Scandinavian Journal of Immunology最新文献_第8页

Antibody responses to immunoevasion proteins BBK32 and OspE constitute part of the serological footprint in neuroborreliosis but are insufficient to prevent the disease 对免疫逃逸蛋白 BBK32 和 OspE 的抗体反应是神经源性疾病血清学足迹的一部分，但不足以预防该疾病

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2024-01-11 DOI: 10.1111/sji.13353

Vinaya Dulipati, Juha Kotimaa, Mikel Rezola, Mikko Kontiainen, Hanna Jarva, Dag Nyman, Seppo Meri

Lyme borreliosis, caused by Borrelia burgdorferi sensu lato, is the most common tickborne disease. Its neuronal form, neuroborreliosis, comprises 3 to 38% of borreliosis cases in Europe. Borrelia outer surface proteins and virulence factors, OspE and BBK32, have been previously reported to help cause infection by promoting attachment to human host epithelial cells and evading complement attack. We assessed the serological responses to BBK32 and OspE in 19 individuals diagnosed with neuroborreliosis to see whether antibodies that could both target the bacteria and neutralize the virulence mechanisms on the microbial surface emerge. Results evaluate levels of total protein, IgG and the chemokine CXCL13, a determinant for B-cell recruitment during neuroinflammation, in patients' cerebrospinal fluid samples. Antibody levels against BBK32 and OspE correlated with those against VlsE, a well-characterized diagnostic serological marker of the disease. A dual serological profile of the patients was observed. K-means clustering split the cohort into two discrete groups presenting distinct serological and CNS responses. One group contained young patients with low levels of anti-BBK32 and OspE antibodies. The other group showed stronger responses, possibly following prolonged infections or reinfections. Additionally, we assessed anti-ganglioside antibodies that could cause autoimmunity or complement dysregulation but observed that they did not correlate with neuroborreliosis in our patient cohort. The dual nature of antibody responses against the virulence factors BBK32 and OspE in neuroborreliosis patients may suggest the necessity of repeated exposures for efficient immune responses. Better protection could be achieved if the virulence factors were formulated into vaccines.

由常染色体包柔氏包虫病（Borrelia burgdorferi sensu lato）引起的莱姆包虫病是最常见的蜱媒疾病。在欧洲，神经型包虫病占包虫病病例的 3% 至 38%。据报道，包柔氏菌的外表面蛋白和致病因子 OspE 和 BBK32 能促进包柔氏菌附着在人类宿主上皮细胞上并逃避补体攻击，从而帮助引起感染。我们评估了 19 名确诊为神经源性疾病患者对 BBK32 和 OspE 的血清反应，以了解是否出现了既能针对细菌又能中和微生物表面毒力机制的抗体。结果评估了患者脑脊液样本中总蛋白、IgG 和趋化因子 CXCL13（神经炎症期间 B 细胞招募的决定因素）的水平。针对 BBK32 和 OspE 的抗体水平与针对 VlsE 的抗体水平相关，而 VlsE 是一种特征明确的疾病诊断血清学标志物。患者的血清学特征具有双重性。K-means 聚类方法将患者分为两组，分别表现出不同的血清学和中枢神经系统反应。一组是抗BBK32和OspE抗体水平较低的年轻患者。另一组则表现出较强的反应，可能是在长期感染或再次感染后出现的。此外，我们还评估了可能导致自身免疫或补体失调的抗神经节苷脂抗体，但发现在我们的患者队列中，这些抗体与神经源性疾病并不相关。神经源性疾病患者体内针对毒力因子 BBK32 和 OspE 的抗体反应具有双重性，这可能表明需要反复接触才能产生有效的免疫反应。如果将致病因子制成疫苗，就能获得更好的保护。

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引用次数: 0

Activation of neutrophils excels the therapeutic potential of Mycobacterium indicus pranii and heat-induced promastigotes against antimony-resistant Leishmania donovani infection 激活中性粒细胞可增强胰分枝杆菌和热诱导原核细胞对抗生素耐药的唐氏利什曼病感染的治疗潜力

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2024-01-08 DOI: 10.1111/sji.13350

Kamalika Roy, Sanhita Ghosh, Mintu Karan, Suman Karmakar, Supriya Nath, Bedanta Das, Sharmistha Paul, Pritam Mandal, Monalisa Ray, Mousumi Das, Soumyadip Mukherjee, Somaditya Dey, Chiranjib Pal

Repurposing drugs and adjuvants is an attractive choice of present therapy that reduces the substantial costs, chances of failure, and systemic toxicity. Mycobacterium indicus pranii was originally developed as a leprosy vaccine but later has been found effective against Leishmania donovani infection. To extend our earlier study, here we reported the immunotherapeutic modulation of the splenic and circulatory neutrophils in favour of hosts as neutrophils actually serve as the pro-parasitic portable shelter to extend the Leishmania infection specifically during the early entry into the hosts' circulation. We targeted to disrupt this early pro-parasitic incidence by the therapeutic combination of M. indicus pranii and heat-induced promastigotes against antimony-resistant L. donovani infection. The combination therapy induced the functional expansion of CD11b⁺Ly6C^intLy6G^hi neutrophils both in the post-infected spleen, and also in the circulation of post-treated animals followed by the immediate Leishmania infection. More importantly, the enhanced expression of MHC-II, phagocytic uptake of the parasites by the circulatory neutrophils as well as the oxidative burst were induced that limited the chances of the very early establishment of the infection. The enhanced expression of pro-inflammatory cytokines, like IL-1α and TNF-α indicated resistance to the parasite-mediated takeover of the neutrophils, as these cytokines are critical for the activation of T cell-mediated immunity and host-protective responses. Additionally, the induction of essential transcription factors and cytokines for early granulocytic lineage commitment suggests that the strategy not only contributed to the peripheral activation of the neutrophils but also promoted granulopoiesis in the bone marrow.

药物和佐剂的再利用是目前治疗的一种有吸引力的选择，它可以降低大量成本、失败几率和全身毒性。普拉尼分枝杆菌最初是作为麻风病疫苗开发的，但后来发现它对唐氏利什曼原虫感染有效。为了扩展我们之前的研究，我们在此报告了对脾脏和循环中性粒细胞的免疫治疗调节，以利于宿主，因为中性粒细胞实际上是亲寄生虫的便携式庇护所，特别是在早期进入宿主循环的过程中扩大利什曼病感染。我们的目标是通过将嗜中性粒细胞和热诱导原核细胞结合起来治疗抗锑抗性利什曼病感染，来破坏这种早期原寄生虫的发生。联合疗法诱导 CD11b+Ly6CintLy6Ghi 中性粒细胞在感染后的脾脏中以及在利什曼原虫感染后的动物血液循环中功能性扩增。更重要的是，MHC-II 表达的增强、循环中性粒细胞对寄生虫的吞噬摄取以及氧化猝灭的诱导限制了早期感染的机会。IL-1α和TNF-α等促炎细胞因子的表达增强，表明中性粒细胞对寄生虫介导的接管具有抵抗力，因为这些细胞因子对激活T细胞介导的免疫和宿主保护反应至关重要。此外，诱导早期粒细胞系形成所必需的转录因子和细胞因子表明，该策略不仅有助于中性粒细胞的外周活化，还能促进骨髓中的粒细胞生成。

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引用次数: 0

The inverse association between the apolipoprotein E ε4 allele and C-reactive protein levels is stronger in persons with obesity and diabetes. 在肥胖和糖尿病患者中，载脂蛋白Eε4等位基因与C反应蛋白水平之间的负相关更强。

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2024-01-01 Epub Date: 2023-08-23 DOI: 10.1111/sji.13323

Lasse Melvaer Giil, Silja Hanseth, Ognjen Bojovic, Jan Erik Nordrehaug, Per Magne Ueland, Klaus Meyer, Grethe S Tell

Background: C-reactive protein (CRP) is lower in patients who carry the apolipoprotein E epsilon 4 allele variant (APOEε4) of the APOE gene. This could however be explained by other factors observed in APOEε4 carriers, such as lower body mass index (BMI), possibly less diabetes and more use of statins, all associated with CRP concentrations.

Objectives: To assess the association between CRP and APOEε4 stratified by BMI, statin use and diabetes.

Methods: We included 2700 community-dwelling older adults from the Hordaland health study with genotyping of the APOE gene by a one-step polymerase chain reaction and CRP measured using immuno-MALDI-TOF MS. Differences in CRP concentrations by APOE (ε4 vs no ε4) were assessed using the Mann-Whitney U tests, also stratified by statin use, diabetes and BMI categories. Finally, we performed linear regression with log (CRP) as the outcome and APOEε4 together with statin use, diabetes, BMI and their respective interactions.

Results: CRP was higher in APOEε4 carriers irrespective of BMI, diabetes and statin use. In APOEε4 non-carriers, CRP was elevated with diabetes and obesity as expected. However, this was attenuated or even reversed in APOEε4 carriers. Such differences were not observed for statin use.

Conclusions: Statin use, obesity or diabetes did not confound the known association between the APOEε4 allele and lower CRP. Our data suggest that CRP is less responsive to inflammatory cues involved in diabetes and obesity in APOEε4 carriers. Epidemiological studies should take note of these relationships, as CRP, APOEε4, diabetes and obesity are both linked to neurodegenerative and cardiovascular disease.

背景：携带载脂蛋白Eε4等位基因变体（APOEε4）的患者的C反应蛋白（CRP）较低。然而，这可以通过在APOEε4携带者中观察到的其他因素来解释，如较低的体重指数（BMI）、可能较少的糖尿病和更多的他汀类药物使用，所有这些都与CRP浓度有关。目的：评估根据BMI、他汀类药物使用和糖尿病分层的CRP和APOEε4之间的相关性。方法：我们纳入了来自Hordaland健康研究的2700名居住在社区的老年人，他们通过一步聚合酶链式反应对APOE基因进行基因分型，并使用免疫MALDI TOF MS测量CRP。使用Mann-Whitney U测试评估APOE的CRP浓度差异（ε4与否ε4），并按他汀类药物使用、糖尿病和BMI类别进行分层。最后，我们以log（CRP）为结果，APOEε4与他汀类药物的使用、糖尿病、BMI及其各自的相互作用进行了线性回归。结果：无论BMI、糖尿病和他汀类药物的使用情况如何，APOEε4携带者的CRP均较高。在APOEε4非携带者中，CRP如预期的那样随着糖尿病和肥胖而升高。然而，这在APOEε4载体中被减弱甚至逆转。他汀类药物的使用没有观察到这种差异。结论：他汀类药物的使用、肥胖或糖尿病并没有混淆APOEε4等位基因与低CRP之间的已知关联。我们的数据表明，在APOEε4携带者中，CRP对糖尿病和肥胖相关的炎症提示反应较弱。流行病学研究应该注意这些关系，因为CRP、APOEε4、糖尿病和肥胖都与神经退行性疾病和心血管疾病有关。

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引用次数: 0

MASP-2 deficiency does not prevent the progression of diabetic kidney disease in a mouse model of type 1 diabetes 在 1 型糖尿病小鼠模型中，MASP-2 缺乏不能阻止糖尿病肾病的进展

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-25 DOI: 10.1111/sji.13348

Holt Charlotte Brinck, Halkjær Lene, Dudler Tom, Schwaeble Wilhelm, Hansen Troels Krarup, Thiel Steffen, Østergaard Jakob Appel

Mannan-binding lectin (MBL) initiates the lectin pathway of complement and has been linked to albuminuria and mortality in diabetes. We hypothesize that MBL-associated serine protease 2 (MASP-2) deficiency will protect against diabetes-induced kidney damage. Male C57BL/6J MASP-2 knockout (Masp2^−/−) mice and wildtype (WT) mice were divided into a diabetic group and a non-diabetic group. Renal hypertrophy, albumin excretion, mesangial area and specific mRNA expressions in the renal cortex were measured after 8 and 12 weeks of diabetes. By two-way ANOVA it was tested if MASP-2 modulated the renal effects of diabetes, that is interaction. After 12 weeks of diabetes Masp2^−/− diabetic mice had a smaller mesangium at 21.1% of the glomerular area (95% CI 19.7, 22.6) compared with WT diabetic mice, 25.2% (23.2, 27.2), p(interaction) = 0.001. After 8 weeks of diabetes, plasma cystatin C was 261.5 ng/mL (229.6, 297.8) in the WT diabetic group compared to 459.9 ng/mL (385.7, 548.3) in non-diabetic WT mice, p < 0.001. By contrast, no difference in plasma cystatin C levels was found between the Masp2^−/− diabetic mice, 288.2 ng/mL (260.6, 318.6) and Masp2^−/− non-diabetic mice, 293.5 ng/mL (221.0, 389.7), p = 0.86 and p(interaction) = 0.001. We demonstrated a protective effect of MASP-2 deficiency on mesangial hypertrophy after 12 weeks of diabetes and an effect on plasma cystatin C level. MASP-2 deficiency did, however, fail to protect against diabetic-induced alterations of kidney weight, albuminuria and renal mRNA expression of fibrotic- and oxidative stress markers.

甘露结合凝集素（MBL）启动了补体的凝集素途径，并与糖尿病患者的白蛋白尿和死亡率有关。我们假设，MBL相关丝氨酸蛋白酶2（MASP-2）的缺乏将防止糖尿病引起的肾脏损伤。雄性 C57BL/6J MASP-2 基因敲除（Masp2-/-）小鼠和野生型（WT）小鼠被分为糖尿病组和非糖尿病组。分别在小鼠患糖尿病 8 周和 12 周后测量其肾脏肥大程度、白蛋白排泄量、肾间质面积和肾皮质中特异性 mRNA 的表达。通过双向方差分析检验了 MASP-2 是否调节了糖尿病对肾脏的影响，即相互作用。糖尿病12周后，Masp2-/-糖尿病小鼠肾小球系膜占肾小球面积的21.1%（95% CI 19.7, 22.6），而WT糖尿病小鼠系膜占肾小球面积的25.2%（23.2, 27.2），p（交互作用）= 0.001。糖尿病 8 周后，WT 糖尿病组的血浆胱抑素 C 为 261.5 纳克/毫升（229.6，297.8），而非糖尿病 WT 小鼠为 459.9 纳克/毫升（385.7，548.3），p < 0.001。相比之下，Masp2-/-糖尿病小鼠288.2纳克/毫升（260.6，318.6）和Masp2-/-非糖尿病小鼠293.5纳克/毫升（221.0，389.7）的血浆胱抑素C水平没有差异，p = 0.86，p（交互作用）= 0.001。我们证明了 MASP-2 缺乏对糖尿病 12 周后系膜肥厚的保护作用，以及对血浆胱抑素 C 水平的影响。然而，MASP-2的缺乏并不能防止糖尿病引起的肾脏重量、白蛋白尿以及肾脏纤维化和氧化应激标志物mRNA表达的改变。

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引用次数: 0

From hepatitis B virus infection to acute-on-chronic liver failure: The dynamic role of hepatic macrophages 从乙型肝炎病毒感染到急性-慢性肝衰竭：肝巨噬细胞的动态作用

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-19 DOI: 10.1111/sji.13349

Yu Zhang, Dongsheng Wu, Xiaoling Tian, Bin Chen

Acute-on-chronic liver failure (ACLF) is a progressive disease that is associated with rapid worsening of clinical symptoms and high mortality. A multicentre prospective study from China demonstrated that patients with hepatitis B virus-related ACLF (HBV-ACLF) exhibited worse clinical characteristics and higher mortality rates compared to non-HBV-ACLF patients. Immune dysregulation is closely linked to the potential mechanisms of initiation and progression of ACLF. Innate immune response, which is represented by monocytes/macrophages, is up-regulated across ACLF development. This suggests that monocytes/macrophages play an essential role in maintaining the immune homeostasis of ACLF. Information that has been published in recent years shows that the immune status and function of monocytes/macrophages vary in ACLF precipitated by different chronic liver diseases. Monocytes/macrophages have an immune activation effect in hepatitis B-precipitated-ACLF, but they exhibit an immune suppression in cirrhosis-precipitated-ACLF. Therefore, this review aims to explain whether this difference affects the clinical outcome in HBV-ACLF patients as well as the mechanisms involved. We summarize the novel findings that highlight the dynamic polarization phenotype and functional status of hepatic macrophages from the stage of HBV infection to ACLF development. Moreover, we discuss how different HBV-related liver disease tissue microenvironments affect the phenotype and function of hepatic macrophages. In summary, increasing developments in understanding the differences in immune phenotype and functional status of hepatic macrophages in ACLF patients will provide new perspectives towards the effective restoration of ACLF immune homeostasis.

急性慢性肝衰竭（ACLF）是一种进展性疾病，与临床症状迅速恶化和高死亡率有关。中国的一项多中心前瞻性研究表明，与非乙型肝炎病毒相关的急性-慢性肝衰竭（HBV-ACLF）患者相比，乙型肝炎病毒相关的急性-慢性肝衰竭（HBV-ACLF）患者的临床特征更差，死亡率更高。免疫失调与 ACLF 的潜在发病和进展机制密切相关。以单核细胞/巨噬细胞为代表的先天性免疫反应在 ACLF 发展过程中上调。这表明，单核细胞/巨噬细胞在维持 ACLF 的免疫平衡方面发挥着重要作用。近年来发表的资料显示，在不同慢性肝病引发的 ACLF 中，单核细胞/巨噬细胞的免疫状态和功能各不相同。单核细胞/巨噬细胞在乙型肝炎诱发的 ACLF 中具有免疫激活作用，但在肝硬化诱发的 ACLF 中却表现出免疫抑制作用。因此，本综述旨在解释这种差异是否会影响 HBV-ACLF 患者的临床预后以及相关机制。我们总结了一些新发现，这些发现强调了肝巨噬细胞从 HBV 感染阶段到 ACLF 发展过程中的动态极化表型和功能状态。此外，我们还讨论了不同的 HBV 相关肝病组织微环境如何影响肝巨噬细胞的表型和功能。总之，对 ACLF 患者肝巨噬细胞免疫表型和功能状态差异的认识不断加深，将为有效恢复 ACLF 免疫平衡提供新的视角。

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引用次数: 0

Chlamydia pathogenesis in mice: Male immunity and the outcome of female infection 小鼠衣原体致病机理：雄性免疫力与雌性感染的结果

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-15 DOI: 10.1111/sji.13347

P. Höglund

引用次数: 0

Unveiling the intricacies of COVID-19: Autoimmunity, multi-organ manifestations and the role of autoantibodies 揭开 COVID-19 的神秘面纱：自身免疫、多器官表现和自身抗体的作用

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-10 DOI: 10.1111/sji.13344

Zetao Ding, Xingyi Wei, Haoyu Pan, Hui Shi, Yue Shi

COVID-19 is a severe infectious disease caused by a SARS-CoV-2 infection. It has caused a global pandemic and can lead to acute respiratory distress syndrome (ARDS). Beyond the respiratory system, the disease manifests in multiple organs, producing a spectrum of clinical symptoms. A pivotal factor in the disease's progression is autoimmunity, which intensifies its severity and contributes to multi-organ injuries. The intricate interaction between the virus' spike protein and human proteins may engender the generation of autoreactive antibodies through molecular mimicry. This can further convolute the immune response, with the potential to escalate into overt autoimmunity. There is also emerging evidence to suggest that COVID-19 vaccinations might elicit analogous autoimmune responses. Advanced technologies have pinpointed self-reactive antibodies that target diverse organs or immune-modulatory proteins. The interplay between autoantibody levels and multi-organ manifestations underscores the importance of regular monitoring of serum antibodies and proinflammatory markers. A combination of immunosuppressive treatments and antiviral therapy is crucial for managing COVID-19-associated autoimmune diseases. The review will focus on the generation of autoantibodies in the context of COVID-19 and their impact on organ health.

COVID-19 是一种由 SARS-CoV-2 感染引起的严重传染病。它已在全球范围内引起大流行，并可导致急性呼吸窘迫综合征（ARDS）。除呼吸系统外，该疾病还表现为多个器官，产生一系列临床症状。自身免疫是疾病发展的一个关键因素，它加剧了疾病的严重性，并导致多器官损伤。病毒的尖峰蛋白与人类蛋白质之间错综复杂的相互作用可能会通过分子模拟产生自体反应性抗体。这可能会进一步干扰免疫反应，并有可能升级为明显的自身免疫。还有新的证据表明，接种 COVID-19 疫苗可能会引起类似的自身免疫反应。先进的技术已经确定了针对不同器官或免疫调节蛋白的自身反应性抗体。自身抗体水平与多器官表现之间的相互作用强调了定期监测血清抗体和促炎标志物的重要性。免疫抑制治疗和抗病毒治疗相结合对于控制 COVID-19 相关自身免疫性疾病至关重要。本综述将重点讨论 COVID-19 引起的自身抗体的产生及其对器官健康的影响。

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引用次数: 0

Gut bacteria at 6 months of age are associated with immune cell status in 1-year-old children 6 个月大时的肠道细菌与 1 岁儿童的免疫细胞状况有关

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-07 DOI: 10.1111/sji.13346

Morten Nilsen, Unni Cecilie Nygaard, Petter Brodin, Karin Cecilie Lødrup Carlsen, Cecilie Fredheim, Guttorm Haugen, Gunilla Hedlin, Christine Monceyron Jonassen, Unni Lise Albertsdottir Jonsmoen, Tadepally Lakshmikanth, Björn Nordlund, Axel Olin, Eva Maria Rehbinder, Håvard O. Skjerven, Lars Snipen, Anne Cathrine Staff, Cilla Söderhäll, Riyas Vettukattil, Knut Rudi

Age-related gut bacterial changes during infancy have been widely studied, but it remains still unknown how these changes are associated with immune cell composition. This study's aim was to explore if the temporal development of gut bacteria during infancy prospectively affects immune cell composition. Faecal bacteria and short-chain fatty acids were analysed from 67 PreventADALL study participants at four timepoints (birth to 12 months) using reduced metagenome sequencing and gas chromatography. Immune cell frequencies were assessed using mass cytometry in whole blood samples at 12 months. The infants clustered into four groups based on immune cell composition: clusters 1 and 2 showed a high relative abundance of naïve cells, cluster 3 exhibited increased abundance of classical- and non-classical monocytes and clusters 3 and 4 had elevated neutrophil levels. At all age groups, we did observe significant associations between the gut microbiota and immune cell clusters; however, these were generally from low abundant species. Only at 6 months of age we observed significant associations between abundant (>8%) species and immune cell clusters. Bifidobacterium adolescentis and Porphyromonadaceae are associated with cluster 1, while Bacteroides fragilis and Bifidobacterium longum are associated with clusters 3 and 4 respectively. These species have been linked to T-cell polarization and maturation. No significant correlations were found between short-chain fatty acids and immune cell composition. Our findings suggest that abundant gut bacteria at 6 months may influence immune cell frequencies at 12 months, highlighting the potential role of gut microbiota in shaping later immune cell composition.

婴儿时期与年龄相关的肠道细菌变化已被广泛研究，但这些变化与免疫细胞组成之间的关系仍是未知数。本研究旨在探讨婴儿期肠道细菌的时间性发展是否会对免疫细胞的组成产生前瞻性影响。研究人员使用还原元基因组测序和气相色谱法分析了 67 名 PreventADALL 研究参与者在四个时间点（出生至 12 个月）的粪便细菌和短链脂肪酸。在 12 个月大时，使用质谱仪对全血样本中的免疫细胞频率进行了评估。根据免疫细胞的组成，婴儿被分为四组：第 1 组和第 2 组的幼稚细胞相对较多，第 3 组的经典和非经典单核细胞较多，第 3 组和第 4 组的中性粒细胞水平较高。在所有年龄组中，我们都观察到了肠道微生物群与免疫细胞群之间的显著关联；然而，这些关联通常来自低丰度物种。只有在 6 个月大时，我们才观察到丰富物种（>8%）与免疫细胞群之间的显著关联。青春期双歧杆菌（Bifidobacterium adolescentis）和卟啉单胞菌（Porphyromonadaceae）与第1群相关，而脆弱双歧杆菌（Bacteroides fragilis）和长双歧杆菌（Bifidobacterium longum）则分别与第3群和第4群相关。这些物种与 T 细胞极化和成熟有关。在短链脂肪酸和免疫细胞组成之间没有发现明显的相关性。我们的研究结果表明，6 个月时丰富的肠道细菌可能会影响 12 个月时的免疫细胞频率，这凸显了肠道微生物群在塑造日后免疫细胞组成方面的潜在作用。

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引用次数: 0

To be remembered: B cell memory response against SARS-CoV-2 and its variants in vaccinated and unvaccinated individuals 值得纪念：接种疫苗和未接种疫苗者体内针对 SARS-CoV-2 及其变种的 B 细胞记忆反应

IF 3.7 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-06 DOI: 10.1111/sji.13345

Nafees Ahmed, Atharv Athavale, Ankita H. Tripathi, Adarsh Subramaniam, Santosh K. Upadhyay, Anil Kumar Pandey, Ramesh Chandra Rai, Amit Awasthi

COVID-19 disease has plagued the world economy and affected the overall well-being and life of most of the people. Natural infection as well as vaccination leads to the development of an immune response against the pathogen. This involves the production of antibodies, which can neutralize the virus during future challenges. In addition, the development of cellular immune memory with memory B and T cells provides long-lasting protection. The longevity of the immune response has been a subject of intensive research in this field. The extent of immunity conferred by different forms of vaccination or natural infections remained debatable for long. Hence, understanding the effectiveness of these responses among different groups of people can assist government organizations in making informed policy decisions. In this article, based on the publicly available data, we have reviewed the memory response generated by some of the vaccines against SARS-CoV-2 and its variants, particularly B cell memory in different groups of individuals.

COVID-19 疾病困扰着世界经济，影响着大多数人的整体福祉和生活。自然感染和接种疫苗会导致对病原体产生免疫反应。这包括产生抗体，在未来的挑战中能够中和病毒。此外，记忆性 B 细胞和 T 细胞形成的细胞免疫记忆可提供持久的保护。免疫反应的持久性一直是这一领域深入研究的课题。长期以来，人们对不同形式的疫苗接种或自然感染所产生的免疫程度一直存在争议。因此，了解这些反应在不同人群中的有效性有助于政府组织做出明智的政策决定。在本文中，我们根据可公开获得的数据，回顾了一些针对 SARS-CoV-2 及其变种的疫苗所产生的记忆反应，特别是不同人群的 B 细胞记忆。

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引用次数: 0

Sphingosine 1-phosphate combining with S1PR4 promotes regulatory T cell differentiation related to FAO through Nrf2/PPARα. 鞘氨醇1-磷酸与S1PR4联合通过Nrf2/PPARα促进与FAO相关的调节性T细胞分化

IF 4.1 4区医学 Q2 IMMUNOLOGY

Scandinavian Journal of Immunology

Pub Date : 2023-12-01 Epub Date: 2023-08-29 DOI: 10.1111/sji.13322

Rui Feng, Chuang Liu, Zilin Cui, Zirong Liu, Yamin Zhang

Metabolism and metabolic processes have long been considered to shape the tumour immunosuppressive microenvironment. Recent research has demonstrated that T regulatory cells (Tregs) display high rates of fatty acid oxidation (FAO) and a relatively low rate of glycolysis. Sphingosine 1-phosphate (S1P), which is a G protein signalling activator involved in immune regulation and FAO modulation, has been implicated in Treg differentiation. However, the precise relation between Treg differentiation and S1P remains unclear. In this study, we isolated naïve CD4⁺ T cells from the spleens of 6-8-week-old BALB/c mice using magnetic bead sorting, which was used in our study for Treg differentiation. S1P stimulation was performed during Treg differentiation. We examined the oxygen consumption and palmitic acid metabolism of the differentiated Tregs and evaluated the expression levels of various proteins, including Nrf2, CPT1A, Glut1, ACC1 and PPARα, through Western blotting. Our results demonstrate that S1P promotes Treg differentiation and enhances FAO, and that the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and peroxisome proliferator-activated receptor α (PPARα) is upregulated. Furthermore, Nrf2 or PPARα knockdown dampened the Treg differentiation and FAO that were promoted by S1P, confirming that S1P can bind with S1PR4 to promote Treg differentiation through the Nrf2/PPARα signalling pathway, which may be related to FAO facilitation.

长期以来，代谢和代谢过程一直被认为是形成肿瘤免疫抑制微环境的因素。最近的研究表明，T调节细胞（Tregs）显示出高的脂肪酸氧化率（FAO）和相对较低的糖酵解率。鞘氨醇1-磷酸（S1P）是一种参与免疫调节和FAO调节的G蛋白信号激活剂，与Treg分化有关。然而，Treg分化与S1P之间的确切关系尚不清楚。在这项研究中，我们使用磁珠分选从6-8周龄BALB/c小鼠的脾脏中分离出幼稚的CD4+T细胞，该分选用于我们的Treg分化研究。在Treg分化过程中进行S1P刺激。我们检测了分化的Tregs的耗氧量和棕榈酸代谢，并通过蛋白质印迹评估了各种蛋白质的表达水平，包括Nrf2、CPT1A、Glut1、ACC1和PPARα。我们的研究结果表明，S1P促进Treg分化并增强FAO，核因子（红系衍生2）样2（Nrf2）和过氧化物酶体增殖物激活受体α（PPARα）的表达上调。此外，Nrf2或PPARα敲低抑制了S1P促进的Treg分化和FAO，证实S1P可以通过Nrf2/PPARα信号通路与S1PR4结合促进Treg分化，这可能与FAO的促进有关。

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引用次数: 0