Mucosal Immunology最新文献_第7页

Lifelong partners: Gut microbiota-immune cell interactions from infancy to old age. 终生伙伴：从婴儿到老年，肠道微生物群与免疫细胞之间的相互作用。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2025-01-23 DOI: 10.1016/j.mucimm.2025.01.006

Julia A Brown, Hilal Bashir, Melody Y Zeng

{"title":"Lifelong partners: Gut microbiota-immune cell interactions from infancy to old age.","authors":"Julia A Brown, Hilal Bashir, Melody Y Zeng","doi":"10.1016/j.mucimm.2025.01.006","DOIUrl":"10.1016/j.mucimm.2025.01.006","url":null,"abstract":"<p><p>Our immune system and gut microbiota are intricately coupled from birth, both going through maturation during early life and senescence during aging almost in a synchronized fashion. The symbiotic relationship between the human host and microbiota is critically dependent on a healthy immune system to keep our microbiota in check, while the microbiota provides essential functions to promote the development and fitness of our immune system. The partnership between our immune system and microbiota is particularly important during early life, when microbial ligands and metabolites shape the development of the immune cells and immune tolerance; during aging, having sufficient beneficial gut bacteria is critical for the maintenance of intact mucosal barriers, immune metabolic fitness, and strong immunity against pathogens. The immune system during childhood is programmed, with the support of the microbiota, to develop robust immune tolerance, and limit autoimmunity and metabolic dysregulation, which are prevalent during aging. This review comprehensively explores the mechanistic underpinnings of gut microbiota-immune cell interactions during infancy and old age, with the goal to gain a better understanding of potential strategies to leverage the gut microbiota to combat age-related immune decline.</p>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":" ","pages":""},"PeriodicalIF":7.9,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143040338","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

Immune crosstalk between respiratory and intestinal mucosal tissues in respiratory infections. 呼吸道感染中呼吸道和肠粘膜组织间的免疫串扰。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2025-01-02 DOI: 10.1016/j.mucimm.2024.12.013

Min Zhao, Lei Zhou, Shuo Wang

引用次数: 0

Deciphering the therapeutic potential of Myeloid-Specific JAK2 inhibition in acute respiratory distress syndrome 解读髓系特异性 JAK2 抑制在急性呼吸窘迫综合征中的治疗潜力

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.008

Shupei Gao , Wenjuan Li , Zhiwen Huang , Jeffrey A. Deiuliis , Zachary Braunstein , Xinxin Liu , Xinlu Li , Mohammadreza Kosari , Jun Chen , Xinwen Min , Handong Yang , Quan Gong , Zheng Liu , Yingying Wei , Ziyang Zhang , Lingli Dong , Jixin Zhong

{"title":"Deciphering the therapeutic potential of Myeloid-Specific JAK2 inhibition in acute respiratory distress syndrome","authors":"Shupei Gao , Wenjuan Li , Zhiwen Huang , Jeffrey A. Deiuliis , Zachary Braunstein , Xinxin Liu , Xinlu Li , Mohammadreza Kosari , Jun Chen , Xinwen Min , Handong Yang , Quan Gong , Zheng Liu , Yingying Wei , Ziyang Zhang , Lingli Dong , Jixin Zhong","doi":"10.1016/j.mucimm.2024.08.008","DOIUrl":"10.1016/j.mucimm.2024.08.008","url":null,"abstract":"<div><div>Acute respiratory distress syndrome (ARDS) is a life-threatening condition characterized by severe inflammation and pulmonary dysfunction. Despite advancements in critical care, effective pharmacological interventions for ARDS remain elusive. While Janus kinase 2 (JAK2) inhibitors have emerged as an innovative treatment for numerous autoinflammatory diseases, their therapeutic potential in ARDS remains unexplored. In this study, we investigated the contribution of JAK2 and its underlying mechanisms in ARDS utilizing myeloid-specific JAK2 knockout murine models alongside a pharmacological JAK2 inhibitor. Notably, myeloid-specific JAK2 knockout led to a notable attenuation of ARDS induced by intratracheal administration of LPS, accompanied by reduced levels of neutrophils and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and lung tissue. Intriguingly, the ameliorative effects were abolished upon the depletion of monocyte-derived alveolar macrophages (Mo-AMs) rather than tissue-resident alveolar macrophages (TR-AMs). JAK2 deficiency markedly reversed LPS-induced activation of STAT5 in macrophages. Remarkably, pharmacological JAK2 inhibition using baricitinib failed to substantially alleviate neutrophils infiltration, implying that specific inhibition of JAK2 in Mo-AMs is imperative for ARDS amelioration. Collectively, our data suggest that JAK2 may mitigate ARDS progression through the JAK2 pathway in Mo-AMs, underscoring JAK2 in alveolar macrophages, particularly Mo-AMs, as a promising therapeutic target for ARDS treatment.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1273-1284"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142036439","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

Distinct cell death pathways induced by granzymes collectively protect against intestinal Salmonella infection 颗粒酶诱导的不同细胞死亡途径共同抵御肠道沙门氏菌感染。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.006

Amanpreet Singh Chawla , Maud Vandereyken , Maykel Arias , Llipsy Santiago , Dina Dikovskaya , Chi Nguyen , Neema Skariah , Nicolas Wenner , Natasha B. Golovchenko , Sarah J. Thomson , Edna Ondari , Marcela Garzón-Tituaña , Christopher J. Anderson , Megan Bergkessel , Jay C. D. Hinton , Karen L. Edelblum , Julian Pardo , Mahima Swamy

{"title":"Distinct cell death pathways induced by granzymes collectively protect against intestinal Salmonella infection","authors":"Amanpreet Singh Chawla , Maud Vandereyken , Maykel Arias , Llipsy Santiago , Dina Dikovskaya , Chi Nguyen , Neema Skariah , Nicolas Wenner , Natasha B. Golovchenko , Sarah J. Thomson , Edna Ondari , Marcela Garzón-Tituaña , Christopher J. Anderson , Megan Bergkessel , Jay C. D. Hinton , Karen L. Edelblum , Julian Pardo , Mahima Swamy","doi":"10.1016/j.mucimm.2024.08.006","DOIUrl":"10.1016/j.mucimm.2024.08.006","url":null,"abstract":"<div><div>Intestinal intraepithelial T lymphocytes (IEL) constitutively express high amounts of the cytotoxic proteases Granzymes (Gzm) A and B and are therefore thought to protect the intestinal epithelium against infection by killing infected epithelial cells. However, the role of IEL granzymes in a protective immune response has yet to be demonstrated. We show that GzmA and GzmB are required to protect mice against oral, but not intravenous, infection with <em>Salmonella enterica</em> serovar Typhimurium<em>,</em> consistent with an intestine-specific role. IEL-intrinsic granzymes mediate the protective effects by controlling intracellular bacterial growth and aiding in cell-intrinsic pyroptotic cell death of epithelial cells. Surprisingly, we found that both granzymes play non-redundant roles. <em>GzmB<sup>-/-</sup></em> mice carried significantly lower burdens of <em>Salmonella</em>, as predominant GzmA-mediated cell death effectively reduced bacterial translocation across the intestinal barrier. Conversely, in <em>GzmA<sup>-/-</sup></em> mice, GzmB-driven apoptosis favored luminal <em>Salmonella</em> growth by providing nutrients, while still reducing translocation across the epithelial barrier. Together, the concerted actions of both GzmA and GzmB balance cell death mechanisms at the intestinal epithelium to provide optimal control that <em>Salmonella</em> cannot subvert.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1242-1255"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141976178","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

Dietary fiber promotes antigen presentation on intestinal epithelial cells and development of small intestinal CD4+CD8αα+ intraepithelial T cells 膳食纤维可促进肠上皮细胞的抗原呈递和小肠 CD4+CD8αα+ 上皮内 T 细胞的发育。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.010

Naomi Rodriguez-Marino , Charlotte J. Royer , Dormarie E. Rivera-Rodriguez , Emma Seto , Isabelle Gracien , Rheinallt M. Jones , Christopher D. Scharer , Adam D. Gracz , Luisa Cervantes-Barragan

{"title":"Dietary fiber promotes antigen presentation on intestinal epithelial cells and development of small intestinal CD4+CD8αα+ intraepithelial T cells","authors":"Naomi Rodriguez-Marino , Charlotte J. Royer , Dormarie E. Rivera-Rodriguez , Emma Seto , Isabelle Gracien , Rheinallt M. Jones , Christopher D. Scharer , Adam D. Gracz , Luisa Cervantes-Barragan","doi":"10.1016/j.mucimm.2024.08.010","DOIUrl":"10.1016/j.mucimm.2024.08.010","url":null,"abstract":"<div><div>The impact of dietary fiber on intestinal T cell development is poorly understood. Here we show that a low fiber diet reduces MHC-II antigen presentation by small intestinal epithelial cells (IECs) and consequently impairs development of CD4<sup>+</sup>CD8αα<sup>+</sup> intraepithelial lymphocytes (DP IELs) through changes to the microbiota. Dietary fiber supports colonization by Segmented Filamentous Bacteria (SFB), which induces the secretion of IFNγ by type 1 innate lymphoid cells (ILC1s) that lead to MHC-II upregulation on IECs. IEC MHC-II expression caused either by SFB colonization or exogenous IFNγ administration induced differentiation of DP IELs. Finally, we show that a low fiber diet promotes overgrowth of <em>Bifidobacterium pseudolongum</em>, and that oral administration of <em>B. pseudolongum</em> reduces SFB abundance in the small intestine. Collectively we highlight the importance of dietary fiber in maintaining the balance among microbiota members that allow IEC MHC-II antigen presentation and define a mechanism of microbiota-ILC-IEC interactions participating in the development of intestinal intraepithelial T cells.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1301-1313"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145986","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

Sensory neuroimmune interactions at the barrier 屏障上的感官神经免疫相互作用

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.10.001

Zhen Wang , Keaton Song , Brian S. Kim , John Manion

引用次数: 0

Dynamic regulation of innate lymphoid cell development during ontogeny 先天性淋巴细胞在本体发育过程中的动态调控

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.009

Tao Wu , Sijie Chen , Xinyi Zhu , Jie Ma , Maocai Luo , Yuanhao Wang , Yujie Tian , Qingqing Sun , Xiaohuan Guo , Jianhong Zhang , Xuegong Zhang , Yunping Zhu , Li Wu

{"title":"Dynamic regulation of innate lymphoid cell development during ontogeny","authors":"Tao Wu , Sijie Chen , Xinyi Zhu , Jie Ma , Maocai Luo , Yuanhao Wang , Yujie Tian , Qingqing Sun , Xiaohuan Guo , Jianhong Zhang , Xuegong Zhang , Yunping Zhu , Li Wu","doi":"10.1016/j.mucimm.2024.08.009","DOIUrl":"10.1016/j.mucimm.2024.08.009","url":null,"abstract":"<div><div>The helper-like ILC contains various functional subsets, such as ILC1, ILC2, ILC3 and LTi cells, mediating the immune responses against viruses, parasites, and extracellular bacteria, respectively. Among them, LTi cells are also crucial for the formation of peripheral lymphoid tissues, such as lymph nodes. Our research, along with others’, indicates a high proportion of LTi cells in the fetal ILC pool, which significantly decreases after birth. Conversely, the proportion of non-LTi ILCs increases postnatally, corresponding to the need for LTi cells to mediate lymphoid tissue formation during fetal stages and other ILC subsets to combat diverse pathogen infections postnatally. However, the regulatory mechanism for this transition remains unclear. In this study, we observed a preference for fetal ILC progenitors to differentiate into LTi cells, while postnatal bone marrow ILC progenitors preferentially differentiate into non-LTi ILCs. Particularly, this differentiation shift occurs within the first week after birth in mice. Further analysis revealed that adult ILC progenitors exhibit stronger activation of the Notch signaling pathway compared to fetal counterparts, accompanied by elevated <em>Gata3</em> expression and decreased <em>Rorc</em> expression, leading to a transition from fetal LTi cell-dominant states to adult non-LTi ILC-dominant states. This study suggests that the body can regulate ILC development by modulating the activation level of the Notch signaling pathway, thereby acquiring different ILC subsets to accommodate the varying demands within the body at different developmental stages.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1285-1300"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142004854","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

Dysregulated NOX1-NOS2 activity as hallmark of ileitis in mice NOX1-NOS2 活性失调是小鼠回肠炎的标志。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.012

Julie Drieu La Rochelle , Josie Ward , Emily Stenke , Yuting Yin , Misaki Matsumoto , Richard Jennings , Gabriella Aviello , Ulla G. Knaus

{"title":"Dysregulated NOX1-NOS2 activity as hallmark of ileitis in mice","authors":"Julie Drieu La Rochelle , Josie Ward , Emily Stenke , Yuting Yin , Misaki Matsumoto , Richard Jennings , Gabriella Aviello , Ulla G. Knaus","doi":"10.1016/j.mucimm.2024.08.012","DOIUrl":"10.1016/j.mucimm.2024.08.012","url":null,"abstract":"<div><div>Inflammation of the ileum, or ileitis, is commonly caused by Crohn’s disease (CD) but can also accompany ulcerative colitis (backwash ileitis), infections or drug-related damage. Oxidative tissue injury triggered by reactive oxygen species (ROS) is considered part of the ileitis etiology. However, not only elevated ROS but also permanently decreased ROS are associated with inflammatory bowel disease (IBD). While very early onset IBD (VEO-IBD) is associated with a spectrum of <em>NOX1</em> variants, how NOX1 inactivation contributes to disease development remains ill-defined. Besides propagating signaling responses, NOX1 provides superoxide for peroxynitrite formation in the epithelial barrier. Here we report that NOX4, an H<sub>2</sub>O<sub>2</sub>-generating NADPH oxidase with documented tissue protective effects in the intestine and other tissues, limits the generation of ileal peroxynitrite by NOX1/NOS2. Deletion of NOX4 leads to persistent peroxynitrite excess, hyperpermeability, villus blunting, muscular hypertrophy, chemokine/cytokine upregulation and dysbiosis. Conversely, SAMP1/YitFc mice, a CD-like ileitis model, showed age-dependent NOX1/NOS2 downregulation preventing ileal peroxynitrite formation in homeostasis and LPS-induced acute inflammation. Deficiency in NOX1 correlated with the upregulation of antimicrobial peptides, suggesting that ileal peroxynitrite acts as chemical barrier and microbiota modifier in the ileum.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1326-1336"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142154590","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

Exposure to bacterial PAMPs before RSV infection exacerbates innate inflammation and disease via IL-1α and TNF-α 在感染 RSV 之前接触细菌 PAMPs 会通过 IL-1α 和 TNF-α 加剧先天性炎症和疾病。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.002

Amber R. Owen , Ana Farias , Anne-Marie Levins , Ziyin Wang , Sophie L. Higham , Matthias Mack , John S. Tregoning , Cecilia Johansson

{"title":"Exposure to bacterial PAMPs before RSV infection exacerbates innate inflammation and disease via IL-1α and TNF-α","authors":"Amber R. Owen , Ana Farias , Anne-Marie Levins , Ziyin Wang , Sophie L. Higham , Matthias Mack , John S. Tregoning , Cecilia Johansson","doi":"10.1016/j.mucimm.2024.08.002","DOIUrl":"10.1016/j.mucimm.2024.08.002","url":null,"abstract":"<div><div>Respiratory syncytial virus (RSV) can cause severe lower respiratory tract infections. Understanding why some individuals get more serious disease may help with diagnosis and treatment. One possible risk factor underlying severe disease is bacterial exposure before RSV infection. Bacterial exposure has been associated with increased respiratory viral-induced disease severity but the mechanism remains unknown. Respiratory bacterial infections or exposure to their pathogen associated molecular patterns (PAMPs) trigger innate immune inflammation, characterised by neutrophil and inflammatory monocyte recruitment and the production of inflammatory cytokines. We hypothesise that these changes to the lung environment alter the immune response and disease severity during subsequent RSV infection. To test this, we intranasally exposed mice to LPS, LTA or <em>Acinetobacter baumannii</em> (an airway bacterial pathogen) before RSV infection and observed an early induction of disease, measured by weight loss, at days 1–3 after infection. Neutrophils or inflammatory monocytes were not responsible for driving this exacerbated weight loss. Instead, exacerbated disease was associated with increased IL-1α and TNF-α, which orchestrated the recruitment of innate immune cells into the lung. This study shows that exposure to bacterial PAMPs prior to RSV infection increases the expression of IL-1α and TNF-α, which dysregulate the immune response resulting in exacerbated disease.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1184-1198"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11631774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141913316","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

Conserved B cell signaling, activation, and differentiation in porcine jejunal and ileal Peyer’s patches despite distinct immune landscapes 猪空肠和回肠佩耶氏斑块的 B 细胞信号传导、激活和分化是一致的，尽管它们的免疫环境各不相同。

IF 7.9 2区医学

Mucosal Immunology Pub Date : 2024-12-01 DOI: 10.1016/j.mucimm.2024.08.005

Jayne E. Wiarda , Adrienne L. Shircliff , Sage R. Becker , Judith B. Stasko , Sathesh K. Sivasankaran , Mark R. Ackermann , Crystal L. Loving

{"title":"Conserved B cell signaling, activation, and differentiation in porcine jejunal and ileal Peyer’s patches despite distinct immune landscapes","authors":"Jayne E. Wiarda , Adrienne L. Shircliff , Sage R. Becker , Judith B. Stasko , Sathesh K. Sivasankaran , Mark R. Ackermann , Crystal L. Loving","doi":"10.1016/j.mucimm.2024.08.005","DOIUrl":"10.1016/j.mucimm.2024.08.005","url":null,"abstract":"<div><div>Peyer’s patches (PPs) are B cell-rich sites of intestinal immune induction, yet PP-associated B cell signaling, activation, and differentiation are poorly defined. Single-cell and spatial transcriptomics were completed to study B cells from porcine jejunum and ileum containing PPs. Intestinal locations had distinct immune landscapes, including more follicular B cells in ileum and increased MHC-II-encoding gene expression in jejunal B cells. Despite distinct landscapes, conserved B cell dynamics were detected across intestinal locations, including B cell signaling to <em>CD4<sup>+</sup></em> macrophages that are putative phagocytic, cytotoxic, effector cells and deduced routes of B cell activation/differentiation, including resting B cells migrating into follicles to replicate/divide or differentiate into antibody-secreting cells residing in intestinal crypts. A six-biomarker panel recapitulated transcriptomics findings of B cell phenotypes, frequencies, and spatial locations via <em>ex vivo</em> and <em>in situ</em> staining. Findings convey conserved B cell dynamics across intestinal locations containing PPs, despite location-specific immune environments. Results establish a benchmark of B cell dynamics for understanding intestinal immune induction important to promoting gut/overall health.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":"17 6","pages":"Pages 1222-1241"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141988354","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