Immunology letters最新文献_第5页

Taurohyodeoxycholic acid ameliorates inflammatory response in a murine model of ovalbumin (OVA)-induced allergic asthma 牛磺酸去氧胆酸改善卵清蛋白（OVA）诱导的过敏性哮喘小鼠模型的炎症反应。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-26 DOI: 10.1016/j.imlet.2025.107096

Ye You , Jing Li , Jiayi Wang , Xianglan Luo , Jingyuan Liu , Xinmiao Wang , Shichen Yi , Ruizhi He , Yating Shi , Jie Xu , Mengqing Hou , Yanjun Cao , Yang Li , Jing Dong , Jiao He

Taurohyodeoxycholic acid (THDCA), a naturally occurring conjugated bile acid compound formed by the condensation of taurine and deoxycholic acid, possesses various biological activities. Present study attempted to assess whether THDCA can alleviate airway inflammation in allergic asthma through regulating the immune balance among CD4⁺ T cell subgroups. Mice were exposed with ovalbumin (OVA) to build allergic asthma model and THDCA was administrated orally. Pulmonary histopathology analysis was evaluated by H&E and PAS staining. The typical cytokines and transcription factors of CD4⁺ T cell subgroups were determined, and the proportion of CD4⁺ T cell subgroups were analyzed. The oral administration of THDCA attenuated OVA-induced asthma by decreasing inflammatory cell counts in the bronchoalveolar lavage fluid (BALF), reducing tIgE and OVA-sIgE concentration in the serum, and improving histopathological changes in the lung tissue. In addition, THDCA reduced the secretion of IL-4, IL-5, IL-13, IL-6, TNF-α, IL-17A, and TGF-β1, but increased the production of IFN-γ, IL-10, and IL-35 in the BALF and lung tissue. Meanwhile, THDCA inhibited GATA3 and RORγt expression, and STAT3 phosphorylation, but improved T-bet and Foxp3 expression in the lung tissue. Besides, THDCA restored the proportion of CD4⁺ T cell subgroups in the spleen and peripheral blood. These findings indicated that THDCA may have therapeutic potential for treating allergic asthma by regulating the immune balance of CD4⁺ T cell subgroups.

牛磺酸-脱氧胆酸（Taurohyodeoxycholic acid， THDCA）是牛磺酸与脱氧胆酸缩合形成的天然共轭胆汁酸化合物，具有多种生物活性。本研究试图评估THDCA是否通过调节CD4+ T细胞亚群间的免疫平衡来缓解过敏性哮喘气道炎症。用卵清蛋白（OVA）建立小鼠变应性哮喘模型，并口服四氢二甲酸（THDCA）。肺组织病理学分析采用H&E和PAS染色。测定CD4+ T细胞亚群的典型细胞因子和转录因子，并分析CD4+ T细胞亚群的比例。口服THDCA通过降低支气管肺泡灌洗液（BALF）中的炎症细胞计数、降低血清中tIgE和OVA-sIgE浓度、改善肺组织的组织病理学改变来减轻ova诱导的哮喘。此外，THDCA降低了BALF和肺组织中IL-4、IL-5、IL-13、IL-6、TNF-α、IL-17A、TGF-β1的分泌，增加了IFN-γ、IL-10、IL-35的分泌。同时，THDCA抑制肺组织中GATA3、rorr γt的表达和STAT3的磷酸化，但提高T-bet和Foxp3的表达。此外，THDCA还能恢复脾脏和外周血中CD4+ T细胞亚群的比例。这些发现表明THDCA可能通过调节CD4+ T细胞亚群的免疫平衡而具有治疗过敏性哮喘的治疗潜力。

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引用次数: 0

Restoration of Fli1 expression as a potential therapeutic approach in Systemic Sclerosis: Effects on age-associated B cells 恢复Fli1表达作为系统性硬化症的潜在治疗方法：对年龄相关B细胞的影响

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-26 DOI: 10.1016/j.imlet.2025.107094

Athanasios Sachinidis , Malamatenia Lamprinou , Theodoros Dimitroulas

Fli1 is a transcription factor playing a major role in the regulation of normal hematopoiesis and vasculogenesis. Its deficiency has been associated with the development of fibrosis in various diseases, including systemic sclerosis/scleroderma (SSc), a rare autoimmune rheumatic disease. In addition, in Fli1 B cell conditional knockout mice, a striking increase of age-associated B cells (ABCs) has been observed. These cells constitute a CD11c⁺CD21^low/- B cell population that displays an expansion in autoimmunity and drives disease pathogenesis. The exact role and functions of ABCs, though, are not yet fully understood. Taking into consideration all the above, regarding Fli1 deficiency in SSc pathogenesis and ABC expansion, we propose restoration of this specific transcription factor’s expression as a potential therapeutic approach for the aforementioned rheumatic disease. Moreover, we provide some interventions that aim to restore Fli1 expression via modulating the signals of TGF-β pathway, whose activation is considered as crucial for fibrosis development in SSc.

Fli1是一种转录因子，在正常造血和血管发生的调节中起重要作用。它的缺乏与各种疾病纤维化的发展有关，包括系统性硬化症/硬皮病（SSc），一种罕见的自身免疫性风湿病。此外，在Fli1 B细胞条件敲除小鼠中，观察到年龄相关B细胞（abc）的显著增加。这些细胞构成CD11c+CD21low/- B细胞群，在自身免疫中表现出扩张并驱动疾病发病机制。然而，abc的确切作用和功能尚不完全清楚。综上所述，关于SSc发病机制中的Fli1缺陷和ABC扩增，我们建议恢复这一特定转录因子的表达作为上述风湿性疾病的潜在治疗方法。此外，我们提供了一些干预措施，旨在通过调节TGF-β通路的信号来恢复Fli1的表达，TGF-β通路的激活被认为是SSc纤维化发展的关键。

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引用次数: 0

Tryptophan metabolism in health and disease- implications for non-communicable diseases 健康和疾病中的色氨酸代谢-对非传染性疾病的影响。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-25 DOI: 10.1016/j.imlet.2025.107093

Andiswa Msizi Gabela, Nontobeko Mthembu, Sabelo Hadebe

Tryptophan, an essential amino acid, is primarily metabolized through four key pathways: the kynurenine pathway, serotonin pathways, indole pathways and interleukin 4-induced gene 1 (IL-4I1) pathways. Dysregulation of tryptophan metabolism is implicated in various non-communicable diseases including psychiatric disorders, inflammatory and autoimmune diseases, as well as metabolic diseases. The dogma in the field is that tryptophan is metabolized via the kynurenine pathway in the liver mainly by indoleamine 2,3-dioxygenase 1/2 (IDO 1/2) and Tryptophan dioxygenase 2 (TDO2) enzymes. However, there is growing evidence demonstrating that IL-4I1 and tryptophanase are also crucial tryptophan catabolizing enzymes resulting in metabolites that activate aryl hydrocarbon receptor (AhR) and modulate immune responses. Tryptophan metabolism is crucial in cellular, tissue and organismal function and its disruption is linked to conditions such as inflammatory bowel disease (IBD), multiple sclerosis (MS), and psychiatric disorders like depression, anxiety and metabolic diseases such as obesity and Type 2 diabetes. It is unclear though whether only specific tryptophan pathways are associated with disease or there is a level of redundancy. Some key metabolites from tryptophan catabolism can come from multiple pathways, with opposing or converging effects on cellular functions. This review will explore the critical role of tryptophan metabolism in health and diseases, focusing on its implications in non-communicable diseases. Importantly, this review will focus on recent developments in tryptophan metabolism and strengthen the argument for a revised schematic tryptophan catabolic pathway.

色氨酸是一种必需氨基酸，主要通过四个关键途径代谢：犬尿氨酸途径、血清素途径、吲哚途径和白细胞介素4诱导基因1 （IL-4I1）途径。色氨酸代谢失调与各种非传染性疾病有关，包括精神疾病、炎症和自身免疫性疾病以及代谢性疾病。该领域的教条是，色氨酸在肝脏中主要通过吲哚胺2,3-双加氧酶1/2 （IDO 1/2）和色氨酸双加氧酶2 （TDO2）酶代谢犬尿氨酸途径。然而，越来越多的证据表明，IL-4I1和色氨酸酶也是关键的色氨酸分解代谢酶，其代谢产物激活芳烃受体（AhR）并调节免疫反应。色氨酸代谢对细胞、组织和机体功能至关重要，它的破坏与炎症性肠病（IBD）、多发性硬化症（MS）、抑郁症、焦虑症等精神疾病以及肥胖和2型糖尿病等代谢性疾病有关。目前尚不清楚是否只有特定的色氨酸途径与疾病有关，还是存在一定程度的冗余。色氨酸分解代谢的一些关键代谢物可以通过多种途径产生，对细胞功能具有相反或趋同的作用。本文将探讨色氨酸代谢在健康和疾病中的关键作用，重点关注其在非传染性疾病中的意义。重要的是，本综述将关注色氨酸代谢的最新进展，并加强对修订后的色氨酸分解代谢途径示意图的论证。

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引用次数: 0

Beyond HNA-1: The anti-HNA-3 autoantibody as a protagonist in autoimmune neutropenia 超越HNA-1：抗hna -3自身抗体在自身免疫性中性粒细胞减少症中的作用。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-25 DOI: 10.1016/j.imlet.2025.107095

Renato Cerqueira , Elyse Moritz , Josefina A.P. Braga , Akemi K. Chiba , João B. Pesquero , José O. Bordin

Introduction

Autoimmune neutropenia (AIN), a common cause of chronic neutropenia, has been categorized as primary (pAIN) and secondary (sAIN). This study investigates the specificity of anti-HNA autoantibodies in both types.

Materials and Methods

A prospective cohort study of 85 chronic neutropenia patients included those with detectable anti-HNA autoantibodies. Anti-HNA was assessed using granulocyte agglutination (GAT), granulocyte immunofluorescence (GIFT), and LABScreen Multi Kit (LSM). Molecular analysis was performed to assess HNA expression.

Results

Of 85 patients, 7 had pAIN and 8 had sAIN. All pAIN patients exhibited only anti-HNA-1, while anti-HNA-3 was found in 3/8 sAIN patients. All patients with anti-HNA-3 tested positive in LSM; one was positive in both GAT and GIFT.

Discussion

While anti-HNA-3 has been described exclusively as an alloantibody, this is the first report of anti-HNA-3 as an autoantibody in AIN.

Conclusion

Anti-HNA-3 autoantibody is associated only with sAIN, suggesting distinct mechanisms in pAIN and sAIN.

自身免疫性中性粒细胞减少症（AIN）是慢性中性粒细胞减少症的常见原因，可分为原发性（pAIN）和继发性（sAIN）。本研究探讨了两种类型的抗海航自身抗体的特异性。材料和方法：对85例慢性中性粒细胞减少患者进行前瞻性队列研究，其中包括可检测到的抗海航自身抗体。采用粒细胞凝集（GAT）、粒细胞免疫荧光（GIFT）和LABScreen Multi Kit （LSM）检测抗海航抗体。通过分子分析评估海航蛋白的表达。结果：85例患者中，pAIN 7例，sAIN 8例。所有pAIN患者均有抗hna -1，而3/8的sAIN患者有抗hna -3。LSM患者抗hna -3阳性；1例GAT和GIFT均阳性。讨论：虽然抗hna -3被描述为一种专门的同种异体抗体，但这是AIN中首次报道的抗hna -3作为自身抗体。结论：抗hna -3自身抗体仅与sAIN相关，提示在pAIN和sAIN中存在不同的机制。

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引用次数: 0

Fatty acid binding protein 2 (FATP2/SLC27A2) blockade with Lipofermata elicits dual effects on inflammatory responses in human monocytes and macrophages 脂fermata阻断脂肪酸结合蛋白2 （FATP2/SLC27A2）可对人单核细胞和巨噬细胞的炎症反应产生双重影响。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-25 DOI: 10.1016/j.imlet.2025.107092

Nico Hahn , Serhii Chornyi , Daan Heister , Helga E. de Vries , Martin Giera , Mariëtte R. Boon , Gijs Kooij , Jan Van den Bossche

Inflammatory responses often involve metabolic rewiring within immune cells to support effector functions. Targeting metabolic pathways in immune cells therefore represents a promising strategy to modulate inflammatory diseases and improve therapeutic outcomes. Acyl-CoA synthesis by fatty acid transporter 2 (FATP2/SLC27A2) facilitates the transport of long-chain fatty acids into the cell. It represents a key step in fatty acid metabolism and the subsequent production of bioactive lipid mediators (LMs) with immunoregulatory functions. While the FATP2 inhibitor Lipofermata is currently evaluated for lipid-lowering therapies in metabolic diseases, and to revert the suppressive nature of myeloid cells in cancer, its effect on inflammatory responses in human macrophages remains elusive.

Here, we show that Lipofermata reduced LPS-induced inflammatory responses in whole blood and human monocytes. This anti-inflammatory effect was paralleled by a decreased biosynthesis of arachidonic acid-derived inflammatory LMs, including prostaglandin E2 (PGE2) and thromboxane 2 (TxB2). These findings suggest an anti-inflammatory effect mediated by Lipofermata-mediated redirection of lipid metabolism in monocytes.

Conversely, in mature human monocyte-derived macrophages, Lipofermata treatment enhanced LPS-induced cytokine production and induced cell death, likely through inflammasome activation. Together, these results underscore the cell type-specific effects of FATP2 inhibition and highlight the dual role of Lipofermata in modulating inflammatory immune responses. As such, targeting lipid metabolism with Lipofermata could have therapeutic potential with both anti- and pro-inflammatory applications, depending on the target cell type and context.

炎症反应通常涉及免疫细胞内的代谢重新布线，以支持效应功能。因此，靶向免疫细胞中的代谢途径代表了一种有希望的策略来调节炎症性疾病并改善治疗结果。脂肪酸转运蛋白2 （FATP2/SLC27A2）合成酰基辅酶a促进长链脂肪酸转运到细胞内。它是脂肪酸代谢和随后产生具有免疫调节功能的生物活性脂质介质（LMs）的关键步骤。虽然FATP2抑制剂Lipofermata目前被评估用于代谢性疾病的降脂治疗，并恢复骨髓细胞在癌症中的抑制性质，但其对人类巨噬细胞炎症反应的影响仍然难以捉摸。在这里，我们发现Lipofermata降低了全血和人单核细胞中脂多糖诱导的炎症反应。这种抗炎作用与花生四烯酸衍生的炎症性LMs的生物合成减少相一致，包括前列腺素E2 （PGE2）和血栓素2 （TxB2）。这些发现表明，脂fermata介导的单核细胞脂质代谢重定向介导了抗炎作用。相反，在成熟的人单核细胞源性巨噬细胞中，Lipofermata处理可能通过炎症小体激活，增强了lps诱导的细胞因子产生并诱导细胞死亡。总之，这些结果强调了FATP2抑制的细胞类型特异性效应，并强调了脂fermata在调节炎症免疫反应中的双重作用。因此，用Lipofermata靶向脂质代谢可能具有抗炎和促炎的治疗潜力，这取决于靶细胞类型和环境。

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引用次数: 0

Tissue resident memory B cells mediate protective immunity to respiratory pathogens in the airways 组织常驻记忆B细胞介导呼吸道病原体的保护性免疫。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-16 DOI: 10.1016/j.imlet.2025.107091

Ivy M. Akehurst, Louisa K. James

Respiratory pathogens pose a significant risk to public health and are responsible for burdening health care by causing worldwide morbidity and mortality. The immune environment in the airway is critical for protection from respiratory pathogens and comprises several specialist subsets of resident lymphocytes and myeloid cells. Tissue resident-memory B cells (B_RM) are a subset of memory B cell which reside in mucosal tissues, including the airways. Although, B_RM have only recently been characterised, they have a crucial role in generating robust and localised immune responses to respiratory infections, particularly secondary responses, by rapidly differentiating into antibody-secreting cells. A greater understanding of their role in protecting the airways from respiratory pathogens will enable the development of immunisation strategies against respiratory disease. This mini-review aims to summarise the current knowledge of B_RM and highlight areas for future research.

呼吸道病原体对公共卫生构成重大风险，并通过在世界范围内造成发病率和死亡率，给卫生保健造成负担。气道内的免疫环境对保护机体免受呼吸道病原体的侵袭至关重要，它由若干专门的淋巴细胞和骨髓细胞亚群组成。组织驻留记忆B细胞（Tissue resident-memory B cells， BRM）是记忆B细胞的一个子集，存在于包括气道在内的粘膜组织中。尽管BRM最近才被描述，但它们通过迅速分化为抗体分泌细胞，在产生针对呼吸道感染的强大和局部免疫反应，特别是继发性反应方面发挥着至关重要的作用。更好地了解它们在保护呼吸道免受呼吸道病原体侵害方面的作用，将有助于制定针对呼吸道疾病的免疫策略。这篇小型综述旨在总结BRM的当前知识，并强调未来研究的领域。

引用次数: 0

Coordination of cellular responses to SARS-CoV-2 during severe COVID-19 illness 严重COVID-19疾病期间细胞对SARS-CoV-2反应的协调

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-15 DOI: 10.1016/j.imlet.2025.107090

Assia Samri , Raphael Lhote , Alice Rousseau , Véronique Morin , Nadine Tarantino , Stéphane Marot , Aude Jary , Delphine Sterlin , Anne-Geneviève Marcelin , Zahir Amoura , Guy Gorochov , Vincent Vieillard , Amélie Guihot

The early cellular and humoral immune responses to SARS-CoV-2 result in a wide range of COVID-19 disease severity. Here we conducted an observational study of these three arms of the immune responses (T, B and NK) to SARS-CoV-2 in 17 patients hospitalized for severe COVID-19 at median of 31 days after first symptoms. We found that the main T cell response was directed against two specific regions of the spike viral protein, called B and E, which are inversely correlated with the expression of the KIR2DL1 inhibitory receptor on NK cells (p = 0.03, and p = 0.0001 respectively). Furthermore, expression of the inhibitory receptor ILT2 on NK cells was only correlated with T cell responses against the specific E region (p = 0.02), suggesting that HLA-G may play a role in the extinction of the NK response to the T cell response. Moreover, the antibody response was mainly directed against the nucleocapsid, whereas the antibody neutralizing response was inversely correlated with the cellular response to spike (p < 0.003). Taken together these data suggest a strong coordination between the innate and adaptive immune responses during the acute phase of infection, which could reflect the further resolution of COVID-19 patients with severe disease.

对SARS-CoV-2的早期细胞和体液免疫反应导致COVID-19疾病严重程度的广泛变化。在这里，我们对17名因严重COVID-19住院的患者在首次出现症状后中位31天内对SARS-CoV-2的这三个免疫反应进行了观察性研究。我们发现，主要的T细胞反应是针对刺突病毒蛋白的两个特定区域，称为B和E，它们与NK细胞上KIR2DL1抑制受体的表达呈负相关（p=0.03和p=0.0001）。此外，NK细胞上抑制受体ILT2的表达仅与T细胞对特定E区的反应相关（p=0.02），提示HLA-G可能在NK对T细胞反应的消除中起作用。此外，抗体反应主要针对核衣壳，而抗体中和反应与细胞对spike的反应呈负相关(p

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引用次数: 0

Immune checkpoint molecules as predictive markers of COVID-19 severity: A comprehensive univariable and multivariable analysis 免疫检查点分子作为COVID-19严重程度的预测标志物：一项综合单变量和多变量分析

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-15 DOI: 10.1016/j.imlet.2025.107089

Adam Majchrzak , Paulina Niedźwiedzka-Rystwej , Dominika Bębnowska , Bogusz Aksak-Wąs , Malwina Karasińska-Cieślak , Danuta Cembrowska-Lech , Karolina Skonieczna-Żydecka , Kaja Mielczak , Anna Urbańska , Rafał Hrynkiewicz , Filip Lewandowski , Miłosz Parczewski

Immune dysregulation plays a key role in the deterioration of COVID-19. This study evaluated immune checkpoint molecules (ICMs) as markers of disease severity. Immunophenotyping of 525 hospitalised patients with moderate (n=464) and severe (n=61) COVID-19 was performed at admission and analysed alongside clinical, laboratory, and imaging data. The strongest correlations with severe outcomes and mortality were found for CD200R+CD3+ T and CD19+ B cells. Significant differences in PD-1+ and PD-L1+ lymphocyte subsets were observed between severity groups. Machine learning (SHAP) confirmed that ICM expression was at least as predictive as conventional risk factors. These findings suggest that markers of immune exhaustion, especially PD-1, PD-L1, and CD200R, may help predict COVID-19 severity. Further research is needed to determine whether targeting immune checkpoints could improve outcomes.

免疫失调是COVID-19恶化的关键因素。这项研究评估了免疫检查点分子（ICMs）作为疾病严重程度的标志物。在入院时对525名中度（n=464）和重度（n=61） COVID-19住院患者进行免疫分型，并结合临床、实验室和影像学数据进行分析。CD200R+CD3+ T和CD19+ B细胞与严重结局和死亡率的相关性最强。严重程度组间PD-1+和PD-L1+淋巴细胞亚群差异有统计学意义。机器学习（SHAP）证实，ICM表达至少与传统风险因素一样具有预测性。这些发现表明，免疫衰竭标志物，特别是PD-1、PD-L1和CD200R，可能有助于预测COVID-19的严重程度。需要进一步的研究来确定靶向免疫检查点是否可以改善结果。

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引用次数: 0

Establishing a system to identify correlations among immune system components for exploring alternative pathways for immune information transfer 建立一个系统来识别免疫系统成分之间的相关性，探索免疫信息传递的替代途径。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-09 DOI: 10.1016/j.imlet.2025.107085

Yaron Ilan

Introduction

The classic immune system information transfer occurs through direct cell-to-cell contact and the secretion of mediators. However, certain immune phenomena suggest alternative pathways exist between immune components that operate independently of these conventional mechanisms.

Methods

We used 24 male C57Bl/6 J mice, divided into six groups, to establish a system for testing alternative immune information transfer pathways. Two triggers—splenectomy and 24-hour fasting—were applied in various combinations. Splenocytes were prepared from operated mice and placed in sterile tubes within cages of different treatment groups. Ex vivo lymphocyte responses were measured using fluorescence-activated cell sorting (FACS) for cell epitope expression (CD4, CD8, CD25, Foxp3) and enzyme-linked immunosorbent assay (ELISA) for cytokine secretion (IFN-γ, TNF-α, IL-10, TGF-β).

Results

Significant changes were observed in CD25 and CD8+CD25 expression, as well as in IL-10 secretion, following the application of the triggers. The system exhibited inherent variability with trends toward altered immune responses in isolated splenocytes that had no direct contact with the trigger-exposed animals. Non-parametric analysis indicates a trend for these markers, even though there is significant variability within the groups..

Conclusions

The data suggest a system where correlations between immune components may occur through alternative pathways, indicating the possibility of non-conventional information transfer mechanisms in the immune system that require further investigation.

经典的免疫系统信息传递是通过细胞间的直接接触和介质的分泌来实现的。然而，某些免疫现象表明，在独立于这些常规机制的免疫成分之间存在替代途径。方法：选取24只雄性C57Bl/6J小鼠，分为6组，建立免疫信息传递替代途径检测系统。脾切除术和24小时禁食两种触发法以不同的组合应用。取手术后小鼠脾细胞，置于不同处理组笼内无菌管中。体外淋巴细胞反应采用荧光活化细胞分选（FACS）检测细胞表位表达（CD4、CD8、CD25、Foxp3），酶联免疫吸附法（ELISA）检测细胞因子分泌（IFN-γ、TNF-α、IL-10、TGF-β）。结果：应用触发剂后，CD25和CD8+CD25的表达以及IL-10的分泌发生了显著变化。该系统表现出固有的可变性，在与暴露于触发器的动物没有直接接触的分离脾细胞中，有改变免疫反应的趋势。非参数分析表明了这些标记物的趋势，尽管在组内存在显著的差异。结论：数据表明免疫成分之间的相关性可能通过其他途径发生，表明免疫系统中非传统信息传递机制的可能性需要进一步研究。

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引用次数: 0

Analysis of islet antigen-specific autoreactive T cells from Japanese patients with slowly progressive insulin-dependent diabetes mellitus 日本缓慢进展型胰岛素依赖型糖尿病患者胰岛抗原特异性自身反应性T细胞分析。

IF 2.8 4区医学 Q3 IMMUNOLOGY

Immunology letters

Pub Date : 2025-09-09 DOI: 10.1016/j.imlet.2025.107084

Noriyuki Kitagawa , Nobuko Kitagawa , Ayaka Kobayashi , Takuro Okamura , Masahide Hamaguchi , Michiaki Fukui

Pancreatic islet antigen-specific autoreactive T cells are involved in inflammation in slowly progressive insulin-dependent diabetes mellitus (SPIDDM). Pancreatic islet antigens, such as glutamic acid decarboxylase 65 (GAD), insulinoma-associated protein 2 (IA-2), and insulin, are associated with SPIDDM. However, the association between pancreatic islet antigen-specific T cells and SPIDDM incidence remains unclear.

We aimed to identify the characteristics of pancreatic islet antigen autoreactive T cells in Japanese patients with SPIDDM.

Peripheral blood mononuclear cells were obtained from Japanese patients with type 1 diabetes mellitus (T1DM) enrolled in our diabetic cohort study. An ex vivo cytokine assay using overlapping peptides of GAD, IA-2, and insulin was performed. The production of tumor necrosis factor-alpha (TNF-α) by CD4⁺ T cells and the fractions of TNF-α⁺ CD4⁺ T cell fractions were measured by fluorescence-activated cell sorting.

The %parent of TNF-α⁺ CD4⁺ T cells and the effector memory TNF-α⁺ CD4⁺ T cells increased after stimulation with overlapping GAD and IA-2 peptides. The response to overlapping peptides was varied among individual SPIDDM case. Response to overlapping peptides of GAD, IA-2, and insulin were observed in each group of T1DM.

Islet antigen-specific autoreactive TNF-α⁺ CD4⁺ T cells from Japanese patients with SPIDDM were activated by overlapping GAD and IA-2 peptides.

胰岛抗原特异性自身反应性T细胞参与缓慢进展型胰岛素依赖型糖尿病（SPIDDM）的炎症。胰岛抗原，如谷氨酸脱羧酶65 （GAD）、胰岛素瘤相关蛋白2 （IA-2）和胰岛素，与SPIDDM有关。然而，胰岛抗原特异性T细胞与SPIDDM发病率之间的关系尚不清楚。我们的目的是确定日本SPIDDM患者胰岛抗原自身反应性T细胞的特征。我们的糖尿病队列研究从日本1型糖尿病患者（T1DM）中获得外周血单个核细胞。使用GAD， IA-2和胰岛素的重叠肽进行体外细胞因子测定。采用荧光活化细胞分选法检测CD4 + T细胞产生肿瘤坏死因子α (TNF-α)和TNF-α + CD4 + T细胞组分。TNF-α + CD4 + T细胞和效应记忆TNF-α + CD4 + T细胞的%亲本在GAD和IA-2肽重叠刺激后增加。不同的SPIDDM病例对重叠肽的反应不同。观察各组T1DM患者对GAD、IA-2和胰岛素重叠肽的反应。来自日本SPIDDM患者的胰岛抗原特异性自反应性TNF-α + CD4+ T细胞被重叠的GAD和IA-2肽激活。

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