Mucosal Immunology最新文献_第8页

Exogenous ephrin-A3 reverses loss of vaginal epithelial barrier protection in progestin-treated mice 外源性ephrin-A3逆转孕激素处理小鼠阴道上皮屏障保护的丧失。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.06.007

Mohan Liu , Rodolfo D. Vicetti Miguel , Kristen Aceves , Thomas L. Cherpes

Desmosomes are junctional complexes that confer mechanical strength and enhance barrier protection at mucosal epithelial surfaces by anchoring intermediate filaments to plasma membrane. These roles are best defined in cutaneous epithelium, but we previously identified lower levels of the desmosomal cadherins desmoglein-1 (DSG1) and desmocollin-1 (DSC1) and loss of barrier function in vaginal epithelium of mice treated systemically with the progestin depot medroxyprogesterone acetate (DMPA). We also showed these changes were avoided in mice treated with both DMPA and a conjugated equine estrogen vaginal cream. We extend these earlier results in the current investigation, identifying ephrin-A3 (EFNA3) as an important regulator of desmosomal cadherin gene expression in murine vaginal epithelial tissue. Moreover, topical treatment of mice with recombinant EFNA3 (rEFNA3) significantly increased vaginal expression of DSG1 and partially reversed the loss of vaginal epithelial barrier function induced by DMPA treatment. Consistent with this improvement in vaginal epithelial barrier protection, mortality caused by genital herpes simplex virus type 2 infection was delayed, but not prevented, in mice administered DMPA and rEFNA3 vs. DMPA alone. Together, current studies identify EFNA3 as a key regulator of desmosomal structure and function in vaginal epithelium and newly suggest that ephrin-Eph signaling pathways will provide an important target for enhancing vaginal epithelial integrity and barrier function.

桥粒是连接复合物，通过将中间丝锚定在质膜上，赋予粘膜上皮表面机械强度并增强屏障保护。这些作用在皮肤上皮中得到了最好的定义，但我们之前发现，在全身注射黄体酮醋酸甲羟孕酮（DMPA）的小鼠阴道上皮中，桥粒体钙粘蛋白桥粒素-1 （DSG1）和桥粒素-1 （DSC1）的水平较低，屏障功能丧失。我们还发现，在使用DMPA和结合马雌激素阴道乳膏的小鼠中，这些变化是避免的。我们在当前的研究中扩展了这些早期的结果，确定了ephrin-A3 （EFNA3）是小鼠阴道上皮组织中桥粒钙粘蛋白基因表达的重要调节因子。此外，用重组EFNA3 （rEFNA3）局部处理小鼠可显著增加阴道DSG1的表达，并部分逆转DMPA处理引起的阴道上皮屏障功能丧失。与阴道上皮屏障保护的改善相一致，在给予DMPA和rEFNA3的小鼠中，与单独给予DMPA相比，生殖器单纯疱疹病毒2型感染引起的死亡率延迟，但不能预防。总之，目前的研究发现EFNA3是阴道上皮桥胞体结构和功能的关键调节因子，并且新的研究表明ephrin-Eph信号通路将为增强阴道上皮完整性和屏障功能提供重要靶点。

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引用次数: 0

Single-cell RNA profiling identifies immune cell population shifts in diabetes associated mucosal inflammation 单细胞RNA谱鉴定糖尿病相关粘膜炎症中免疫细胞群的变化。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.06.008

Bushra Alghamdi , Min Liu , Xin Huang , Rahul Debnath , Hamideh Afzali , Michael Troka , Akira Hasuike , Quinn Easter , Mi Zhou , Kevin Byrd , Michael Gonzalez , Kang I. Ko , Dana T. Graves

Poorly controlled diabetes significantly worsens periodontal disease, affecting millions worldwide, yet the mechanisms driving this destructive synergy remain unclear. We generated single-cell RNA sequencing profiles of diabetic periodontal tissue, revealing increased γ^δ T-cells, a loss of Tregs and greater neutrophil polarization as key mediators of diabetes-enhanced periodontitis. Flow cytometry confirmed significant expansion of IL-17A⁺ γ^δ+ T-cells and reduced Tregs in diabetic mice, with parallel findings of elevated CD3⁺IL-17A⁺ cells and reduced Tregs in human diabetic periodontal specimens. scRNAseq determined that diabetes caused a global increase in pro-inflammatory and a decrease in pro-resolving transcripts and enhanced inflammatory neutrophil polarization. Selective γ^δ T-cell inhibition reversed diabetes-enhanced periodontal destruction while minimally affecting normoglycemic controls and returned neutrophil infiltration to normoglycemic levels. These findings point to unique aspects of diabetes-induced dysregulation, implicate γ^δ T-cells as a driving factor and point to them as a potential therapeutic target in periodontitis and other diabetic complications.

控制不良的糖尿病显著地将牙周病从可控制转变为晚期，影响全世界数百万人，但驱动这种破坏性协同作用的机制尚不清楚。为了研究这些病理相互作用，我们生成了糖尿病牙周组织的单细胞RNA测序图谱，揭示了γδ t细胞是以前未被识别的糖尿病增强牙周破坏的中心介质。流式细胞术验证证实，与血糖正常的小鼠相比，糖尿病小鼠体内产生IL-17A的γδ t细胞显著扩增，同时在人类糖尿病牙周标本中也发现IL-17A + 细胞升高。选择性γδ t细胞抑制可显著逆转糖尿病增强的牙周破坏，同时对正常血糖控制的影响最小，并使中性粒细胞浸润恢复到正常血糖水平。scRNAseq发现了其他因素，包括中性粒细胞向促炎表型的更大极化和treg的丢失。这些发现指出了糖尿病诱导失调的独特方面，并暗示γδ t细胞在这一过程中是一个驱动因素。结果还指出γδ t细胞是牙周炎和其他糖尿病并发症的治疗靶点。

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引用次数: 0

Dysbiosis of the gut microbiome may contribute to the pathogenesis of oral lichen planus through Treg dysregulation 肠道菌群失调可能通过Treg失调导致口腔扁平苔藓的发病。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.05.009

Shiho Yokomizo , Naoki Kaneko , Hu Chen , Lijing Yan , Shoji Tsuji , Shohei Akagawa , Junsei Sameshima , Tomoki Sueyoshi , Haruki Nagano , Yuka Miyahara , Yasuhisa Kamikaseda , Hajime Kido , Yoshikazu Hayashi , Masaki Yamauchi , Tamotsu Kiyoshima , Yuichi Goto , Yukiko Ohyama , Kazunari Kaneko , Masafumi Moriyama , Shintaro Kawano

Oral lichen planus (OLP) is a chronic inflammatory disorder with autoimmune features and malignant transformation risk, lacking a definitive treatment, with CD4⁺ T cells being pivotal in its pathogenesis. Dysbiosis, an imbalance in the microbiome, is linked to various autoimmune and inflammatory diseases, where CD4⁺ T cells play a significant role. Given these insights, the development of OLP might be influenced by dysbiosis. This study investigates the association between dysbiosis and CD4⁺ T cells in OLP. We collected stool and saliva samples from OLP patients, conducting 16S rRNA gene analysis and mass spectrometry, and assessed CD4⁺ T cell characteristics in lesions through multiplex immunofluorescence and single-cell RNA sequencing. Peripheral blood samples were subjected to flow cytometry and cell culture assays. Results showed extensive gut dysbiosis in OLP patients, notably a reduction in short-chain fatty acid (SCFA)-producing bacteria essential for regulatory T cell (Treg) differentiation. While various CD4⁺ T cell subsets, including Tregs, were present in tissues, these Tregs as unresponsive to specific antigens, showing reduced immunosuppressive molecule expression. The decline in SCFA-producing bacteria correlated with fewer activated Tregs in tissues and blood. These findings suggest that gut dysbiosis may contribute to OLP by impairing Treg regulation, influencing disease pathogenesis.

口腔扁平苔藓（OLP）是一种具有自身免疫特征和恶性转化风险的慢性炎症性疾病，缺乏明确的治疗方法，CD4+ T细胞在其发病机制中起关键作用。生态失调是一种微生物组失衡，与各种自身免疫性和炎症性疾病有关，其中CD4+ T细胞起着重要作用。鉴于这些见解，OLP的发展可能受到生态失调的影响。本研究探讨了OLP中生态失调与CD4+ T细胞的关系。我们收集OLP患者的粪便和唾液样本，进行16S rRNA基因分析和质谱分析，并通过多重免疫荧光和单细胞RNA测序评估病变中CD4+ T细胞的特征。外周血标本行流式细胞术和细胞培养检测。结果显示，OLP患者存在广泛的肠道生态失调，特别是产生短链脂肪酸（SCFA）的细菌减少，这是调节性T细胞（Treg）分化所必需的。虽然组织中存在各种CD4+ T细胞亚群，包括treg，但这些treg对特定抗原无反应，表现出免疫抑制分子表达减少。产生scfa的细菌的减少与组织和血液中活性treg的减少有关。这些发现表明，肠道生态失调可能通过损害Treg调节，影响疾病发病机制，从而促进OLP的发生。

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引用次数: 0

TRIM33 prevents the exacerbation of allergic asthma by restricting the overactivation of alveolar macrophages TRIM33通过限制肺泡巨噬细胞的过度活化来防止过敏性哮喘的加重。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.07.003

Jiaoyan Lv , Ziyan Su , Tao Wu , Yujie Tian , Xin Liu , Jiachen Liu , Xiaoguang Li , Wenlong Lai , Chen Dong , Li Wu

Alveolar macrophages (AMs) and dendritic cells (DCs) are the two major types of primary innate immune cells in allergic asthma and their functions were elaborately regulated during the progression of asthma. Tripartite motif-containing protein 33 (TRIM33) is a multifunctional protein that regulates differentiation and function of immune cells. However, its role in AMs and DCs in the context of allergic asthma remained unclear. Herein, we found that specific deletion of TRIM33 in AM and DCs (Itgax^Cre-GFPTrim33^fl/fl mice) affected their homeostasis in lung and induced aggravated allergic asthma. Though reduced in number in steady state, antigen-exposed Trim33^−/− CD11b⁺ DCs exhibited comparable potency in triggering allergic asthma. Replacing Trim33^−/− AMs with normal AMs could alleviate the aggravated HDM-induced airway inflammation and Th2 responses in Itgax^Cre-GFPTrim33^fl/fl mice. Moreover, Trim33^−/− AMs exhibited stronger activation status and became an additional cellular source of CCL2 when encountered the allergen, thereby promoting the recruitment of CD11b⁺ DCs into lung and draining lymph nodes where they amplifying Th2 responses in Itgax^Cre-GFPTrim33^fl/fl mice. Our study revealed a crucial role of TRIM33 in controlling the aggravation of allergic asthma via repressing AM overactivation.

肺泡巨噬细胞（Alveolar macrophages, AMs）和树突状细胞（dendritic cells, dc）是过敏性哮喘的两种主要先天性免疫细胞，它们的功能在哮喘的发展过程中受到精心调节。Tripartite motif-containing protein 33 （TRIM33）是一种调节免疫细胞分化和功能的多功能蛋白。然而，其在过敏性哮喘am和dc中的作用尚不清楚。在本研究中，我们发现AM和dc （ItgaxCre-GFPTrim33fl/fl小鼠）中TRIM33的特异性缺失影响了它们的肺内稳态，并诱发了加重的过敏性哮喘。虽然数量减少，但TRIM33缺陷CD11b±dc在引发过敏性哮喘方面表现出相当的效力。用正常am替代Trim33-/- am可减轻ItgaxCre-GFPTrim33fl/fl小鼠hdm诱导的加重气道炎症和Th2反应。此外，Trim33-/- AMs表现出更强的激活状态，并在遇到过敏原时成为CCL2的额外细胞来源，从而促进CD11b+ dc募集到肺和引流淋巴结，并在ItgaxCre-GFPTrim33fl/fl小鼠中扩增Th2反应。我们的研究揭示了TRIM33通过抑制AM过度激活在控制过敏性哮喘加重中的关键作用。

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引用次数: 0

Dynamics of virus-specific CD8+ T cells in the human nasal cavity 病毒特异性CD8+ T细胞在人鼻腔中的动态变化。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.07.007

Joey Ming Er Lim , Sabrina Ottolini , Shou Kit Hang , Martin Daniel Qui , Adeline Chia , Jenny Guek Hong Low , Nina Le Bert , Anthony Tanoto Tan , Antonio Bertoletti

The nasal cavity is the entry site for respiratory viruses. Understanding how the nasal cavity sustains memory CD8+ T cell is essential for improving respiratory virus management and vaccine development. Here, we sampled CD8+ T cells from the upper nasal turbinate and peripheral blood of healthy adults. We analysed their transcriptomic profile and antigen specificity for respiratory (SARS-CoV-2, Influenza A) and non-respiratory (HCMV) viruses.

Transcriptomic analysis revealed that nasal CD8+ T cells failed to upregulate STAT1 following TCR stimulation, potentially enabling clonal expansion despite the antiproliferative effects of IFN signalling. They also exhibited a cytotoxic, Th1-like profile with tissue-residency markers but lacked TCF7 expression, suggesting limited self-renewal capacity. The CD8+ T cell analysis of antigen specificity demonstrates that local nasal exposure is indispensable for virus-specific CD8+ T cell detection. Only SARS-CoV-2 and influenza-specific but not HCMV-specific CD8+ T cells were detected in the nasal compartment. However, their persistence over time in the nasal cavity appears linked to repetitive viral exposure.

Our findings provide insights into the adaptations of nasal-resident CD8+ T cells and highlight challenges in eliciting durable nasal T cell immunity, with important implications for vaccine strategies against respiratory pathogens.

鼻腔是呼吸道病毒的进入点。了解鼻腔如何维持记忆CD8+ T细胞对于改善呼吸道病毒管理和疫苗开发至关重要。在这里，我们从健康成人的上鼻甲和外周血中取样了CD8+ T细胞。我们分析了它们对呼吸道（SARS-CoV-2、流感）和非呼吸道（HCMV）病毒的转录组谱和抗原特异性。转录组学分析显示，鼻腔CD8+ T细胞在TCR刺激后无法上调STAT1，尽管IFN信号传导具有抗增殖作用，但仍有可能实现克隆扩增。它们还表现出细胞毒性，th1样的组织驻留标记，但缺乏TCF7表达，表明自我更新能力有限。CD8+ T细胞抗原特异性分析表明，局部鼻暴露对于病毒特异性CD8+ T细胞检测是必不可少的。鼻室中仅检测到SARS-CoV-2和流感特异性CD8+ T细胞，未检测到hcmv特异性CD8+ T细胞。然而，它们在鼻腔中持续存在的时间似乎与反复接触病毒有关。我们的研究结果提供了对鼻腔驻留CD8+ T细胞适应性的见解，并强调了引发持久鼻腔T细胞免疫的挑战，对针对呼吸道病原体的疫苗策略具有重要意义。

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引用次数: 0

Single cell transcriptional analysis of human adenoids identifies molecular features of airway microfold cells 人腺样体单细胞转录分析鉴定气道微褶细胞的分子特征。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.07.006

Samuel Alvarez-Arguedas , Khadijah Mazhar , Andi Wangzhou , Ishwarya Sankaranarayanan , Gabriela Gaona , John T. Lafin , Ron B. Mitchell , Theodore J. Price , Michael U. Shiloh

The nasal, oropharyngeal, and bronchial mucosa are primary contact points for airborne pathogens like Mycobacterium tuberculosis (Mtb), SARS-CoV-2, and influenza virus. While mucosal surfaces can function as both entry points and barriers to infection, mucosa-associated lymphoid tissues (MALT) facilitate early immune responses to mucosal antigens. MALT contains a variety of specialized epithelial cells, including a rare cell type called a microfold cell (M cell) that functions to transport apical antigens to basolateral antigen-presenting cells, a crucial step in the initiation of mucosal immunity. M cells have been extensively characterized in the gastrointestinal (GI) tract in murine and human models. However, the precise development and functions of human airway M cells are unknown. Here, using single-nucleus RNA sequencing (snRNA-seq), we generated an atlas of cells from the human adenoid and identified 26 unique cell types representing basal, club, hillock, and hematopoietic lineages, defined their developmental trajectories, and determined cell-cell relationships. Using trajectory analysis, we found that human airway M cells develop from progenitor club cells and express a gene signature distinct from intestinal M cells. Surprisingly, we also identified a heretofore unknown epithelial cell type demonstrating a robust interferon-stimulated gene signature. Our analysis of human adenoid cells enhances our understanding of mucosal immune responses and the role of M cells in airway immunity. This work also provides a resource for understanding early interactions of pathogens with airway mucosa and a platform for development of mucosal vaccines.

鼻、口咽和支气管粘膜是空气传播病原体如结核分枝杆菌（Mtb）、SARS-CoV-2和流感病毒的主要接触点。虽然粘膜表面可以作为感染的入口和屏障，但粘膜相关淋巴组织（MALT）促进对粘膜抗原的早期免疫反应。MALT包含多种特化上皮细胞，包括一种称为微褶细胞（M细胞）的罕见细胞类型，其功能是将根尖抗原转运到基底外侧抗原呈递细胞，这是启动粘膜免疫的关键步骤。在小鼠和人类的胃肠道模型中，M细胞已经被广泛地表征。然而，人类气道M细胞的确切发育和功能尚不清楚。在这里，我们使用单核RNA测序（snRNA-seq），生成了来自人类腺样体的细胞图谱，并鉴定了26种独特的细胞类型，代表了基础、俱乐部、丘和造血谱系，定义了它们的发育轨迹，并确定了细胞-细胞关系。通过轨迹分析，我们发现人类气道M细胞由祖俱乐部细胞发育而来，并表达与肠道M细胞不同的基因特征。令人惊讶的是，我们还发现了一种迄今未知的上皮细胞类型，显示出强大的干扰素刺激基因特征。我们对人腺样细胞的分析增强了我们对粘膜免疫反应和M细胞在气道免疫中的作用的理解。这项工作也为了解病原体与气道粘膜的早期相互作用提供了资源，并为开发粘膜疫苗提供了平台。

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引用次数: 0

Fibroblast-derived CSF1 maintains colonization of gut mucosal macrophage to resist bacterial infection 成纤维细胞衍生的CSF1维持肠道粘膜巨噬细胞的定植以抵抗细菌感染。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.06.011

Daichi Nonaka , Soichiro Yoshida , Kenta Nakano , Xiaojun Li , Tadashi Okamura , Eiji Umemoto , Taisho Yamada , Miyuki Watanabe , Shozo Jinno , Minako Ito , Makoto Tsuda , Naoto Noguchi , Jean X Jiang , Eriko Sumiya , Shinichiro Sawa

Macrophages play essential roles in immune defense and tissue homeostasis, but the mechanisms underlying their colonization in the gut mucosa remain incompletely understood. Here, we identify CSF1, primarily derived from fibroblasts, as the dominant factor maintaining mucosal macrophage colonization, whereas IL-34 deficiency alone has a minimal impact. We reveal that CSF1R ligands originate from distinct cellular sources: macrophages at the upper villus region depend on fibroblast-derived CSF1 and IL-34, while macrophages in the lower villus and the submucosal (lower villus + SM) region are regulated by CSF1 from both fibroblasts and endothelial cells. Additionally, within the lower villus + SM region, CSF1-producing CD81⁺ LepR⁺ fibroblasts directly interact with CD163⁺ macrophages, forming a localized niche. The loss of CSF1 in fibroblasts results in accelerated systemic dissemination of Salmonella Typhimurium, highlighting fibroblast-derived CSF1 as a key regulator of gut macrophage function in host defense. Collectively, our findings uncover a previously unrecognized fibroblast-macrophage crosstalk that governs gut macrophage homeostasis and immunity.

巨噬细胞在免疫防御和组织稳态中发挥着重要作用，但其在肠道粘膜中的定植机制尚不完全清楚。在这里，我们发现主要来源于成纤维细胞的CSF1是维持粘膜巨噬细胞定植的主要因素，而IL-34缺乏本身的影响很小。我们发现CSF1R配体起源于不同的细胞来源：上绒毛区域的巨噬细胞依赖于成纤维细胞衍生的CSF1和IL-34，而下绒毛和粘膜下（下绒毛 + SM）区域的巨噬细胞受成纤维细胞和内皮细胞的CSF1调节。此外，在下绒毛 + SM区域，产生csf1的CD81+ LepR+成纤维细胞直接与CD163+巨噬细胞相互作用，形成局部生态位。成纤维细胞中Csf1的缺失导致鼠伤寒沙门氏菌的全身传播加速，这表明成纤维细胞衍生的Csf1在宿主防御中是肠道巨噬细胞功能的关键调节因子。总的来说，我们的发现揭示了一种以前未被识别的成纤维细胞-巨噬细胞串扰，它控制着肠道巨噬细胞的稳态和免疫。

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引用次数: 0

Editing B cells at the IGHA2 gene position provides alternative route to therapeutic IgA production 在IGHA2基因位置编辑B细胞为治疗性IgA生产提供了另一种途径。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-10-01 DOI: 10.1016/j.mucimm.2025.06.001

Marine Cahen , Jenny Léonard , Ophélie Dézé , Laurent Deleurme , Maiwenn Pineau , Anne-Laure Tanguy , Stéphane Paul , Jérome Moreaux , Grégory Noël , Natsuko Ueda , Yannic Danger , Michel Cogné

As professional and long-lived immunoglobulin (Ig) producers, B cells represent attractive candidates for adoptive immunotherapy and their highly expressed Ig heavy (IgH) chain locus is ideal for editing. Each of its constant genes, expressed after class switch recombination (CSR), affords an attractive platform where an adoptive Ig variable domain would acquire IgM, IgG, IgE or IgA class-specific functions. In particular, IgA plays a unique role in mucosal immunity but has remained excluded from therapeutic applicability due to unfavorable chemistry, manufacturing, and control (CMC) issues. To test whether these barriers could be overcome by producing IgA in vivo rather than in vitro, we edited the human B cell-specific IGHA2 gene and found it to be a suitable platform for inserting gene cassettes for expression in B cells. Targeted deletions can also induce CSR to IgA2, while, by combining IgA2 CSR with the insertion of a linked VH and a complete light chain, we have replaced the endogenous Ig chains with a customized full-size but single-chain IgA carrying an adoptive antigen specificity.

Taken together, we show that IGHA2-editing of B cells could provide a novel avenue to B-cell targeted delivery of therapeutic IgA, overcoming the problems that have so far excluded IgA from clinical use.

作为专业和长寿的免疫球蛋白（Ig）生产者，B细胞是过继免疫治疗的有吸引力的候选者，它们高表达的Ig重（IgH）链位点是理想的编辑位点。在类转换重组（CSR）后表达的每一个恒定基因，都提供了一个有吸引力的平台，在这个平台上，采用的Ig变量结构域将获得IgM、IgG、IgE或IgA类特异性功能。特别是，IgA在粘膜免疫中起着独特的作用，但由于不利的化学、制造和控制（CMC）问题，仍被排除在治疗适用性之外。为了测试是否可以通过在体内而不是在体外产生IgA来克服这些障碍，我们编辑了人类B细胞特异性IGHA2基因，发现它是插入基因盒在B细胞中表达的合适平台。靶向缺失也可以诱导IgA2的CSR，而通过将IgA2 CSR与连接的VH和完整轻链的插入结合，我们已经用定制的全尺寸单链IgA取代了内源性Ig链，携带过继抗原特异性。综上所述，我们表明，对B细胞进行igha2编辑可以为B细胞靶向递送治疗性IgA提供一种新的途径，克服了迄今为止将IgA排除在临床应用之外的问题。

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引用次数: 0

A zebrafish model of intestinal epithelial damage reveals macrophages and igfbp1a as major modulators of mucosal healing 斑马鱼肠上皮损伤模型显示巨噬细胞和igfbp1a是粘膜愈合的主要调节剂。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-08-01 DOI: 10.1016/j.mucimm.2025.04.004

Rodrigo A. Morales Castro , Bianca C. Kern , Angélica Díaz-Basabe , Eveline R. Meinen , Danxia Zhao , Yuqing Zhou , Francisca Castillo , Gustavo Monasterio , Vlad Farcas , Myra N. Chávez , Jennifer Fransson , Eduardo J. Villablanca

Promoting intestinal regeneration and enhancing mucosal healing have emerged as promising therapeutic alternatives for treating intestinal disorders that compromise epithelial barrier integrity and function. However, the cellular and molecular mechanisms underlying these processes remain poorly understood. This knowledge gap is partly due to the lack of reliable and cost-effective in vivo models for studying the mechanisms governing intestinal damage and regeneration. Here, we developed a controlled, inducible, and targeted intestinal epithelial cell (IEC) ablation transgenic zebrafish model that recapitulates features of intestinal damage and regeneration observed in humans. Single-cell RNAseq and live imaging revealed accumulation of macrophages in the recovering intestine, contributing to its regeneration. Furthermore, we observed overexpression of insulin-like growth factor binding protein 1a (igfbp1a) during intestinal damage. Morpholino-mediated knockdown of igfbp1a exacerbated intestinal damage and impaired subsequent regeneration. In summary, we introduced a novel zebrafish model of intestinal damage that enables in vivo high-throughput screening for identifying and validating novel modulators of mucosal healing and intestinal regeneration.

促进肠道再生和增强粘膜愈合已成为治疗损害上皮屏障完整性和功能的肠道疾病的有希望的治疗选择。然而，这些过程背后的细胞和分子机制仍然知之甚少。这种知识差距部分是由于缺乏可靠和具有成本效益的体内模型来研究肠道损伤和再生的机制。在这里，我们建立了一个受控的、诱导的、靶向的肠上皮细胞（IEC）消融转基因斑马鱼模型，该模型再现了在人类中观察到的肠道损伤和再生的特征。单细胞RNAseq和实时成像显示巨噬细胞在恢复的肠道中积累，有助于其再生。此外，我们观察到胰岛素样生长因子结合蛋白1a （igfbp1a）在肠道损伤期间过表达。morpholino介导的igfbp1a敲低加重了肠道损伤和随后的再生受损。总之，我们介绍了一种新的肠道损伤斑马鱼模型，该模型能够在体内进行高通量筛选，以识别和验证粘膜愈合和肠道再生的新型调节剂。

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引用次数: 0

A novel link driving immune cell-fibroblast interactions in intestinal fibrosis 肠道纤维化中驱动免疫细胞-成纤维细胞相互作用的新联系。

IF 7.6 2区医学 Q1 IMMUNOLOGY

Mucosal Immunology

Pub Date : 2025-08-01 DOI: 10.1016/j.mucimm.2025.06.009

Gaurav Chauhan , Ido Veisman , Florian Rieder

引用次数: 0