Mucosal Immunology最新文献

{"title":"Interleukin-10 production by innate lymphoid cells restricts intestinal inflammation in mice","authors":"Jing Li ,&nbsp;Justin Jacobse ,&nbsp;Jennifer M. Pilat ,&nbsp;Harsimran Kaur ,&nbsp;Weihong Gu ,&nbsp;Seung Woo Kang ,&nbsp;Mark Rusznak ,&nbsp;Hsin-I Huang ,&nbsp;Julio Barrera ,&nbsp;Pauline A. Oloo ,&nbsp;Joseph T. Roland ,&nbsp;Caroline V. Hawkins ,&nbsp;Andrew P. Pahnke ,&nbsp;Marian Khalil ,&nbsp;M.Kay Washington ,&nbsp;Keith T. Wilson ,&nbsp;Christopher S. Williams ,&nbsp;R.Stokes Peebles Jr ,&nbsp;Liza Konnikova ,&nbsp;Yash A. Choksi ,&nbsp;Jeremy A. Goettel","doi":"10.1016/j.mucimm.2025.02.005","DOIUrl":"10.1016/j.mucimm.2025.02.005","url":null,"abstract":"<div><div>Interleukin-10 (IL-10) is an immunomodulatory cytokine critical for intestinal immune homeostasis. IL-10 is produced by various immune cells but IL-10 receptor signaling in intestinal CX₃CR1⁺ mononuclear phagocytes is necessary to prevent spontaneous colitis in mice. Here, we utilized fluorescent protein reporters and cell-specific targeting and found that <em>Rorc</em>-expressing innate lymphoid cells (ILCs) produce IL-10 in response to anti-CD40-mediated intestinal inflammation. Deletion of <em>Il10</em> specifically in <em>Rorc</em>-expressing ILCs led to phenotypic changes in intestinal macrophages and exacerbated both innate and adaptive immune-mediated models of experimental colitis. The population of IL-10⁺ producing ILCs shared markers with both ILC2 and ILC3 with nearly all ILC3s being of the NCR⁺ subtype. Interestingly, <em>Ccl26</em> was enriched in IL-10⁺ ILCs and was markedly reduced in IL-10-deficient ILC3s. Since CCL26 is a ligand for CX₃CR1, we employed RNA <em>in situ</em> hybridization and observed increased numbers of ILCs in close proximity to <em>Cx3cr1</em>-expressing cells under inflammatory conditions. Finally, we generated transgenic <em>Rorc</em>^tdTomato reporter mice that faithfully marked RORγt⁺ cells that could rescue disease pathology and aberrant macrophage phenotype following adoptive transfer into mice with selective <em>Il10</em> deficiency in ILC3s. These results demonstrate that IL-10 production by a population of ILCs functions to promote immune homeostasis in the intestine possibly via direct effects on intestinal macrophages.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 643-655"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483613","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":"Immune crosstalk between respiratory and intestinal mucosal tissues in respiratory infections","authors":"Min Zhao ,&nbsp;Lei Zhou ,&nbsp;Shuo Wang","doi":"10.1016/j.mucimm.2024.12.013","DOIUrl":"10.1016/j.mucimm.2024.12.013","url":null,"abstract":"<div><div>Mucosal tissues, including those in the respiratory and gastrointestinal tracts, are critical barrier surfaces for pathogen invasion. Infections at these sites not only trigger local immune response, but also recruit immune cells from other tissues. Emerging evidence in the mouse models and human samples indicates that the immune crosstalk between the lung and gut critically impacts and determines the course of respiratory disease. Here we summarize the current knowledge of the immune crosstalk between the respiratory and gastrointestinal tracts, and discuss how immune cells are recruited and migrate between these tissues during respiratory infections. We also discuss how commensal bacteria contribute to these processes.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 501-508"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927532","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":"Triggering mouth-resident antiviral CD8+ T cells potentiates experimental periodontitis","authors":"Flávia M. Saavedra ,&nbsp;Danielle B. Brotto ,&nbsp;Vineet Joag ,&nbsp;Courtney A. Matson ,&nbsp;Pavel P. Nesmiyanov ,&nbsp;Mark C. Herzberg ,&nbsp;Vaiva Vezys ,&nbsp;David Masopust ,&nbsp;J. Michael Stolley","doi":"10.1016/j.mucimm.2025.02.003","DOIUrl":"10.1016/j.mucimm.2025.02.003","url":null,"abstract":"<div><div>Emerging evidence indicates that gingival-resident helper CD4⁺ T cells are major drivers of periodontal inflammation in response to commensal and pathogenic oral microorganisms. Whether tissue-resident memory CD8⁺ T cells (T_RM), which principally safeguard against viruses and cancer but also drive certain autoimmune and inflammatory conditions, impact periodontitis progression and severity remain unknown. We asked whether local reactivation of oral CD8⁺ T_RM of a defined antigen specificity could exacerbate ligature-induced periodontitis (LIP), a well-established model of periodontal disease in mice. Topical application of virus-mimicking peptides to the oral mucosa concurrent with LIP 1) intensified alveolar bone loss, 2) amplified gingival and cervical lymph node inflammation, and 3) stimulated gingival transcriptional changes in genes related to innate immune sensing and cell-mediated cytotoxicity. Therapeutic depletion of CD103-expressing oral CD8⁺ T_RM in advance of LIP prevented exacerbation of disease. These observations provide evidence that oral CD103⁺ CD8⁺ T_RM have the potential to participate in gingival inflammation, alveolar bone loss, and periodontitis.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 620-630"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483673","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":"Female sex hormones and the oral contraceptive pill modulate asthma severity through GLUT-1","authors":"Alexandra C. Brown ,&nbsp;Olivia R. Carroll ,&nbsp;Jemma R. Mayall ,&nbsp;Nazanin Zounemat-Kermani ,&nbsp;Samantha L.E. Vinzenz ,&nbsp;Henry M. Gomez ,&nbsp;Ed F. Mills ,&nbsp;Richard Y. Kim ,&nbsp;Chantal Donovan ,&nbsp;Katherine J. Baines ,&nbsp;Evan J. Williams ,&nbsp;Bronwyn S. Berthon ,&nbsp;Katie Wynne ,&nbsp;Hayley A. Scott ,&nbsp;James W. Pinkerton ,&nbsp;Yike Guo ,&nbsp;Philip M. Hansbro ,&nbsp;Paul S. Foster ,&nbsp;Peter A.B. Wark ,&nbsp;Sven-Erik Dahlen ,&nbsp;Jay C. Horvat","doi":"10.1016/j.mucimm.2025.02.006","DOIUrl":"10.1016/j.mucimm.2025.02.006","url":null,"abstract":"<div><div>Females are disproportionately affected by asthma. An increased understanding of how female sex hormones influence key pathophysiological processes that underpin asthma may identify new, more effective asthma therapies, particularly for females with severe, poorly controlled asthma.</div><div>We assessed the effects of oral ethinylestradiol/levonorgestrel (representing OCP use) and depot-medroxyprogesterone acetate (DMPA) and estradiol injections on key features of experimental asthma, and determined their effects on glucose transporter-1 (GLUT-1). The effects of OCP use on clinical asthma outcomes, and the relationships between estrogen receptors and type 2 (T2), non-T2, and GLUT-1 responses, in clinical asthma were also determined.</div><div>OCP and DMPA reduce T2 responses, disease features, and lung expression of GLUT-1, whereas estradiol increases lung expression of GLUT-1, and results in severe, corticosteroid-insensitive, neutrophil-enriched disease, in experimental asthma. OCP use is associated with reduced T2 cytokine and GLUT-1 responses in clinical asthma. GLUT-1 expression is increased in sputum of severe asthmatics, and positively correlates with estrogen receptor expression and both T2 and non-T2 inflammatory responses. Significantly, OCP or GLUT-1 inhibition protects against obesity-associated or estradiol-induced, severe, experimental asthma, respectively.</div><div>Together, these data show how female sex hormones and the OCP likely modulate asthma severity by modifying GLUT-1 responses in the airways.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 656-667"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531659","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":"Antibiotic-induced dysbiosis of the ocular microbiome affects corneal circadian rhythmic activity in mice","authors":"Xinwei Jiao ,&nbsp;Yan Li ,&nbsp;Yu Hu ,&nbsp;Ruyu Yan ,&nbsp;Ting Fu ,&nbsp;Jun Liu ,&nbsp;Zhijie Li","doi":"10.1016/j.mucimm.2025.01.010","DOIUrl":"10.1016/j.mucimm.2025.01.010","url":null,"abstract":"<div><div>The ocular surface microbiota plays a critical role in maintaining corneal homeostasis, but its disruption and subsequent effects on corneal functions remain poorly understood. This study investigates how antibiotic-induced microbial depletion affects the corneal circadian transcriptome in C57BL/6J mice. Dysbiosis was induced using a topical antibiotic cocktail, and RNA sequencing was employed to analyze gene expression across eight time points over 24 h. Antibiotic treatment disrupted corneal circadian rhythms, eliminating rhythmicity in 1,812 genes and introducing rhythmicity in 1,928 previously arrhythmic genes. Furthermore, epithelial adhesion was impaired, inflammation was elevated, and neural sensitivity was reduced. More than 50 % of ocular microbial genera exhibited daily oscillations, with six genera showing significant correlations with corneal rhythmic transcripts. Additionally, the administration of TLR agonists restored circadian gene expression patterns, with partial recovery of corneal barrier function and immune homeostasis, further highlighting the potential of microbiota-targeted therapies in treating ocular surface disorders. These findings underscore the critical role of the ocular microbiota in regulating corneal health and suggest that restoring microbial balance via TLR activation may offer new therapeutic avenues for eye diseases.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 562-582"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374452","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":"Airway epithelial cells as drivers of severe asthma pathogenesis","authors":"Del Dorscheid ,&nbsp;Gail M. Gauvreau ,&nbsp;Steve N. Georas ,&nbsp;Pieter S. Hiemstra ,&nbsp;Gilda Varricchi ,&nbsp;Bart N. Lambrecht ,&nbsp;Gianni Marone","doi":"10.1016/j.mucimm.2025.03.003","DOIUrl":"10.1016/j.mucimm.2025.03.003","url":null,"abstract":"<div><div>Our understanding of the airway epithelium’s role in driving asthma pathogenesis has evolved over time. From being regarded primarily as a physical barrier that could be damaged <em>via</em> inflammation, the epithelium is now known to actively contribute to asthma development through interactions with the immune system. The airway epithelium contains multiple cell types with specialized functions spanning barrier action, mucociliary clearance, immune cell recruitment, and maintenance of tissue homeostasis. Environmental insults may cause direct or indirect injury to the epithelium leading to impaired barrier function, epithelial remodelling, and increased release of inflammatory mediators. In severe asthma, the epithelial barrier repair process is inhibited and the response to insults is exaggerated, driving downstream inflammation. Genetic and epigenetic mechanisms also maintain dysregulation of the epithelial barrier, adding to disease chronicity. Here, we review the role of the airway epithelium in severe asthma and how targeting the epithelium can contribute to asthma treatment.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 524-536"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742558","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":"Tear duct M cells exacerbate allergic conjunctivitis by facilitating germinal-center reactions","authors":"Yuki Oya ,&nbsp;Shunsuke Kimura ,&nbsp;Maho Uemura ,&nbsp;Yumiko Fujimura ,&nbsp;Koji Hase","doi":"10.1016/j.mucimm.2025.01.009","DOIUrl":"10.1016/j.mucimm.2025.01.009","url":null,"abstract":"<div><div>The ocular mucosal surface regularly encounters external materials in the air and tear fluids. Microfold (M) cells, specialized epithelial cells for antigen uptake, are present in tear duct-associated lymphoid tissue (TALT) within the nasolacrimal sac; however, their immunological significance is unclear. We generated <em>Krt5</em>-Cre <em>Tnfrsf11a</em>^flox/flox mice, which lack functional M cells in the TALT, as evidenced by the absence of M-cell markers and reduced nanoparticle uptake. M cell deficiency resulted in fewer T follicular helper (Tfh) and germinal center (GC) B cells in the TALT under steady-state conditions. Upon induction of allergic conjunctivitis, control mice exhibited itching and increased Tfh and immunoglobulin E (IgE⁺) GC B cells in the TALT. However, M cell-deficient mice showed ameliorated allergic symptoms with fewer Tfh and IgE⁺ GC B cells. These findings suggest that M cells in TALT contribute to ocular surface immunosurveillance, whereas, upon allergen exposure, they play a critical role in the development of allergic conjunctivitis.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 549-561"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122946","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":"Spatially separated epithelium-associated and lamina propria neutrophils present distinct functional identities in the inflamed colon mucosa","authors":"Lenore K. Yalom ,&nbsp;Caroline J. Herrnreiter ,&nbsp;Triet M. Bui ,&nbsp;Joey Lockhart ,&nbsp;Enzo B. Piccolo ,&nbsp;Xingsheng Ren ,&nbsp;Cenfu Wei ,&nbsp;Anastasiia Serdiukova ,&nbsp;Edward B. Thorp ,&nbsp;Parambir S. Dulai ,&nbsp;Ronen Sumagin","doi":"10.1016/j.mucimm.2025.02.008","DOIUrl":"10.1016/j.mucimm.2025.02.008","url":null,"abstract":"<div><div>Inflammatory Bowel Disease (IBD) features <em>en masse</em> neutrophil (PMN) infiltration of the colon tissue, where PMNs occupy spatially distinct niches, including the lamina propria mucosa (LPNs) and the crypt epithelium (epithelium-associated neutrophils or EANs). Spatial PMN localization is currently used as a clinical disease scoring parameter, and EAN presence has been correlated with disease severity prognosis and reduced response to therapy. Surprisingly, although PMN heterogeneity and their clinical relevance in IBD is now well-recognized, localization-driven PMN specialization has not been investigated. We found that following initial PMN influx during the active disease phase, EANs were near-completely resolved in both UC remission patients and in murine colitis, whereas LPNs persisted throughout the resolution phase, implicating EANs as likely drivers of disease. Local profiling of transcriptional programs (by murine and human single-cell RNA sequencing, coupled with human spatial RNA transcriptomics) and functional phenotypes, including real-time intravital imaging of murine LPNs versus EANs in inflamed colon revealed LPNs and EANs to have distinct functional identities. LPN programs allowed for heightened motility and pathogen uptake, whereas EANs were overrepresented by hyperactivated/pro-apoptotic states with elevated ROS and inflammatory TNFα production. Thus, we demonstrate that colon LPNs and EANs have distinct functional identities, with EANs exhibiting activated states and apparent cytotoxicity, which may actively contribute to tissue damage. Our findings further identify EANs as potential therapeutic targets for improving mucosal healing and sustaining clinical remission in UC.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 685-699"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586255","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":"Influenza virus-induced type I interferons disrupt alveolar epithelial repair and tight junction integrity in the developing lung","authors":"Abigail P. Onufer ,&nbsp;Joshua Chang Mell ,&nbsp;Laura Cort ,&nbsp;Abhishek Rao ,&nbsp;Nontokozo V. Mdluli ,&nbsp;Alison J. Carey","doi":"10.1016/j.mucimm.2025.02.002","DOIUrl":"10.1016/j.mucimm.2025.02.002","url":null,"abstract":"<div><div>Recently, we demonstrated that influenza A virus (IAV)-infected murine neonates lacking a functional IFN-I receptor (IFNAR^−/−) had significantly improved survival and reduced lung pathology relative to wild-type (WT) neonates. In direct contrast, adult IFNAR^−/− mice display enhanced morbidity following IAV infection relative to WT adults. We hypothesized that IAV-induced IFN-I signaling in primary neonatal type II alveolar epithelial cells (TIIECs), the main cell type of IAV infection and initiator of host response in the lung, contributed to age-specific viral pathogenesis. Multifactorial transcriptional analysis of purified TIIECs revealed age, not infection status, as the primary driver of transcriptional differences in TIIECs. Subsequent pathway analysis demonstrated IAV-infected IFNAR^−/− neonates significantly upregulated cell proliferation, tissue repair and tight junction genes at 2-days post-infection (dpi), compared to WT neonates. Next, to determine if these growth and repair differences persisted later in infection, targeted analysis of repair gene expression and immunofluorescent quantification of pulmonary sealing tight junction molecules ZO-1 and occludin was performed at 6-dpi. Relative to WT neonates, IFNAR^−/− neonates had significantly higher whole lung occludin staining and repair gene expression. Together, our data demonstrates IFN-I signaling is extremely pathogenic in the developing lung by disrupting alveolar repair and pulmonary barrier integrity.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 607-619"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143472767","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":"Hematopoietic MyD88 orchestrates the control of gut colonization by segmented filamentous bacteria","authors":"Marie Cherrier ,&nbsp;Teck Hui Teo ,&nbsp;Renan Oliveira Corrêa ,&nbsp;Marion Picard ,&nbsp;Aurélie Couesnon ,&nbsp;Corinne Lebreton ,&nbsp;Francesco Carbone ,&nbsp;Cécile Masson ,&nbsp;Pamela Schnupf ,&nbsp;Nadine Cerf-Bensussan ,&nbsp;Valérie Gaboriau-Routhiau","doi":"10.1016/j.mucimm.2025.03.002","DOIUrl":"10.1016/j.mucimm.2025.03.002","url":null,"abstract":"<div><h3>Summary</h3><div>Host-microbiota cooperation is critical for successful intestinal homeostasis. The commensal segmented filamentous bacteria (SFB) are crucial for orchestrating the post-natal maturation of the host gut immune system and establishing a healthy state of physiological inflammation, which largely depends on their intimate attachment to the ileal mucosa. However, the signaling pathways used by SFB to induce gut immune responses and how such responses ultimately control SFB colonization remain controversial. Using gnotobiotic approaches, we showed that SFB load is controlled by complex interactions involving the gut microbiota and the host immune system. Therefore, to clearly determine the role of host immune responses induced by SFB in directly controlling their growth, immunodeficient mice monocolonized with SFB were used. Here, we show that in the absence of a complex microbiota, the humoral immune response is dispensable to control SFB growth in the jejunum and ileum, shortly and later after colonization. In contrast, MyD88 signaling in myeloid cells is critical for licensing interleukin (IL)-22 production by type 3 innate lymphoid cells (ILC3) and CD4⁺ T cells, which ultimately limits SFB expansion. Thus, by revisiting the hierarchy of immune mechanisms that directly control SFB growth, our results emphasize the necessary and sufficient role of a hematopoietic MyD88/IL-22 axis.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"18 3","pages":"Pages 717-729"},"PeriodicalIF":7.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143639752","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}