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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
New Engineered-Chimeric Botulinum Neurotoxin Mutant Acts as an Effective Bivalent Vaccine Against Botulinum Neurotoxin Serotype A and E. 新设计的嵌合型肉毒杆菌神经毒素突变体可作为针对肉毒杆菌神经毒素血清型 A 和 E 的有效双价疫苗
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-10-01 DOI: 10.1111/imm.13867
Jingrong Wang, Jiansheng Lu, Bolin Li, Xiaoyu Liu, Rong Wang, Peng Du, Shuo Yu, Zhixin Yang, Yunzhou Yu

Botulinum neurotoxins (BoNTs), including serotypes A and E, are potent biotoxins known to cause human poisoning. In addition to the critical protective antigen found in the full BoNT molecule, the receptor binding domain (Hc domain), BoNTs also harbour another essential protective antigen-the light chain-translocation domain (L-HN domain). Leveraging these pivotal protective antigens, we genetically engineered a series of inactivated chimeric molecules incorporating L-HN and Hc domains of BoNT/A and E. The structure of these chimeric molecules, mirror BoNT/A and E, but are devoid of enzyme activity. Experimental findings demonstrated that a lead candidate mEL-HN-mAHc harnessing the inactivated protease LCHN/E with the mutated gangliosides binding site Hc/A (mE-mA) elicited robust immune protection against BoNT/A and E simultaneously in a mouse model, requiring low immune dosages and minimal immunisations. Moreover, mE-mA exhibited high protective efficacy against BoNT/A and E in guinea pigs and New Zealand white rabbits, resulting in elevated neutralising antibody titres. Furthermore, mE-mA proved to be a more stable and safer vaccine compared to formaldehyde-inactivated toxoid. Our data underscore the genetically engineered mE-mA as a highly effective bivalent vaccine against BoNT/A and E, paving the way for the development of polyvalent vaccines against biotoxins.

肉毒杆菌神经毒素(BoNTs),包括血清型 A 和 E,是已知可导致人类中毒的强效生物毒素。除了完整 BoNT 分子中的关键保护性抗原--受体结合结构域(Hc 结构域)外,BoNTs 还含有另一个重要的保护性抗原--轻链-转座结构域(L-HN 结构域)。利用这些关键的保护性抗原,我们从基因上设计了一系列灭活的嵌合分子,其中包含 BoNT/A 和 E 的 L-HN 和 Hc 结构域。实验结果表明,候选药物 mEL-HN-mAHc 利用失活的蛋白酶 LCHN/E 和变异的神经节苷脂结合位点 Hc/A(mE-mA),在小鼠模型中同时对 BoNT/A 和 E 产生强大的免疫保护作用,只需较低的免疫剂量和最低限度的免疫接种。此外,mE-mA 对豚鼠和新西兰白兔的 BoNT/A 和 E 具有很高的保护效力,从而导致中和抗体滴度升高。此外,与甲醛灭活的类毒素相比,mE-mA 被证明是一种更稳定、更安全的疫苗。我们的数据强调了基因工程改造的 mE-mA 是一种高效的二价疫苗,可预防 BoNT/A 和 E,为开发多价生物毒素疫苗铺平了道路。
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引用次数: 0
How maternal factors shape the immune system of breastfed infants to alleviate food allergy: A systematic and updated review. 母体因素如何塑造母乳喂养婴儿的免疫系统以缓解食物过敏:系统性最新综述。
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-30 DOI: 10.1111/imm.13864
Yuhong Wu, Bihua Chen, Huan Wu, Jinyan Gao, Xuanyi Meng, Hongbing Chen

What infants eat early in life may shape the immune system and have long-standing consequences on the health of the host during later life. In the early months post-birth, breast milk serves as the exclusive and optimal nourishment for infants, facilitating crucial molecular exchanges between mother and infant. Recent advances have uncovered that some maternal factors influence breastfed infant outcomes, including the risk of food allergy (FA). To date, accumulated data show that breastfed infants have a lower risk of FA. However, the issue remains disputed, some reported preventive allergy effects, while others did not confirm such effects, or if identified, protective effects were limited to early childhood. The disputed outcomes may be attributed to the maternal status, as it determines the compounds of the breast milk that breastfed infants are exposed to. In this review, we first detail the compounds in breast milk and their roles in infant FA. Then, we present maternal factors resulting in alterations in breast milk compounds, such as maternal health status, maternal diet intake, and maternal food allergen intake, which subsequently impact FA in breastfed infants. Finally, we analyze how these compounds in breast milk alleviated the infant FA by mother-to-infant transmission. Altogether, the mechanisms are primarily linked to the synergetic and direct effects of compounds in breast milk, via promoting the colonization of gut microbiota and the development of the immune system in infants.

婴儿生命早期的饮食可能会塑造其免疫系统,并对宿主日后的健康产生长期影响。在婴儿出生后的最初几个月里,母乳是婴儿唯一的最佳营养品,促进了母婴之间重要的分子交换。最近的研究发现,一些母亲因素会影响母乳喂养婴儿的结果,包括食物过敏(FA)的风险。迄今为止,积累的数据显示,母乳喂养的婴儿患食物过敏症的风险较低。然而,这一问题仍存在争议,一些研究报告称母乳喂养具有预防过敏的作用,而另一些研究则没有证实母乳喂养具有这种作用,或者即使证实了母乳喂养具有保护作用,也仅限于幼儿期。这些有争议的结果可能归因于母亲的状况,因为这决定了母乳喂养的婴儿所接触到的母乳中的化合物。在本综述中,我们首先详细介绍了母乳中的化合物及其在婴儿 FA 中的作用。然后,我们介绍了导致母乳化合物变化的母体因素,如母体健康状况、母体饮食摄入量和母体食物过敏原摄入量,这些因素随后会影响母乳喂养婴儿的 FA。最后,我们分析了母乳中的这些化合物如何通过母婴传播减轻婴儿的 FA。总之,这些机制主要与母乳中的化合物通过促进婴儿肠道微生物群的定植和免疫系统的发育而产生的协同和直接效应有关。
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引用次数: 0
RNA technology and nanocarriers empowering in vivo chimeric antigen receptor therapy 为体内嵌合抗原受体疗法赋能的 RNA 技术和纳米载体。
IF 4.9 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-28 DOI: 10.1111/imm.13861
Jingsheng Cai, Shaoyi Chen, Zheng Liu, Haoran Li, Peiyu Wang, Fan Yang, Yun Li, Kezhong Chen, Ming Sun, Mantang Qiu

The remarkable success of mRNA-based coronavirus 2019 (COVID-19) vaccines has propelled the advancement of nanomedicine, specifically in the realm of RNA technology and nanomaterial delivery systems. Notably, significant strides have been made in the development of RNA-based in vivo chimeric antigen receptor (CAR) therapy. In comparison to the conventional ex vivo CAR therapy, in vivo CAR therapy offers several benefits including simplified preparation, reduced costs, broad applicability and decreased potential for carcinogenic effects. This review summarises the RNA-based CAR constructs in in vivo CAR therapy, discusses the current applications of in vivo delivery vectors and outlines the immune cells edited with CAR molecules. We aim for the conveyed messages to contribute towards the advancement of in vivo CAR application.

基于 mRNA 的冠状病毒 2019(COVID-19)疫苗取得了巨大成功,推动了纳米医学的发展,特别是在 RNA 技术和纳米材料递送系统领域。值得注意的是,基于 RNA 的体内嵌合抗原受体(CAR)疗法的开发取得了重大进展。与传统的体外 CAR 疗法相比,体内 CAR 疗法具有多种优势,包括准备工作简化、成本降低、适用性广以及致癌作用的可能性降低。本综述总结了体内 CAR 疗法中基于 RNA 的 CAR 构建,讨论了体内递送载体的当前应用,并概述了使用 CAR 分子编辑的免疫细胞。我们希望所传达的信息能为推进体内 CAR 应用做出贡献。
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引用次数: 0
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