Mucosal Immunology最新文献_第7页

Localization of TCR-expressing natural intraepithelial lymphocytes in the colon epithelium depends on GPR15 and epithelium-derived C10ORF99 结肠上皮中表达tcr的天然上皮内淋巴细胞的定位取决于GPR15和上皮源性C10ORF99。

IF 5.5 2区医学

Mucosal Immunology Pub Date : 2026-08-01 Epub Date: 2026-06-01 DOI: 10.1016/j.mucimm.2026.100355

Gerald J. O’Connor, Jihae C. Choi, Nguyen T. Van, Anthony M. Klutkoski, Lucia C. Robertson, Sangwon V. Kim

{"title":"Localization of TCR-expressing natural intraepithelial lymphocytes in the colon epithelium depends on GPR15 and epithelium-derived C10ORF99","authors":"Gerald J. O’Connor, Jihae C. Choi, Nguyen T. Van, Anthony M. Klutkoski, Lucia C. Robertson, Sangwon V. Kim","doi":"10.1016/j.mucimm.2026.100355","DOIUrl":"10.1016/j.mucimm.2026.100355","url":null,"abstract":"<div><div>Intraepithelial lymphocytes (IELs) are among the largest lymphocyte populations in the body and play a crucial role in maintaining the integrity of epithelial barriers at mucosal sites, which are highly immunostimulatory. Therefore, understanding how these cells are generated, localized within the epithelium, and contribute to barrier immunity is essential. Although most research on IEL biology has focused on the small intestine, IELs are also present in the large intestinal epithelium. Additionally, the homing receptor-ligand pairs that regulate T cell localization in the lamina propria beneath the epithelium differ between the small and large intestines: CCL25-CCR9 in the small intestine and C10ORF99-GPR15 in the large intestine. CCL25-CCR9 is also necessary for proper localization of IELs in the small intestine, but the mechanisms controlling IEL localization in the large intestine remain unknown. Here, we demonstrate that the C10ORF99-GPR15 pathway is crucial for the presence of TCR + natural IELs in the large intestinal epithelium, a process that requires epithelium-derived C10ORF99 (GPR15L).</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 4","pages":"Article 100355"},"PeriodicalIF":5.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148150635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A neuro-epithelial unit regulates immunohomeostasis at barrier surfaces 神经上皮单位调节屏障表面的免疫稳态。

IF 5.5 2区医学

Mucosal Immunology Pub Date : 2026-08-01 Epub Date: 2026-06-17 DOI: 10.1016/j.mucimm.2026.100363

Manuel O. Jakob, Eliane Dohner, Patrycja M. Forster, Christoph S.N. Klose

{"title":"A neuro-epithelial unit regulates immunohomeostasis at barrier surfaces","authors":"Manuel O. Jakob, Eliane Dohner, Patrycja M. Forster, Christoph S.N. Klose","doi":"10.1016/j.mucimm.2026.100363","DOIUrl":"10.1016/j.mucimm.2026.100363","url":null,"abstract":"<div><h3>Summary</h3><div>Barrier tissues are sites of constant environmental exposure and require tightly coordinated mechanisms to maintain immune homeostasis while preserving tissue integrity. Emerging evidence supports the concept of a neuro-epithelial unit, in which neurons and epithelial cells function as integrated regulatory modules. In this review, we discuss how epithelial cells and peripheral neurons communicate to sense environmental cues and orchestrate immune responses. Epithelial cells provide a physical and biochemical barrier, while neurons rapidly detect perturbations and modulate local immune and stromal compartments through neuropeptide release. This coordinated interaction shapes immune cell recruitment, activation, and tolerance at barrier surfaces, such as the intestine. Here, we highlight recent advances demonstrating that neuronal signaling directly influences epithelial renewal, barrier function, and inflammatory responses. Furthermore, we explore how dysregulation of this neuro-epithelial axis contributes to chronic inflammatory diseases. Understanding the principles governing neuro-epithelial crosstalk may uncover novel therapeutic strategies to restore tissue homeostasis and treat barrier-associated disorders.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 4","pages":"Article 100363"},"PeriodicalIF":5.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148272434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beyond antibodies: Emerging roles of B cells in gastrointestinal inflammation and disease. 超越抗体：B细胞在胃肠道炎症和疾病中的新角色。

IF 5.5 2区医学

Mucosal Immunology Pub Date : 2026-07-25 DOI: 10.1016/j.mucimm.2026.100390

Marina Costa Fujishima, Jing Ouyang, Thomas T Murooka, Deanna M Santer

引用次数: 0

Adaptive immune responses against Lachnospiraceae-derived flagellins and their role in inflammatory bowel disease. 针对毛螺杆菌衍生鞭毛蛋白的适应性免疫反应及其在炎症性肠病中的作用。

IF 5.5 2区医学

Mucosal Immunology Pub Date : 2026-06-22 DOI: 10.1016/j.mucimm.2026.100365

Daniëlle M H Barendregt, Qing Zhao, Janneke N Samsom, Charles O Elson

引用次数: 0

Inhaled Acinetobacter lwoffii exposure promotes lung PD-L1+ neutrophils and dampens viral-induced type 2 immunity 吸入不动杆菌lwoffii暴露促进肺PD-L1+中性粒细胞和抑制病毒诱导的2型免疫。

IF 7.6 2区医学

Mucosal Immunology Pub Date : 2026-06-01 Epub Date: 2026-02-27 DOI: 10.1016/j.mucimm.2026.02.007

Kunyuan Tian , Lucia Labeur-Iurman , Simone A. Walker , Dimple Zope , Erika von Mutius , James A. Harker , Clare M. Lloyd , Sejal Saglani

引用次数: 0

Macrophage SIRT6 promotes allergic airway inflammation through ATG3 deacetylation-mediated autophagy 巨噬细胞SIRT6通过ATG3去乙酰化介导的自噬促进过敏性气道炎症。

IF 7.6 2区医学

Mucosal Immunology Pub Date : 2026-06-01 Epub Date: 2026-03-19 DOI: 10.1016/j.mucimm.2026.03.009

Yuting Lei , Zhilin Xiong , Mengting Zhang , Shihai Li , Guomei Su , Ruina Huang , Jielin Duan , Xiao Gao , Tianwen Lai

{"title":"Macrophage SIRT6 promotes allergic airway inflammation through ATG3 deacetylation-mediated autophagy","authors":"Yuting Lei , Zhilin Xiong , Mengting Zhang , Shihai Li , Guomei Su , Ruina Huang , Jielin Duan , Xiao Gao , Tianwen Lai","doi":"10.1016/j.mucimm.2026.03.009","DOIUrl":"10.1016/j.mucimm.2026.03.009","url":null,"abstract":"<div><div>Chronic airway inflammation is a central driver of asthma pathogenesis, in which macrophages play a pivotal role. While autophagy is known to regulate macrophage function, the specific molecular mechanisms linking autophagy to allergic airway inflammation remain unclear. Here, we identify macrophage sirtuin 6 (SIRT6) as a critical regulator of autophagy and allergic inflammation in asthma. SIRT6 expression was elevated in lung tissues and macrophages from asthmatic mice. Myeloid-specific <em>Sirt6</em> deletion attenuated allergic airway inflammation in asthma murine model. Mechanistically, SIRT6 promoted proinflammatory cytokine expression via autophagy-related 3 (ATG3)-mediated autophagy in macrophages. We further demonstrated that SIRT6 directly bound to ATG3 and deacetylated it at lysine 77 (K77), a modification required for driving the proinflammatory response. Importantly, pharmacological inhibition of SIRT6 with OSS_128167 suppressed macrophage autophagy and alleviated allergic inflammation. Our findings establish SIRT6 as a key promoter of allergic airway inflammation through ATG3 deacetylation and enhanced autophagy in macrophages, highlighting SIRT6 inhibition as a potential novel therapeutic strategy for asthma.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 3","pages":"Article 100335"},"PeriodicalIF":7.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147494052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Androgens protect ILC2S from functional suppression during influenza virus infection 雄激素保护ILC2S免受流感病毒感染时的功能抑制。

IF 7.6 2区医学

Mucosal Immunology Pub Date : 2026-06-01 Epub Date: 2026-03-27 DOI: 10.1016/j.mucimm.2026.03.011

Sapana Kadel , Reegan A.J. Miller , Anna Karlik , Abigael P. Williams , Sean Turner , Erola Ainsua-Enrich , Ibrahim Hatipoglu , Joshua W. Garton , Richard Pelikan , Harini Bagavant , José Alberola-Ila , Susan Kovats

{"title":"Androgens protect ILC2S from functional suppression during influenza virus infection","authors":"Sapana Kadel , Reegan A.J. Miller , Anna Karlik , Abigael P. Williams , Sean Turner , Erola Ainsua-Enrich , Ibrahim Hatipoglu , Joshua W. Garton , Richard Pelikan , Harini Bagavant , José Alberola-Ila , Susan Kovats","doi":"10.1016/j.mucimm.2026.03.011","DOIUrl":"10.1016/j.mucimm.2026.03.011","url":null,"abstract":"<div><div>Biological sex differences in morbidity upon influenza A virus (IAV) infection are linked to stronger IFN-centered immune responses in females, yet the regulatory role of sex steroid receptors in immune cell subsets is incompletely understood. Lung-resident group 2 innate lymphoid cells (ILC2s) express notably high levels of androgen receptors (AR). In IAV infection, ILC2s produce type 2 cytokines and facilitate tissue repair, but they also may be functionally suppressed by type 1 cytokines. Here, we report sex differences in the magnitude of ILC2 functional suppression at the peak of sublethal IAV infection. Relative to males, ILC2s in females show attenuated proliferation, decreased propensity for IL-5 and amphiregulin production, and reduced expression of GATA3 and IL-33R, features supported by divergent transcriptomes. Equivalent inflammatory cytokine levels and viral load suggested sex differences in ILC2-intrinsic factors. Indeed, naïve female ILC2s showed elevated IFNGR expression and higher phospho-STAT1 levels following IFNγ stimulation, and lymphocyte-restricted STAT1 deficiency reversed IAV-induced suppression of female ILC2s. ILC2-restricted AR deficiency increased IFNGR expression and loss of androgens via orchiectomy led to suppression of male ILC2s. Thus, ILC2-intrinsic AR activity attenuates IFNGR-STAT1 signaling pathways to preserve canonical ILC2 function in males during IAV infection.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 3","pages":"Article 100337"},"PeriodicalIF":7.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147574521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential effects of SARS-CoV-2-targeted infection of ATII, club cells, and macrophages on lung immunopathology and antiviral responses sars - cov -2靶向ATII、俱乐部细胞和巨噬细胞感染对肺免疫病理和抗病毒反应的差异影响

IF 7.6 2区医学

Mucosal Immunology Pub Date : 2026-06-01 Epub Date: 2026-04-06 DOI: 10.1016/j.mucimm.2026.04.001

Austin W. Todd , Sergey A. Shein , Anna A. Korchagina , Vasily A. Kudinov , Brianna N. Faz , Ramya S. Barre , Raehum Paik , Emma C. Collins , Kizil A. Yusoof , Ishana Khetarpal , Korri S. Weldon , Zhao Lai , Dias Kurmashev , Jordi B. Torrelles , Elizabeth A. Leadbetter , Yan Xiang , Yidong Chen , Luis Martinez-Sobrido , Ekaterina Koroleva , Alexei V. Tumanov

{"title":"Differential effects of SARS-CoV-2-targeted infection of ATII, club cells, and macrophages on lung immunopathology and antiviral responses","authors":"Austin W. Todd , Sergey A. Shein , Anna A. Korchagina , Vasily A. Kudinov , Brianna N. Faz , Ramya S. Barre , Raehum Paik , Emma C. Collins , Kizil A. Yusoof , Ishana Khetarpal , Korri S. Weldon , Zhao Lai , Dias Kurmashev , Jordi B. Torrelles , Elizabeth A. Leadbetter , Yan Xiang , Yidong Chen , Luis Martinez-Sobrido , Ekaterina Koroleva , Alexei V. Tumanov","doi":"10.1016/j.mucimm.2026.04.001","DOIUrl":"10.1016/j.mucimm.2026.04.001","url":null,"abstract":"<div><div>The specific contributions of lung epithelial and immune cells to SARS-CoV-2–induced immunopathology and antiviral responses remain unclear. To address this, we generated mouse models with inducible expression of human angiotensin-converting enzyme 2 (hACE2) in specific lung cell types. Infection of mice expressing hACE2 on club cells triggered early type I interferon responses, limited viral replication, and caused transient, mild lung pathology. In contrast, hACE2-driven infection of type II alveolar epithelial cells (ATIIs) resulted in higher viral loads and moderate lung damage, accompanied by expansion of interstitial macrophages, virus-specific CD8<sup>+</sup> T cell responses, and production of anti-SARS-CoV-2 IgG. Additionally, infection of mice expressing hACE2 on ATIIs increased CD11c<sup>+</sup> CD8<sup>+</sup> effector T cells and proinflammatory cytokines in the lungs, including IFN-γ, CXCL9, and CXCL10. However, neutralization of CXCL9 and CXCL10 exacerbated disease severity. Moreover, infection of mice with hACE2 targeted to ATIIs and macrophages led to severe lung injury, increased viral burden, enhanced T-cell and neutrophil infiltration, higher IgG responses, and sustained lung pathology. In contrast, hACE2 expression limited to endothelial cells was insufficient to promote SARS-CoV-2 replication in the lung or cause pathology. Together, these findings demonstrate that ACE2-driven infection of ATIIs, club cells, and macrophages plays distinct but cooperative roles in driving SARS-CoV-2-induced lung immunopathology and antiviral immunity.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 3","pages":"Article 100340"},"PeriodicalIF":7.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147639341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Allergic lung inflammation can be modulated by niacin and drives the development of glycolytic eosinophils 变应性肺部炎症可由烟酸调节，并驱动糖酵解嗜酸性粒细胞的发展。

IF 7.6 2区医学

Mucosal Immunology Pub Date : 2026-06-01 Epub Date: 2026-03-28 DOI: 10.1016/j.mucimm.2026.03.013

Rossana Azzoni , Kara J. Filbey , Maria Z. Krauss , Matthew R. Hepworth , Joanne E. Konkel , Edith M. Hessel , Yashaswini Kannan , Nicola L. Harris , John R. Grainger

{"title":"Allergic lung inflammation can be modulated by niacin and drives the development of glycolytic eosinophils","authors":"Rossana Azzoni , Kara J. Filbey , Maria Z. Krauss , Matthew R. Hepworth , Joanne E. Konkel , Edith M. Hessel , Yashaswini Kannan , Nicola L. Harris , John R. Grainger","doi":"10.1016/j.mucimm.2026.03.013","DOIUrl":"10.1016/j.mucimm.2026.03.013","url":null,"abstract":"<div><div>Eosinophils are key contributors to allergic pathology, however, increasingly eosinophils are described to have important roles in organ health and immunoregulation. The factors that define and regulate these diverse eosinophil functions remain poorly understood. Here we show the emergence of a lung-specific Siglec-F<sup>hi</sup> inflammatory eosinophil subset that exhibits high glycolytic activity, mTOR activation and increased amino acid and glucose uptake. The emergence of glycolytic Siglec-F<sup>hi</sup> inflammatory eosinophils was apparent in the lung in multiple models of type 2 inflammation and in response to influenza infection. Siglec-F<sup>hi</sup> eosinophils present in the lung during allergic inflammation also expressed the niacin and butyrate receptor GPR109A and were niacin responsive. These findings reveal a unique metabolic phenotype of activated lung eosinophils and reveal niacin-GPR109A signaling as a regulator of allergic type 2 immune responses.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 3","pages":"Article 100339"},"PeriodicalIF":7.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Autoantibodies induced by Mycoplasma pneumoniae infection underlie the severity of acute lung injury in children 肺炎支原体感染诱导的自身抗体是儿童急性肺损伤严重程度的基础。

IF 7.6 2区医学

Mucosal Immunology Pub Date : 2026-06-01 Epub Date: 2026-03-21 DOI: 10.1016/j.mucimm.2026.03.008

Haoying Huang , Xiaoping Yuan , Sen Li , Qiong Zi , Chen Liu , Kuimiao Deng , Haiyan Liu , Xuehua Xu , Wanli Liu , Jingyou Yu , Gen Lu , Xiaohui Wang

{"title":"Autoantibodies induced by Mycoplasma pneumoniae infection underlie the severity of acute lung injury in children","authors":"Haoying Huang , Xiaoping Yuan , Sen Li , Qiong Zi , Chen Liu , Kuimiao Deng , Haiyan Liu , Xuehua Xu , Wanli Liu , Jingyou Yu , Gen Lu , Xiaohui Wang","doi":"10.1016/j.mucimm.2026.03.008","DOIUrl":"10.1016/j.mucimm.2026.03.008","url":null,"abstract":"<div><div><em>Mycoplasma pneumoniae</em> (MP) infection directly damages lung tissue and triggers dysregulated immune responses, yet the immunopathology underlying the severe pneumonia remains unknown. Here we analyzed cellular and molecular features in the peripheral blood and bronchoalveolar lavage fluid from patients to define the systemic immune landscape associates with severity of MP pneumonia (MPP). Cytokine and cellular profiling found severe MPP is associated with type I inflammation potentiated by γδ T and NK T cells. Severe MPP patients were found to have significantly enriched autoantibodies targeting non-protein antigens such as double-stranded DNA, phosphatidylserine and cardiolipin, and a broad panel of peptide antigen such as Cullin 4B (CUL4B), a core component of the Cullin-RING ligase 4B (CRL4B) E3 ubiquitin ligase complex. Mechanistically, we identified elevated plasma cells correlating with increased autoantibody levels, as well as disease severity. These findings suggest a potential association between cellular immune responses and autoantibody generation, advancing our understanding of MPP pathogenesis and revealing novel potential therapeutic targets.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 3","pages":"Article 100334"},"PeriodicalIF":7.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0