体反应。然而,人们对胎盘疟疾仍然知之甚少。为了评估母亲-新生儿夫妇对恶性疟原虫衍生的 MSP3 和 UB05 候选疟疾疫苗的特异性抗体反应,我们在分娩时采集了母亲的外周血和新生儿的脐带血样本。疟疾诊断后,使用 ELISA 方法测定血浆中针对 UB05、MSP3 和 UB05-MSP3 的 IgG 和 IgG 亚类反应水平。结果显示,与抗 MSP3 IgG 相比,母亲和新生儿对 UB05 和 UB05-MSP3 的 IgG 反应明显更高(分别为 p s = 0.25,p = 0.04;rs = 0.31,p = 0.01)。UB05MSP3 特异性 IgG3 和 IgG1 亚类反应明显高于 IgG4 亚类(p
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引用次数: 0
NrCAM activates the NF-κB signalling pathway by competitively binding to SUMO-1 and promotes Th17 cell differentiation in Graves' disease. NrCAM 通过与 SUMO-1 竞争性结合激活 NF-κB 信号通路,并促进巴塞杜氏病 Th17 细胞的分化。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-01 Epub Date: 2024-08-19 DOI: 10.1111/sji.13401
Fengjiao Huang, Lijuan Zhang, Yingying Zhou, Shuiying Zhao, Jiao Wang

This study aimed to explore the molecular mechanism of neuronal cell adhesion molecule (NrCAM) by regulating Th17 cell differentiation in the pathogenesis of Graves' disease (GD). Naïve CD4+ T cells were isolated from peripheral blood mononuclear cells of GD patients and healthy control (HC) subjects. During the differentiation of CD4+ T cells into Th17 cells, NrCAM level in GD group was improved. Interference with NrCAM in CD4+ T cells of GD patients decreased the percentage of Th17 cells. NrCAM overexpression in CD4+ T cells of HC subjects increased the percentage of Th17 cells and upregulated p-IκBα, p50, p65, c-Rel protein expressions, and NF-κB inhibitor BAY11-7082 partially reversed NrCAM effect. NrCAM overexpression promoted the degradation of IκBα, and overexpression of small ubiquitin-related modifier 1 (SUMO-1) inhibited IκBα degradation. NrCAM overexpression reduced IκBα binding to SUMO-1. During Th17 cell differentiation in HC group, NrCAM overexpression increased IL-21 levels and secretion, and IL-21 neutralizing antibody reversed this effect. IL-21 level was decreased after p65 interference in CD4+ T cells of HC subjects. p65 interacts with IL-21 promoter region. In conclusion, NrCAM binds to SUMO-1 and increases phosphorylation of IκBα, leading to activation of NF-κB pathway, which promotes Th17 cell differentiation.

本研究旨在探讨神经元细胞粘附分子(NrCAM)调控Th17细胞分化在巴塞杜氏病(GD)发病机制中的分子机制。研究人员从巴塞杜氏病患者和健康对照组(HC)的外周血单核细胞中分离出了幼稚的CD4+ T细胞。在CD4+ T细胞向Th17细胞分化的过程中,GD组的NrCAM水平有所提高。干扰 GD 患者 CD4+ T 细胞中的 NrCAM 会降低 Th17 细胞的比例。在 HC 受试者的 CD4+ T 细胞中过表达 NrCAM 会增加 Th17 细胞的比例,并上调 p-IκBα、p50、p65 和 c-Rel 蛋白的表达,NF-κB 抑制剂 BAY11-7082 可部分逆转 NrCAM 的作用。NrCAM的过表达促进了IκBα的降解,而泛素相关小修饰物1(SUMO-1)的过表达抑制了IκBα的降解。NrCAM的过表达减少了IκBα与SUMO-1的结合。在HC组Th17细胞分化过程中,NrCAM过表达增加了IL-21的水平和分泌,IL-21中和抗体逆转了这一效应。p65与IL-21启动子区域相互作用。总之,NrCAM与SUMO-1结合并增加IκBα的磷酸化,导致NF-κB通路的激活,从而促进Th17细胞的分化。
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引用次数: 0
Can autoantibodies be transferred by immunoglobulin replacement therapy? 免疫球蛋白替代疗法会转移自身抗体吗?
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-01 DOI: 10.1111/sji.13413
Peter Bergman

特应性皮炎是一种常见的炎症性皮肤病。体内微生态菌群失调引发的 TH2 型免疫失衡是特应性皮炎的一个重要机制。皮肤微生态、肠道微生态和肺部微生态参与了特应性皮炎的免疫过程。如需了解更多信息,请阅读本期由 Zhou 等人撰写的综述文章。
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引用次数: 0
Assessment of autoantibodies associated with intravenous immunoglobulin replacement therapy in children with primary immunodeficiency. 评估与原发性免疫缺陷儿童静脉注射免疫球蛋白替代疗法相关的自身抗体。
IF 4.1 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-01 Epub Date: 2024-07-07 DOI: 10.1111/sji.13396
Murat Özer, Seher Tekeli, Selçuk Doğan, Sema Çetin, Rıdvan Selen, Caner Aytekin

While it is known that immunoglobulin replacement therapy (IgRT) used in the treatment of primary immunodeficiency disorders (PIDs) can lead to the passive transfer of autoantibodies, there is no data indicating that these antibodies can cause clinical symptoms in patients. This study aimed to investigate the presence of autoantibodies and their clinical correlation in patients diagnosed with PIDs receiving IgRT. Paediatric patients who were diagnosed with PIDs, and administered IgRT at our immunology clinic between 1 January 2012 and 31 December 2021, were included in the study. The medical records of these patients were retrospectively analysed, and autoantibodies were screened. Autoantibody screening was conducted at least once in 48 cases. Among these cases, 29 cases (60.4%) demonstrated positivity for at least one of the autoantibodies screened in the study. Among these cases, 23 tested positive for anti-TPO, 9 for anti-TG and 2 for both anti-TPO and anti-TG. Only two of these patients were confirmed to have Hashimoto's thyroiditis. In 30 cases, autoantibodies related to Celiac disease (CD) were screened, with at least one being positive in five different cases; CD was not confirmed. The results of our study suggest that passive transfer of autoantibodies to patients with IgRT does not cause any significant clinical findings. In addition, in cases of PID, autoantibodies detected in the blood passed to patients with IgRT can lead to misdiagnosis. Screening for autoantibodies in patients with PID undergoing IgRT may not yield accurate results in terms of detecting autoimmune diseases.

众所周知,用于治疗原发性免疫缺陷病(PID)的免疫球蛋白替代疗法(IgRT)会导致自身抗体的被动转移,但目前还没有数据表明这些抗体会导致患者出现临床症状。本研究旨在调查接受 IgRT 治疗的 PID 患者体内是否存在自身抗体及其临床相关性。研究纳入了2012年1月1日至2021年12月31日期间在本院免疫诊所确诊为PID并接受IgRT治疗的儿科患者。对这些患者的病历进行回顾性分析,并筛查自身抗体。48例患者至少进行了一次自身抗体筛查。在这些病例中,29 例(60.4%)至少有一种自身抗体呈阳性。其中,23 例抗血小板生成素检测呈阳性,9 例抗 TG 检测呈阳性,2 例抗血小板生成素和抗 TG 检测均呈阳性。其中只有两名患者被确诊为桥本氏甲状腺炎。在30例病例中,筛查出了与乳糜泻(CD)相关的自身抗体,其中有5例至少有一种抗体呈阳性;但乳糜泻并未得到确诊。我们的研究结果表明,自身抗体被动转移到 IgRT 患者身上不会引起任何明显的临床症状。此外,在 PID 病例中,从 IgRT 患者的血液中检测到自身抗体可能会导致误诊。对接受 IgRT 的 PID 患者进行自身抗体筛查,可能无法准确检测出自身免疫性疾病。
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引用次数: 0
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Scandinavian Journal of Immunology
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