Mucosal Immunology最新文献

{"title":"IL-13 driven tuft cell hyperplasia is suppressed by retinoic acid in chronic rhinosinusitis with nasal polyps.","authors":"Michael A Kohanski, Li Hui Tan, Deepa Keshari, Cailu Lin, Nithin D Adappa, James N Palmer, Jennifer E Douglas, Danielle R Reed, Noam A Cohen","doi":"10.1016/j.mucimm.2026.100421","DOIUrl":"https://doi.org/10.1016/j.mucimm.2026.100421","url":null,"abstract":"<p><p>Tuft cells are specialized chemosensory epithelial cells that contribute to mucosal immunity, yet how their differentiation is regulated in human airway disease remains unclear. Chronic rhinosinusitis with nasal polyps(CRSwNP) features type 2 inflammation and expansion of sinonasal tuft cells, consistent with type 2 cytokine-driven epithelial remodeling. Using primary human sinonasal epithelial air-liquid interface cultures, we examined tuft cell differentiation across disease phenotypes. IL-13-induced expansion of POU2F3⁺ tuft cells and generated a BMX⁺ subset consistent with a mature or activated phenotype. These IL-13 activated cultures exhibited enhanced responsiveness to chemosensory ligands such as succinate and denatonium, indicating functional activation. Surprisingly, IL-13-driven sinonasal tuft cell differentiation occurred despite inhibition of STAT6 and ERK signaling, suggesting involvement of noncanonical pathways. Retinoic acid(RA) emerged as a selective regulator of tuft cell differentiation specifically in CRSwNP. RA did not alter STAT6 phosphorylation or canonical IL-13-responsive gene expression, indicating that RA suppresses tuft cell differentiation through distinct mechanisms. These findings highlight a noncanonical pathway of IL-13-mediated tuft cell expansion and identify retinoic acid as a context-dependent regulator of tuft cell differentiation in the airway. These findings demonstrate methods to regulate human sinonasal tuft cell differentiation across disease phenotypes, opening avenues for tuft cell-targeted therapeutic strategies.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":"100421"},"PeriodicalIF":5.5,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224504","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}

{"title":"Allergen-induced trained immunity in alveolar macrophages predisposes to long-lasting airway hypersensitivity.","authors":"Lin Tong, Wenjun Song, Lin Su, Mengyao Li, Jing He, Lingman Dai, Huihan Li, Xiling Wu, Qiannan Zhao, Xiaodie Shen, Yuanyuan Zhang, Yushi Yao, Qingqing Wang, Zhimin Chen","doi":"10.1016/j.mucimm.2026.100411","DOIUrl":"https://doi.org/10.1016/j.mucimm.2026.100411","url":null,"abstract":"<p><p>Allergic asthma is characterized by airway hypersensitivity to various allergens and chronic airway inflammation. The mechanisms underlying such a prolonged and broad-responsive airway hypersensitivity remain not fully understood. In this study, we systematically investigated the role of allergen-induced trained immunity in tissue resident alveolar macrophages (AMs) and its impact on long-lasting airway hypersensitivity. Here, we utilized flow cytometry and single-cell transcriptomics to analyze immune cell dynamics in murine asthma model, and we compare the differences between allergen-experienced AMs and naïve AMs. Specifically, we introduce and delve into the concept of allergen-induced trained immunity within these particular cells (Trained alveolar macrophages, Tr-AMs). Our findings demonstrated that Tr-AMs preferentially produce pro-eosinophilic chemokines upon subsequent allergen exposure and, therefore, induce exacerbated eosinophilic inflammation in the lung. The induction of Tr-AMs was potentially associated with their interactions with other immune cells, such as natural killer cells, dendritic cells, and Th2 cells. Both IFN-γ and IL-4 are critical for AM activation, we found that their simultaneous action on AMs induced the development of an MHCII⁺ CD206⁺ Tr-AM phenotype, which was specialized in producing pro-eosinophilic chemokines, including CCL24 (eotaxin-2) and CCL5 (RANTES). This study highlights the establishment and roles of Tr-AMs in pro-asthmatic airway hypersensitivity, providing a new understanding of the pathogenesis and recurrence of allergic asthma.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":"100411"},"PeriodicalIF":5.5,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166920","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}

{"title":"Autoimmune CD4⁺T cells cause Meibomian gland dysfunction in an adoptive transfer model.","authors":"Kaitlin K Scholand, Paola A Guevara Montoya, Emre Aksan, Yangluowa Qu, Sean Paiboonfungfuang, Laura Schaefer, Elizaveta A Demianova, Elaine Vo, Sudhir Verma, Elle Joy J San Juan, Zhiyuan Yu, Tarsis F Gesteira, Vivien J Coulson-Thomas, Cintia S de Paiva","doi":"10.1016/j.mucimm.2026.100419","DOIUrl":"10.1016/j.mucimm.2026.100419","url":null,"abstract":"<p><p>Sjögren disease (SjD) is an autoimmune disease driven by autoimmune CD4⁺T cells that leads to an immune-mediated loss of lacrimal glands (LG). Meibomian glands are lipid-producing glands in the eyelids that help prevent tear evaporation. While the role of T cells in LG-mediated destruction is well established, it is unknown whether pathogenic T cells can cause MG dysfunction (MGD). Herein, we investigated whether autoimmune CD4⁺T cells induce MGD and characterized the pathophysiologic mechanisms using an adoptive transfer model. T cells were isolated from CD25KO (KO^CD4) or wild-type (WT^CD4) mice and transferred into Rag1KO mice. In comparison, KO cells were co-adoptively transferred with WT regulatory T cells (KO^CD4 + WT^Tregs). Our results demonstrate that CD25KO CD4⁺T recipients had MG dropout, CD4⁺IFN-γ⁺ infiltration, increased MHC II presentation within the periglandular area, MG fibrosis, decreased lipid production, and upregulation of pathways related to inflammation, including Type II interferon signaling. Rag1KO, WT^CD4, and KO^CD4 + WT^Tregs recipients exhibited minimal inflammation in the periglandular MG area. These results indicate that autoimmune CD4⁺T cells are sufficient to cause MGD, and healthy young regulatory T cells can prevent T-cell-mediated damage. Our findings provide mechanistic insights into the pathogenesis of autoimmune SjD and could impact how patients are managed in the clinic.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":"100419"},"PeriodicalIF":5.5,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149137815","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}

{"title":"Kinetics of local C3 production orchestrates neutrophil recruitment in lung injury.","authors":"Rafael Aponte Alburquerque, Josue I Hernandez, Aasritha Nallapu, Marick Starick, Jungheun Hyun, John Michael Sanchez, Neelou Etesami, Sandip K Mukherjee, Ayse Naz Ozanturk, Jose Vazquez, Allison Chang, Ashley Zheng, Lorena Garnica, Alberto E Lopez, Andrew E Gelman, John A Belperio, Jae Woo Lee, Devesha H Kulkarni, Alexander Hoffmann, Hrishikesh S Kulkarni","doi":"10.1016/j.mucimm.2026.100412","DOIUrl":"10.1016/j.mucimm.2026.100412","url":null,"abstract":"<p><p>Complement component 3 (C3) is crucial for host defense against bacteria. While the liver is the primary source of circulating C3, local C3 production at barrier surfaces such as the lung is key in early responses. Yet, how local complement-mediated responses are initiated at mucosal barriers-and how locally-derived C3 functions distinctly from its established cytoprotective role-is unknown. This study investigates the kinetics and necessity of lung-derived C3 during the initial hours of an infection. Leveraging models of bacterial pneumonia in ex vivo-perfused human lungs and mice deficient in liver-derived C3, we demonstrate that intrapulmonary C3 production and activation precedes the accumulation of circulating C3 into the bronchoalveolar space. Utilizing conditional knockout mice, we demonstrate that lung epithelial cell-derived C3 is required for early neutrophil recruitment in pneumonia. C3-mediated early neutrophil recruitment depends on a local C3a-C3aR axis that increases epithelial CXCL1 and CXCL2 production and occurs without any difference in epithelial injury, revealing that this activity is mechanistically different from its cytoprotective function. Collectively, our study demonstrates that an initial, entirely local phase of complement-mediated mucosal protection is critical for host defense during lung injury, before alveolar-capillary barrier disruption results in a subsequent, systemic response.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":"100412"},"PeriodicalIF":5.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112290","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}

{"title":"Mechanisms of CD4⁺T tolerance to a corneal epithelial neoantigen.","authors":"Jeremias G Galletti, Kaitlin K Scholand, Jianming Shao, Eric P Fujisaki, Prashant Kumar, Elizaveta A Demianova, Elle Joy J San Juan, Laura Schaefer, Cintia S de Paiva","doi":"10.1016/j.mucimm.2026.100418","DOIUrl":"10.1016/j.mucimm.2026.100418","url":null,"abstract":"<p><p>Tissue-specific peripheral tolerance mechanisms are essential to prevent autoimmunity. The cornea is immune privileged, and anterior chamber-associated immune deviation (ACAID) governs its inner surface. However, the mechanisms governing corneal epithelial (outer surface) antigens remain unknown. Using an inducible, cornea-restricted neoantigen mouse model, we found that tolerance of corneal epithelial antigens is associated with antigen-specific regulatory T cell (Treg) induction. Although the cornea is both avascular and alymphatic, its epithelial antigens are still efficiently presented by ocular surface-derived antigen-presenting cells to T cells in draining lymph nodes under homeostatic conditions, leading to conventional antigen-specific Treg expansion without ocular pathology. This tolerance was not absolute: systemic immunization redirected antigen-specific responses toward pathogenic effector T cells that disrupted epithelial barrier function. These findings identify Treg induction and anergy as mechanisms linked to corneal epithelial immune homeostasis and demonstrate that inflammatory priming can render a previously tolerated corneal antigen into an autoimmune target, providing mechanistic insight into ocular surface disease pathogenesis.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":"100418"},"PeriodicalIF":5.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112221","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}

{"title":"Uterine monocytes and macrophages: New insight into their pivotal homeostatic inflammatory role during reproductive life.","authors":"Isabel M Paterson, Catriona I Laverty, John D Aplin, Elizabeth R Mann","doi":"10.1016/j.mucimm.2026.100409","DOIUrl":"10.1016/j.mucimm.2026.100409","url":null,"abstract":"<p><p>The repeated (menstrual) cycles of tissue proliferation, differentiation, degradation and shedding in the lining of the uterus (endometrium) make this arguably the most dynamic tissue of the body in the steady state. Many of the tissue processes involved resemble those occurring during wound repair, in which there is a wealth of knowledge regarding the contributions of macrophages to tissue remodelling in other tissues. In addition, several inflammatory events also regulate tissue integrity in the uterus including apoptosis, alongside numerous inflammatory myeloid-specific cytokines peaking during the window for embryo implantation. We discuss the key roles that both monocytes and the macrophages that they differentiate into play in regulating tissue integrity in the uterus during the menstrual cycle, and the relevance to reproductive physiology. We describe inflammatory and repair processes, which monocyte or macrophage subsets may be responsible, and at which point of the menstrual cycle. An understanding of macrophage biology in the uterus and their contributions to tissue physiology is essential for understanding the pathophysiology of reproductive diseases that contribute to infertility and pregnancy complications.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":"100409"},"PeriodicalIF":5.5,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112405","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}

{"title":"Mucin degradation by Akkermansia muciniphila promotes Alistipes-dependent tryptophan metabolism and Th17-driven autoimmunity","authors":"Xun Lin,&nbsp;Ankita Singh,&nbsp;Xindi Shan,&nbsp;Suzanne Tawch,&nbsp;Isabel Sakarin,&nbsp;Tej Bahadur,&nbsp;Nancy McLinskey,&nbsp;Patricia Melville,&nbsp;Bettina C. Fries,&nbsp;Patricia K. Coyle,&nbsp;James Collins,&nbsp;Andriy Morgun,&nbsp;Natalia Shulzhenko,&nbsp;Jessica Seeliger,&nbsp;Timothy W. Hand,&nbsp;Lijun Xia,&nbsp;Olga Syritsyna,&nbsp;Pawan Kumar","doi":"10.1016/j.mucimm.2026.100377","DOIUrl":"10.1016/j.mucimm.2026.100377","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is an autoimmune disorder of the central nervous system associated with alterations in gut commensals, including <em>Akkermansia muciniphila</em> (<em>A. muciniphila</em>). However, its role in MS remains unclear. Here, we report elevated serum lipopolysaccharide (LPS) and anti-LPS IgG levels in patients with relapsing-remitting MS (RRMS), indicating compromised gut barrier integrity. Notably, RRMS patients also exhibited increased serum anti-<em>A. muciniphila</em> IgA and enhanced <em>A. muciniphila</em>-induced Th17 responses in peripheral blood mononuclear cells (PBMCs). Using experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, we found that <em>A. muciniphila</em> colonization worsened EAE severity, with increased infiltration of GM-CSF⁺CD4⁺ and IL-17A⁺CD4⁺ T cells in spinal cord. Mechanistically, <em>A. muciniphila</em> colonization enhanced tryptophan metabolism and elevated levels of aryl hydrocarbon receptor (AhR) agonists, including indole derivatives, during EAE. Although <em>A. muciniphila</em> does not directly metabolize tryptophan, it promotes expansion of tryptophan-utilizing bacterium <em>Alistipes onderdonkii</em> (<em>A. onderdonkii</em>) through mucin degradation. We further demonstrate that <em>A. onderdonkii</em> utilizes mucin-derived metabolites, including galactose and <em>N</em>-acetylneuraminic acid (NANA). Importantly, dietary tryptophan restriction significantly attenuated EAE severity. Collectively, these findings reveal a cross-feeding mechanism in which <em>A. muciniphila</em> supports growth of <em>A. onderdonkii</em>, thereby enhancing microbial tryptophan metabolism and production of AhR agonists that drive Th17-mediated neuroinflammation.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 5","pages":"Article 100377"},"PeriodicalIF":5.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13488615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148387799","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}

{"title":"Gammaherpesvirus infection impairs lung fibrosis resolution through PD-L1+ fibroblasts and PD-1+ CD8+ T cell interaction","authors":"Laura Kempen,&nbsp;Domien Vanneste,&nbsp;Justine Javaux,&nbsp;Lorène Dams,&nbsp;Rémy Sandor,&nbsp;Malyvanh Pathammavong,&nbsp;Lele Han,&nbsp;Marjo Donners,&nbsp;Elias Wieland,&nbsp;Marion Gijbels,&nbsp;Marie-Alice Meuwis,&nbsp;Edouard Louis,&nbsp;Moritz Reif,&nbsp;Martina Balsamo,&nbsp;Mika Rohlfing,&nbsp;Dimitri Kasakovski,&nbsp;Erik Biessen,&nbsp;Thomas Marichal,&nbsp;Pieter Goossens,&nbsp;Bénédicte Machiels","doi":"10.1016/j.mucimm.2026.100388","DOIUrl":"10.1016/j.mucimm.2026.100388","url":null,"abstract":"<div><div>Pulmonary fibrosis is a complex disease with poorly understood, multifactorial triggers. Gammaherpesviruses (γHVs), including <em>Epstein-Barr virus</em> in humans and <em>Murid herpesvirus 4</em> (MuHV-4) in mice, have been linked to pulmonary fibrosis exacerbation, although the underlying mechanisms remain unclear. This study explores how γHV infection modulates bleomycin (bleo)-induced lung fibrosis in mice, using flow cytometry and multiplex spectral immunofluorescence (MSI) to analyze cell dynamics, localization, and intercellular crosstalk. Despite the substantial contribution of monocytes (MOs) to the alveolar macrophage (AM) pool following MuHV-4 infection, these cells do not exhibit overt profibrotic properties upon bleo treatment. In contrast, MuHV-4 infection led to the accumulation of activated, IFNγ-producing memory CD8⁺ T cells in the lungs of bleo-treated mice, with MSI revealing their enrichment and colocalization with fibroblasts. Notably, fibroblasts showed increased IFNγ-induced PD-L1 expression, while T cells upregulated PD-1, co-localizing in fibrosis-rich regions. <em>In vivo</em> neutralization of the PD-L1/PD-1 axis after bleo treatment significantly improved the resolution of fibrosis in MuHV-4-infected mice, highlighting the key pathogenic role of this interaction in sequelae persistence. Compared to fibroblasts cocultured with T cells from naïve mice, those cocultured with MuHV-4-induced T cells exhibited significantly increased collagen expression, while this effect was abrogated by PD-1 blockade. Similar results were observed in cocultures of human fibroblasts and CD8⁺ T cells isolated from EBV-infected patients, underscoring the translational potential of these findings. Collectively, our findings identify interactions between PD-1⁺ CD8⁺ T cells and PD-L1⁺ fibroblasts as central drivers of persistent lung fibrosis associated with γHV infection.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 5","pages":"Article 100388"},"PeriodicalIF":5.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148562589","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}

{"title":"BAMBI: A novel regulator of intestinal epithelial integrity in the control of colitis and colon cancer progression","authors":"Marta Muñoz,&nbsp;Luis Gil-de-Gómez,&nbsp;Thais M. Gil,&nbsp;Diego Romero,&nbsp;Paula Pérez-Adrián,&nbsp;Fernando Gallego,&nbsp;Vincenzo Cappitelli,&nbsp;María Luisa Cagigal,&nbsp;José Andrés Vazquez,&nbsp;Juan Ignacio Raba-Díez,&nbsp;María Sauras,&nbsp;Gemma Massonis,&nbsp;María Luisa del Rio,&nbsp;José Ignacio Rodríguez-Barbosa,&nbsp;Iván Gómez,&nbsp;David Merino,&nbsp;Jesús Merino,&nbsp;Victoria Casado-Medrano,&nbsp;Ramón Merino","doi":"10.1016/j.mucimm.2026.100373","DOIUrl":"10.1016/j.mucimm.2026.100373","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease affects approximately 7 million individuals worldwide. Its pathogenesis involves genetic susceptibility, alterations in the gut microbiota, and immune system imbalance, with both innate and adaptive components contributing through aberrant cytokine signaling. The Transforming Growth Factor-β (TGFβ) pathway plays a central role in this context, controlling the differentiation of regulatory T-cells (Tregs) and Th17 lymphocytes within the intestinal mucosa. Given the importance of these populations in maintaining intestinal homeostasis, we investigated the role of the TGFβ inhibitor BAMBI (BMP and Activin Membrane-Bound Inhibitor) in UC progression. In addition, due to the increased risk of colorectal cancer associated with chronic intestinal inflammation, we evaluated the effects of genetic ablation of <em>Bambi</em> (BAMBI-KO) in chronic inflammation-associated colon cancer progression.</div><div>BAMBI expression is predominantly localized in the colonic epithelium, and either its absence or pharmacological inhibition confers protection against Dextran Sodium Sulfate-induced colitis. Mechanistically, this effect is TGFβ-dependent, independent of immune suppression and is associated with enhanced epithelial cell renewal and improved barrier function. Moreover, chronic UC induction in BAMBI-KO mice results in reduced colorectal tumor multiplicity, size and severity. Collectively, these findings identify BAMBI as a critical regulator of intestinal homeostasis and a potential therapeutic target in colorectal disease.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 5","pages":"Article 100373"},"PeriodicalIF":5.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148361617","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}

{"title":"Gone but not forgotten: lung infection history shapes future respiratory immunity","authors":"Alicia Dirlam,&nbsp;Chrysante S. Iliakis,&nbsp;Andreas Wack","doi":"10.1016/j.mucimm.2026.100386","DOIUrl":"10.1016/j.mucimm.2026.100386","url":null,"abstract":"<div><div>After respiratory infection, the lung does not simply return to the prior baseline but adopts a new distinct post-infection steady state involving durable imprints that can shape tissue responses to subsequent challenges. This review introduces the concept of lung tissue memory, whereby prior infection leaves long-term changes across immune and structural compartments, with consequences for tissue repair and disease severity during later, antigenically distinct challenges. Pre-existing and newly emerging cell populations establish networks of cell-cell crosstalk that can initiate and maintain altered cellular states. We discuss to what degree these persistent adaptations reflect shifts in cellular composition, cell-intrinsic reprogramming, changes in inflammatory tone and altered tissue niches. Finally, we propose that infection-experienced models provide a more translationally relevant framework to understand immune networks operating in the lung during infection in humans, and we present how a better understanding of tissue memory informs therapeutic strategies and improved design of antigen-specific and more broadly protective mucosal vaccines.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"19 5","pages":"Article 100386"},"PeriodicalIF":5.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148471288","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}