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LGR4 Deficiency Aggravates Skin Inflammation and Epidermal Hyperplasia in Imiquimod-Induced Psoriasis. LGR4 缺乏会加重咪喹莫特诱导的银屑病的皮肤炎症和表皮增生。
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-20 DOI: 10.1111/imm.13873
Mengfei Xue, Ruijie Yang, Guihong Li, Zhizhan Ni, Yuqing Chao, Kairui Shen, Hua Ren, Bing Du, Juliang Qin, Zhenliang Sun

Psoriasis is a chronic inflammatory skin disease characterised by inflammatory cell infiltration, keratinocyte hyperproliferation and increased neovascularization. Despite extensive research, the precise mechanisms underlying psoriasis pathology and treatment strategies remain unclear because of a complex aetiology and disease progression. Hence, in this study, we aimed to identify potential therapeutic targets for psoriasis and explore their effects on disease progression. We observed that G protein-coupled receptor LGR4 attenuates psoriasis progression. Bioinformatics analysis of publicly available clinical data revealed lower LGR4 expression in the skin lesions of patients with psoriasis than in their non-lesioned skin. Both in vitro (HaCaT cell) and in vivo (mouse) models confirmed this phenomenon. The Lgr4-knockout mouse model further confirmed that LGR4 plays a positive role in psoriasis progression. Specifically, Lgr4 knockout promoted the secretion of inflammatory factors, accumulation of local immunocyte infiltration in skin lesions, and keratinocyte proliferation. In conclusion, we demonstrated that LGR4 is critical to limiting psoriasis progression, suggesting that it is a viable target for the clinical management of this skin condition.

银屑病是一种慢性炎症性皮肤病,以炎症细胞浸润、角质细胞过度增殖和新生血管增多为特征。尽管进行了大量研究,但由于病因和疾病进展复杂,银屑病病理和治疗策略的确切机制仍不清楚。因此,在本研究中,我们旨在确定银屑病的潜在治疗靶点,并探讨它们对疾病进展的影响。我们观察到,G 蛋白偶联受体 LGR4 可减轻银屑病的进展。对公开临床数据进行的生物信息学分析表明,银屑病患者皮损中的 LGR4 表达量低于非皮损皮肤。体外(HaCaT 细胞)和体内(小鼠)模型都证实了这一现象。Lgr4基因敲除小鼠模型进一步证实,LGR4在银屑病的发展过程中起着积极作用。具体而言,Lgr4 基因敲除促进了炎症因子的分泌、皮损局部免疫细胞浸润的积累以及角质细胞的增殖。总之,我们证明了 LGR4 对限制银屑病的发展至关重要,这表明它是临床治疗这种皮肤病的一个可行靶点。
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引用次数: 0
SNX17 Regulates Antigen Internalisation and Phagosomal Maturation by Dendritic Cells. SNX17 调控树突状细胞的抗原内化和吞噬体成熟
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-19 DOI: 10.1111/imm.13878
Sofía Dinamarca, Cristina Croce, Anna Salvioni, Facundo Garrido, Sandra Estrada Fidalgo, Gonzalo Bigliani, Luis S Mayorga, Nicolas Blanchard, Ignacio Cebrian

Antigen cross-presentation is the process whereby small peptides derived from exogenous antigens are attached to MHC-I molecules triggering CD8+ T lymphocyte activation. The endocytic route of dendritic cells (DCs) is highly specialised for cross-presentation to initiate cytotoxic immune responses against numerous intracellular pathogens and tumours. In this study, we identify the endosomal protein sorting nexin (SNX) 17 as a key regulator of antigen internalisation and cross-presentation by DCs. SNX17 expression in DCs guarantees optimal cross-presentation of soluble, particulate, and Toxoplasma gondii-associated antigens. The silencing of SNX17 expression in DCs significantly affected the internalisation of exogenous antigens by fluid-phase endocytosis, phagocytosis, and more strikingly, T. gondii invasion. We show that SNX17 controls proper integrin recycling, actin cytoskeleton organisation, and phagosomal maturation. Altogether, our findings provide compelling evidence that SNX17 plays a central role in the modulation of the DC endocytic network, which is essential for competent antigen cross-presentation.

抗原交叉呈递是指来自外源性抗原的小肽附着在 MHC-I 分子上引发 CD8+ T 淋巴细胞活化的过程。树突状细胞(DCs)的内吞途径高度专业化,用于交叉呈递,启动针对多种细胞内病原体和肿瘤的细胞毒性免疫反应。在这项研究中,我们发现内泌体蛋白分选蛋白(SNX)17 是 DCs 抗原内化和交叉呈递的关键调节因子。SNX17在DC中的表达保证了可溶性、颗粒状和弓形虫相关抗原的最佳交叉呈递。抑制 SNX17 在直流细胞中的表达会显著影响外源抗原通过液相内吞、吞噬作用的内化,更显著的是会影响弓形虫的入侵。我们的研究表明,SNX17 控制着整合素的正常循环、肌动蛋白细胞骨架的组织以及吞噬体的成熟。总之,我们的研究结果提供了令人信服的证据,证明 SNX17 在调节 DC 内细胞网络中发挥着核心作用,而 DC 内细胞网络对有效的抗原交叉呈递至关重要。
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引用次数: 0
Metabolic Regulation of Inflammation: Exploring the Potential Benefits of Itaconate in Autoimmune Disorders. 炎症的代谢调节:探索伊塔康酸对自身免疫性疾病的潜在益处
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-11-14 DOI: 10.1111/imm.13875
Yin Luo, Li-Yan Jiang, Zhe-Zhen Liao, Yuan-Yuan Wang, Ya-Di Wang, Xin-Hua Xiao

Itaconic acid and its metabolites have demonstrated significant therapeutic potential in various immune diseases. Originating from the tricarboxylic acid cycle in immune cells, itaconic acid can modulate immune responses, diminish inflammation, and combat oxidative stress. Recent research has uncovered multiple mechanisms through which itaconic acid exerts its effects, including the inhibition of inflammatory cytokine production, activation of anti-inflammatory pathways, and modulation of immune cell function by regulating cellular metabolism. Cellular actions are influenced by the modulation of metabolic pathways, such as inhibiting succinate dehydrogenase (SDH) activity or glycolysis, activation of nuclear-factor-E2-related factor 2 (Nrf2), boosting cellular defences against oxidative stress, and suppression of immune cell inflammation through the NF-κB pathway. This comprehensive review discusses the initiation, progression, and mechanisms of action of itaconic acid and its metabolites, highlighting their modulatory effects on various immune cell types. Additionally, it examines their involvement in immune disease like rheumatoid arthritis, multiple sclerosis, type 1 diabetes mellitus, and autoimmune hepatitis, offering greater understanding for creating new therapies for these ailments.

衣康酸及其代谢物在治疗各种免疫疾病方面具有显著的潜力。衣康酸来源于免疫细胞中的三羧酸循环,它可以调节免疫反应、减轻炎症反应并对抗氧化应激。最近的研究发现了衣康酸发挥作用的多种机制,包括抑制炎症细胞因子的产生、激活抗炎途径以及通过调节细胞新陈代谢来调节免疫细胞的功能。细胞作用受代谢途径调节的影响,如抑制琥珀酸脱氢酶(SDH)活性或糖酵解、激活核因子-E2 相关因子 2(Nrf2)、增强细胞对氧化应激的防御能力,以及通过 NF-κB 途径抑制免疫细胞炎症。这篇综合性综述讨论了衣康酸及其代谢物的起始、发展和作用机制,强调了它们对各种免疫细胞类型的调节作用。此外,还探讨了它们在类风湿性关节炎、多发性硬化症、1 型糖尿病和自身免疫性肝炎等免疫性疾病中的参与作用,为开发治疗这些疾病的新疗法提供了更深入的理解。
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引用次数: 0
Coexistence of IL12Rβ1 and BTK Mutations in a Family. 一个家族中同时存在 IL12Rβ1 和 BTK 基因突变
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-30 DOI: 10.1111/imm.13874
Hulya Kose, Orhan Gorukmez, Sara Sebnem Kilic
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引用次数: 0
Metabolic Reprogramming in Cancer: Implications for Immunosuppressive Microenvironment. 癌症中的代谢重编程:对免疫抑制微环境的影响
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-27 DOI: 10.1111/imm.13871
Durre Aden, Niti Sureka, Samreen Zaheer, Jai Kumar Chaurasia, Sufian Zaheer

Cancer is a complex and heterogeneous disease characterised by uncontrolled cell growth and proliferation. One hallmark of cancer cells is their ability to undergo metabolic reprogramming, which allows them to sustain their rapid growth and survival. This metabolic reprogramming creates an immunosuppressive microenvironment that facilitates tumour progression and evasion of the immune system. In this article, we review the mechanisms underlying metabolic reprogramming in cancer cells and discuss how these metabolic alterations contribute to the establishment of an immunosuppressive microenvironment. We also explore potential therapeutic strategies targeting metabolic vulnerabilities in cancer cells to enhance immune-mediated anti-tumour responses. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT02044861, NCT03163667, NCT04265534, NCT02071927, NCT02903914, NCT03314935, NCT03361228, NCT03048500, NCT03311308, NCT03800602, NCT04414540, NCT02771626, NCT03994744, NCT03229278, NCT04899921.

癌症是一种复杂的异质性疾病,其特点是细胞不受控制地生长和增殖。癌细胞的特征之一是能够进行新陈代谢重编程,这使它们能够维持快速生长和存活。这种代谢重编程创造了一种免疫抑制微环境,有利于肿瘤的发展和免疫系统的规避。在本文中,我们回顾了癌细胞代谢重编程的内在机制,并讨论了这些代谢改变如何有助于建立免疫抑制微环境。我们还探讨了针对癌细胞代谢脆弱性的潜在治疗策略,以增强免疫介导的抗肿瘤反应。试验注册:ClinicalTrials.gov identifier:NCT02044861、NCT03163667、NCT04265534、NCT02071927、NCT02903914、NCT03314935、NCT03361228、NCT03048500、NCT03311308、NCT03800602、NCT04414540、NCT02771626、NCT03994744、NCT03229278、NCT04899921。
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引用次数: 0
Sphingosine-1-Phosphate Signalling Inhibition Suppresses Th1-Like Treg Generation by Reversing Mitochondrial Uncoupling. 鞘氨醇-1-磷酸信号抑制通过逆转线粒体解偶联抑制 Th1 类 Treg 的生成
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-24 DOI: 10.1111/imm.13870
Rachel Coulombeau, Claudia Selck, Nicolas Giang, Abdulrahman Al-Mohammad, Natalie Ng, Allison K Maher, Rafael Argüello, Antonio Scalfari, James Varley, Richard Nicholas, Margarita Dominguez-Villar

Inflammatory environments induce the generation of dysfunctional IFNγ+T-bet+FOXP3+ Th1-like Tregs, which show defective function and are found in autoimmune conditions including multiple sclerosis (MS). The pathways that control the generation of Th1-like Tregs are not well understood. Sphingosine-1-phosphate (S1P) signalling molecules are upregulated in Th1-like Tregs, and in vivo S1P inhibition with Fingolimod (FTY720) inhibits the expression of genes responsible for Treg plasticity in MS patients. However, the underlying mechanisms are unknown. Here we show that S1P signalling inhibition by FTY720 inhibits the generation of Th1-like Tregs and rescues their suppressive function. These effects are mediated by a decrease in mTORC1 signalling and reversal of the mitochondrial uncoupling that Tregs undergo during their reprogramming into Th1-like Tregs in vitro. Finally, these results are validated in in vivo-generated Th1-like Tregs, as Tregs from MS patients treated with FTY720 display decreased Th1-like Treg frequency, increased suppressive function and mitochondrial metabolism rebalance. These results highlight the involvement of mitochondrial uncoupling in Treg reprogramming and identify S1P signalling inhibition as a target to suppress the generation of dysfunctional Th1-like Tregs.

炎症环境会诱导产生功能失调的 IFNγ+T-bet+FOXP3+ Th1 样 Tregs,这些 Tregs 显示出功能缺陷,并出现在包括多发性硬化症(MS)在内的自身免疫性疾病中。控制 Th1 样 Tregs 生成的途径尚不十分清楚。在 Th1 样 Tregs 中,Sphingosine-1-phosphate(S1P)信号分子上调,用 Fingolimod(FTY720)抑制体内 S1P 可抑制多发性硬化症患者中负责 Treg 可塑性的基因的表达。然而,其潜在机制尚不清楚。在这里,我们展示了通过 FTY720 抑制 S1P 信号可抑制 Th1 样 Tregs 的生成并挽救其抑制功能。这些效应是通过减少 mTORC1 信号传导和逆转线粒体解偶联介导的,Tregs 在体外重编程为 Th1 样 Tregs 的过程中经历了线粒体解偶联。最后,这些结果在体内生成的 Th1 样 Tregs 中得到了验证,因为接受 FTY720 治疗的多发性硬化症患者的 Tregs 显示 Th1 样 Treg 频率降低、抑制功能增强和线粒体代谢恢复平衡。这些结果突显了线粒体解偶联在 Treg 重编程中的参与作用,并确定 S1P 信号抑制是抑制 Th1-like Tregs 功能障碍生成的一个靶点。
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引用次数: 0
RGS10 Deficiency Alleviated Intestinal Mucosal Inflammation Through Suppression of Th1/Th17 Cell Immune Responses in Ulcerative Colitis. RGS10 缺陷通过抑制溃疡性结肠炎患者的 Th1/Th17 细胞免疫反应缓解肠粘膜炎症
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-20 DOI: 10.1111/imm.13869
Yonghong Yang, Yiming Shao, Xizhuang Gao, Zongjing Hu, Yan Wang, Cuimei Ma, Guiyuan Jin, Fengqin Zhu, Guanjun Dong, Guangxi Zhou

Regulator of G-protein signalling (RGS) 10 plays critical roles in several immune related diseases. However, whether RGS10 is involved in colonic inflammation of ulcerative colitis (UC) is still obscure. This study aimed to investigate the role of RGS10 in UC. In this study, RGS10 expression was examined by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, immunohistochemistry, and immunofluorescent analysis. Single-cell RNA sequencing of intestinal mucosa was performed to identify key immune cells with differentially expressed RGS10. RGS10 knockout mice were generated and established dextran sulphate sodium (DSS)-induced colitis. Expression of inflammatory cytokines on mRNA and protein levels was detected by qRT-PCR, enzyme-linked immunosorbent assay, and flow cytometry. We found that RGS10 expression was significantly elevated in UC patients, especially in CD4+ T cells, compared with healthy subjects. Intriguingly, RGS10 deficiency markedly alleviated DSS-induced colitis and decreased the proportion of Th1 and Th17 cells in lamina propria mononuclear cells (LPMCs), peripheral blood (PB), spleens, and mesenteric lymph nodes (mLNs). Mechanistically, RGS10 deficiency blocked the differentiation of Th1 and Th17 cells by inhibiting the phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT3. The co-immunoprecipitation analysis further showed that RGS10 could interact with protein tyrosine phosphatase non-receptor type 2 (PTPN2), and further regulated Th1 and Th17 cells differentiation of CD4+ T cells. In conclusion, RGS10 deficiency alleviated intestinal mucosal inflammation through inhibition of Th1/Th17 cell-mediated immune responses via interaction with PTPN2 in CD4+ T cells. Therefore, targeting RGS10 may represent a novel therapeutic approach for UC treatment.

G 蛋白信号调节器(RGS)10 在多种免疫相关疾病中发挥着关键作用。然而,RGS10是否参与了溃疡性结肠炎(UC)的结肠炎症仍不清楚。本研究旨在探讨 RGS10 在 UC 中的作用。本研究通过实时定量聚合酶链式反应(qRT-PCR)、免疫印迹、免疫组织化学和免疫荧光分析检测了RGS10的表达。对肠粘膜进行了单细胞 RNA 测序,以确定 RGS10 有不同表达的关键免疫细胞。RGS10基因敲除小鼠在葡聚糖硫酸钠(DSS)诱导的结肠炎中发病。通过 qRT-PCR、酶联免疫吸附试验和流式细胞术检测了炎症细胞因子在 mRNA 和蛋白质水平上的表达。我们发现,与健康人相比,UC 患者的 RGS10 表达明显升高,尤其是在 CD4+ T 细胞中。耐人寻味的是,RGS10 的缺乏明显缓解了 DSS 诱导的结肠炎,并降低了固有膜单核细胞(LPMCs)、外周血(PB)、脾脏和肠系膜淋巴结(mLNs)中 Th1 和 Th17 细胞的比例。从机理上讲,RGS10 缺乏会抑制信号转导和转录激活因子(STAT)1 和 STAT3 的磷酸化,从而阻止 Th1 和 Th17 细胞的分化。共免疫沉淀分析进一步表明,RGS10能与蛋白酪氨酸磷酸酶非受体2型(PTPN2)相互作用,并进一步调控CD4+ T细胞的Th1和Th17细胞分化。总之,RGS10缺乏可通过与CD4+ T细胞中的PTPN2相互作用,抑制Th1/Th17细胞介导的免疫反应,从而缓解肠粘膜炎症。因此,靶向 RGS10 可能是治疗 UC 的一种新疗法。
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引用次数: 0
The Immune Regulatory Functions in B Cells Are Restored by CpG to Reduce Experimental Food Allergy. CpG可恢复B细胞的免疫调节功能,减轻实验性食物过敏。
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-09 DOI: 10.1111/imm.13868
Qiao Liu, Dong-Hua Bin, Zhuo-Ya Wang, Ke-Ping Peng, Wang Tang, Jing-Weng Huang, Ling-Zhi Xu, Xiang-Yu Wang, Ping-Chang Yang, Gui-Xiang Tian

Dysfunctional immune regulation contributes to the pathogenesis of food allergy (FA). The mechanism behind regulatory B-cell dysfunction is unclear. CpG has immune regulatory functions. The purpose of this study is to use CpG to recover the immune suppressive functions of B cells in mice with FA. An FA mouse model was created using ovalbumin as the specific antigen. Flow cytometry was used to isolate B cells from the intestinal tissues. The immune regulatory functions of B cells were assessed using immunological approaches. The results showed that the FA response was linked to low IL-10 levels in gut lavage fluids of FA mice. FA mouse intestinal B cells produced lower amounts of IL-10 as compared with B cells isolated from naïve control mice. Impaired immune suppressive functions were observed in B cells isolated from the FA mouse intestine. The inducibility of the Il10 expression in naïve B cells of the intestine of FA mice was defective. The induction of Il10 expression in FA B cells could be restored by CpG through regulating the methylation status of the Cmip promoter. CpG promoted the therapeutic efficacy of allergen specific immunotherapy by restoring the induction of IL-10+ B cells in the intestine. The expression of Il10 in B cells of the FA mouse intestine was impaired. Administration of CpG could restore the expression of Il10 in B cells in the intestine and promote immunotherapy for FA.

免疫调节功能失调是食物过敏(FA)的发病机制之一。调节性 B 细胞功能失调的机制尚不清楚。CpG具有免疫调节功能。本研究的目的是利用 CpG 恢复 FA 小鼠 B 细胞的免疫抑制功能。以卵清蛋白为特异性抗原建立了一个 FA 小鼠模型。使用流式细胞术从肠道组织中分离出 B 细胞。使用免疫学方法评估了 B 细胞的免疫调节功能。结果显示,FA反应与FA小鼠肠道灌洗液中低IL-10水平有关。与分离自天真对照组小鼠的 B 细胞相比,FA 小鼠肠道 B 细胞产生的 IL-10 含量较低。从FA小鼠肠道分离的B细胞的免疫抑制功能受损。在FA小鼠肠道的幼稚B细胞中,Il10表达的诱导性存在缺陷。CpG可以通过调节Cmip启动子的甲基化状态来恢复FA B细胞中Il10的诱导表达。CpG通过恢复肠道中IL-10+ B细胞的诱导,促进了过敏原特异性免疫疗法的疗效。FA小鼠肠道B细胞中Il10的表达受损。服用CpG可恢复肠道B细胞中Il10的表达,促进FA的免疫治疗。
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引用次数: 0
Helios-Illuminating the way for lymphocyte self-control. 太阳神--照亮淋巴细胞自我控制之路
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1111/imm.13866
Iivo Hetemäki, T Petteri Arstila, Eliisa Kekäläinen

Transcription factor Helios, encoded by the IKZF2 gene, has an important role in regulatory T cells by stabilizing their suppressive phenotype. While Helios is prominently expressed in regulatory T cells, its expression extends beyond to include effector T cells, follicular regulatory T cells, B cells, and innate-like lymphocyte populations. Recent characterizations of patients with inborn error of immunity due to damaging IKZF2 variants coupled with translational research on lymphocytes from healthy individuals, have increased our understanding on Helios' multifaceted role in controlling the human adaptive immune system. A less studied role for Helios beyond the stabilizing of regulatory T cells has emerged in directing effector T cell maturation. In the absence of functional Helios, effector T cells acquire more inflammatory phenotype and are prone to senescence. Loss of Helios expression disrupts the regulation of the germinal centre reaction, often resulting in either hypogammaglobulinemia or B cell autoimmunity. This review summarizes findings from studies in both mice and men offering a comprehensive understanding of the impact of the transcription factor Helios on the adaptive immune system.

由 IKZF2 基因编码的转录因子 Helios 在调节性 T 细胞中发挥着重要作用,它能稳定 T 细胞的抑制表型。Helios 主要在调节性 T 细胞中表达,其表达范围还包括效应 T 细胞、滤泡调节性 T 细胞、B 细胞和先天类淋巴细胞群。最近,我们对因IKZF2变体损伤而导致先天性免疫错误的患者进行了特征描述,并对健康人的淋巴细胞进行了转化研究,从而加深了我们对Helios在控制人类适应性免疫系统中的多方面作用的了解。除了稳定调节性T细胞外,Helios在引导效应T细胞成熟方面的作用研究较少。在缺乏功能性 Helios 的情况下,效应 T 细胞会获得更多的炎症表型,并容易衰老。Helios 的表达缺失会破坏生殖中心反应的调控,通常会导致低丙种球蛋白血症或 B 细胞自身免疫。本综述总结了对小鼠和人类的研究结果,以全面了解转录因子Helios对适应性免疫系统的影响。
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引用次数: 0
Downregulation of type I interferon signalling pathway by urate in primary human PBMCs. 尿酸盐下调原代人类 PBMC 的 I 型干扰素信号通路。
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1111/imm.13858
Medeea Badii, Valentin Nica, Ancuța R Straton, Brenda Kischkel, Orsolya Gaal, Georgiana Cabău, Viola Klück, Ioana Hotea, Boris Novakovic, Cristina Pamfil, Simona Rednic, Mihai G Netea, Radu A Popp, Leo A B Joosten, Tania O Crișan

Type I interferons (IFN1s) mediate innate responses to microbial stimuli and regulate interleukin (IL)-1 and IL-1 receptor antagonist (Ra) production in human cells. This study explores interferon-stimulated gene (ISG) alterations in the transcriptome of patients with gout and stimulated human primary cells in vitro in relation to serum urate concentrations. Peripheral blood mononuclear cells (PBMCs) and monocytes of patients with gout were primed in vitro with soluble urate, followed by lipopolysaccharide (LPS) stimulation. Separately, PBMCs were stimulated with various toll-like receptor (TLR) ligands. RNA sequencing and IL-1Ra cytokine measurement were performed. STAT1 phosphorylation was assessed in urate-treated monocytes. Cytokine responses to IFN-β were evaluated in PBMCs cultured with or without urate and restimulated with LPS and monosodium urate (MSU) crystals. Transcriptomics revealed suppressed IFN-related signalling pathways in urate-exposed PBMCs or monocytes which was supported by diminishment of phosphorylated STAT1. The stimulation of PBMCs with IFN-β did not modify the urate-induced inflammation. Interestingly, in vivo, serum urate concentrations were inversely correlated to in vitro ISG expression upon stimulations with TLR ligands. These findings support a deficient IFN1 signalling in the presence of elevated serum urate concentrations, which could translate to increased susceptibility to infections.

I型干扰素(IFN1s)介导对微生物刺激的先天性反应,并调节人体细胞中白细胞介素(IL)-1和IL-1受体拮抗剂(Ra)的产生。本研究探讨了痛风患者和受刺激的体外人类原代细胞转录组中干扰素刺激基因(ISG)的改变与血清尿酸盐浓度的关系。痛风患者的外周血单核细胞(PBMCs)和单核细胞在体外用可溶性尿酸盐诱导,然后用脂多糖(LPS)刺激。另外,用各种收费样受体(TLR)配体刺激 PBMC。进行了 RNA 测序和 IL-1Ra 细胞因子测定。在尿酸盐处理的单核细胞中评估 STAT1 磷酸化。在有尿酸盐或无尿酸盐培养的 PBMC 中评估了细胞因子对 IFN-β 的反应,并用 LPS 和单钠尿酸盐(MSU)晶体进行了再刺激。转录组学显示,尿酸盐暴露的 PBMC 或单核细胞中与 IFN 相关的信号通路受到抑制,磷酸化 STAT1 的减少也证实了这一点。用 IFN-β 刺激 PBMC 并不能改变尿酸盐诱导的炎症。有趣的是,在体内,血清尿酸盐浓度与 TLR 配体刺激后体外 ISG 的表达成反比。这些研究结果表明,在血清尿酸盐浓度升高的情况下,IFN1 信号会出现缺陷,从而导致对感染的易感性增加。
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引用次数: 0
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Immunology
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