Mucosal Immunology最新文献

{"title":"Activation of the SST-SSTR5 signaling pathway enhances corneal wound healing in diabetic mice","authors":"","doi":"10.1016/j.mucimm.2024.06.002","DOIUrl":"10.1016/j.mucimm.2024.06.002","url":null,"abstract":"<div><div>Corneal wound healing in diabetic patients is usually delayed and accompanied by excessive inflammation. However, the underlying cellular and molecular mechanisms remain poorly understood. Here, we found that somatostatin (SST), an immunosuppressive peptide produced by corneal nerve fibers, was significantly reduced in streptozotocin-induced diabetic mice. In addition, we discovered that topical administration of exogenous SST significantly improved re-epithelialization and nerve regeneration following diabetic corneal epithelial abrasion. Further analysis showed that topical SST significantly reduced the expression of injury inflammation-related genes, inhibited neutrophil infiltration, and shifted macrophage polarization from pro-inflammatory M1 to anti-inflammatory M2 in diabetic corneas' healing. Moreover, the application of L-817,818, an agonist of the SST receptor type 5 subtype, significantly reduced the inflammatory response following epithelial injury and markedly improved the process of re-epithelialization and nerve regeneration in mice. Taken together, these data suggest that activation of the SST-SST receptor type 5 pathway significantly ameliorates diabetes-induced abnormalities in corneal wound repair in mice. Targeting this pathway may provide a novel strategy to restore impaired corneal wound closure and nerve regeneration in diabetic patients.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141311210","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":"Cell type-specific modulation of metabolic, immune-regulatory, and anti-microbial pathways by CD101","authors":"","doi":"10.1016/j.mucimm.2024.06.004","DOIUrl":"10.1016/j.mucimm.2024.06.004","url":null,"abstract":"<div><div>T lymphocytes and myeloid cells express the immunoglobulin-like glycoprotein cluster of differentiation (CD)101, notably in the gut. Here, we investigated the cell-specific functions of CD101 during dextran sulfate sodium (DSS)-induced colitis and <em>Salmonella enterica</em> Typhimurium infection. Similar to conventional CD101^−/− mice, animals with a regulatory T cell-specific <em>Cd101</em> deletion developed more severe intestinal pathology than littermate controls in both models. While the accumulation of T helper 1 cytokines in a CD101-deficient environment entertained DSS-induced colitis, it impeded the replication of <em>Salmonella</em> as revealed by studying CD101^−/− x interferon-g^−/− mice. Moreover, CD101-expressing neutrophils were capable to restrain <em>Salmonella</em> infection <em>in vitro</em> and <em>in vivo</em>. Both cell-intrinsic and -extrinsic mechanisms of CD101 contributed to the control of bacterial growth and spreading. The CD101-dependent containment of <em>Salmonella</em> infection required the expression of <em>Irg-1</em> and <em>Nox2</em> and the production of itaconate and reactive oxygen species. The level of intestinal microbial antigens in the sera of inflammatory bowel disease patients correlated inversely with the expression of CD101 on myeloid cells, which is in line with the suppression of CD101 seen in mice following DSS application or <em>Salmonella</em> infection. Thus, depending on the experimental or clinical setting, CD101 helps to limit inflammatory insults or bacterial infections due to cell type-specific modulation of metabolic, immune-regulatory, and anti-microbial pathways.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141432276","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":"Human intestinal stromal cells promote homeostasis in normal mucosa but inflammation in Crohn’s disease in a retinoic acid–deficient manner","authors":"","doi":"10.1016/j.mucimm.2024.06.009","DOIUrl":"10.1016/j.mucimm.2024.06.009","url":null,"abstract":"<div><div>Intestinal stromal cells (SCs), which synthesize the extracellular matrix that gives the mucosa its structure, are newly appreciated to play a role in mucosal inflammation. Here, we show that human intestinal vimentin⁺CD90⁺smooth muscle actin⁻ SCs synthesize retinoic acid (RA) at levels equivalent to intestinal epithelial cells, a function in the human intestine previously attributed exclusively to epithelial cells. Crohn’s disease SCs (Crohn’s SCs), however, synthesized markedly less RA than SCs from healthy intestine (normal SCs). We also show that microbe-stimulated Crohn’s SCs, which are more inflammatory than stimulated normal SCs, induced less RA-regulated differentiation of mucosal dendritic cells (DCs) (circulating pre-DCs and monocyte-derived DCs), leading to the generation of more potent inflammatory interferon-γ^hi/interleukin-17^hi T cells than normal SCs. Explaining these results, Crohn’s SCs expressed more DHRS3, a retinaldehyde reductase that inhibits retinol conversion to retinal and, thus, synthesized less RA than normal SCs. These findings uncover a microbe–SC–DC crosstalk in which luminal microbes induce Crohn’s disease SCs to initiate and perpetuate inflammation through impaired synthesis of RA.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141469516","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":"Impaired neutrophil migration underpins host susceptibility to infectious colitis","authors":"","doi":"10.1016/j.mucimm.2024.06.008","DOIUrl":"10.1016/j.mucimm.2024.06.008","url":null,"abstract":"<div><div><em>Citrobacter rodentium</em> models infection with enteropathogenic <em>Escherichia coli</em> and ulcerative colitis (UC). While C57BL/6 (C57) mice recover, C3H/HeN (C3H) mice succumb to infection, partially due to increased colonic neutrophil elastase activity, also seen in UC patients; however, the underlying cause was unknown. Here, we found that bone marrow, blood, and colonic C57 neutrophils expressed (CD)11b^Hi and reached the infected colonic lumen, where they underwent productive NETosis. In contrast, while the number of C3H neutrophils increased in the bone marrow, blood, and colon, they remained CD11b^Lo and got trapped in the submucosa, away from <em>C. rodentium</em>, where they underwent harmful NETosis. CD11b^Lo neutrophils in C3H mice infected with CR_i9, which triggers expression of neutrophil chemoattractants, reached the colonization site, resulting in host survival. UC patient neutrophils also displayed decreased levels of the activation/differentiation markers CD16/CXCR4. These results, suggesting that neutrophil malfunction contributes to exacerbated colitis, provide insight for future therapeutic prospects.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141469517","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":"Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis","authors":"","doi":"10.1016/j.mucimm.2024.05.007","DOIUrl":"10.1016/j.mucimm.2024.05.007","url":null,"abstract":"<div><div><em>Mycobacterium tuberculosis</em> (Mtb)-infected neutrophils are often found in the airways of patients with active tuberculosis (TB), and excessive recruitment of neutrophils to the lung is linked to increased bacterial burden and aggravated pathology in TB. The basis for the permissiveness of neutrophils for Mtb and the ability to be pathogenic in TB has been elusive. Here, we identified metabolic and functional features of neutrophils that contribute to their permissiveness in Mtb infection. Using single-cell metabolic and transcriptional analyses, we found that neutrophils in the Mtb-infected lung displayed elevated mitochondrial metabolism, which was largely attributed to the induction of activated neutrophils with enhanced metabolic activities. The activated neutrophil subpopulation was also identified in the lung granulomas from Mtb-infected non-human primates. Functionally, activated neutrophils harbored more viable bacteria and displayed enhanced lipid uptake and accumulation. Surprisingly, we found that interferon-γ promoted the activation of lung neutrophils during Mtb infection. Lastly, perturbation of lipid uptake pathways selectively compromised Mtb survival in activated neutrophils. These findings suggest that neutrophil heterogeneity and metabolic diversity are key to their permissiveness for Mtb and that metabolic pathways in neutrophils represent potential host-directed therapeutics in TB.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141284213","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":"Atopic dermatitis and food allergy: More than sensitization","authors":"","doi":"10.1016/j.mucimm.2024.06.005","DOIUrl":"10.1016/j.mucimm.2024.06.005","url":null,"abstract":"<div><div>The increased risk of food allergy in infants with atopic dermatitis (AD) has long been recognized; an epidemiologic phenomenon termed “the atopic march.” Current literature supports the hypothesis that food antigen exposure through the disrupted skin barrier in AD leads to food antigen-specific immunoglobulin E production and food sensitization. However, there is growing evidence that inflammation in the skin drives intestinal remodeling via circulating inflammatory signals, microbiome alterations, metabolites, and the nervous system. We explore how this skin-gut axis helps to explain the link between AD and food allergy beyond sensitization.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141437253","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":"Regulatory T cells restrict immunity and pathology in distal tissue sites following a localized infection","authors":"","doi":"10.1016/j.mucimm.2024.06.007","DOIUrl":"10.1016/j.mucimm.2024.06.007","url":null,"abstract":"<div><div>Regulatory T cells (Tregs) are well-known to mediate peripheral tolerance at homeostasis, and there is a growing appreciation for their role in modulating infectious disease immunity. Following acute and chronic infections, Tregs can restrict pathogen-specific T cell responses to limit immunopathology. However, it is unclear if Tregs mediate control of pathology and immunity in distal tissue sites during localized infections. We investigated the role of Tregs in immunity and disease in various tissue compartments in the context of “mild” vaginal Zika virus infection. We found that Tregs are critical to generating robust virus-specific CD8 T cell responses in the initial infection site. Further, Tregs limit inflammatory cytokines and immunopathology during localized infection; a dysregulated immune response in Treg-depleted mice leads to increased T cell infiltrates and immunopathology in both the vagina and the central nervous system (CNS). Importantly, these CNS infiltrates are not present at the same magnitude during infection of Treg-sufficient mice, in which there is no CNS immunopathology. Our data suggest that Tregs are necessary to generate a robust virus-specific response at the mucosal site of infection, while Treg-mediated restriction of bystander inflammation limits immunopathology both at the site of infection as well as distal tissue sites.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141440697","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":"Inflammation of the nasal mucosa is associated with susceptibility to experimental pneumococcal challenge in older adults","authors":"","doi":"10.1016/j.mucimm.2024.06.010","DOIUrl":"10.1016/j.mucimm.2024.06.010","url":null,"abstract":"<div><div><em>Streptococcus pneumoniae</em> colonization in the upper respiratory tract is linked to pneumococcal disease development, predominantly affecting young children and older adults. As the global population ages and comorbidities increase, there is a heightened concern about this infection. We investigated the immunological responses of older adults to pneumococcal-controlled human infection by analyzing the cellular composition and gene expression in the nasal mucosa. Our comparative analysis with data from a concurrent study in younger adults revealed distinct gene expression patterns in older individuals susceptible to colonization, highlighted by neutrophil activation and elevated levels of CXCL9 and CXCL10. Unlike younger adults challenged with pneumococcus, older adults did not show recruitment of monocytes into the nasal mucosa following nasal colonization. However, older adults who were protected from colonization showed increased degranulation of cluster of differentiation 8+ T cells, both before and after pneumococcal challenge. These findings suggest age-associated cellular changes, in particular enhanced mucosal inflammation, that may predispose older adults to pneumococcal colonization.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476988","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":"Git2 deficiency promotes MDSCs recruitment in intestine via NF-κB-CXCL1/CXCL12 pathway and ameliorates necrotizing enterocolitis","authors":"Huijuan Le ,&nbsp;Yanyan Wang ,&nbsp;Jiefei Zhou ,&nbsp;Dan Li ,&nbsp;Zizhen Gong ,&nbsp;Fangxinxing Zhu ,&nbsp;Jian Wang ,&nbsp;Chunyan Tian ,&nbsp;Wei Cai ,&nbsp;Jin Wu","doi":"10.1016/j.mucimm.2024.07.006","DOIUrl":"10.1016/j.mucimm.2024.07.006","url":null,"abstract":"<div><div>Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease in preterm infants and the most common cause of neonatal death, whereas the molecular mechanism of intestinal injury remains unclear accompanied by deficiency of effective therapeutic approaches. GIT2 (G-protein-coupled receptor kinase interacting proteins 2) can affect innate and adaptive immunity and has been involved in multiple inflammatory disorders. In this study, we investigated whether GIT2 participates in the pathogenesis of NEC. Here we found that intestinal <em>Git2</em> gene expression was significantly increased in NEC patients and NEC mice, which positively correlated with the tissue damage severity, and <em>Git2</em> deficiency could potently protect against NEC development in mice. Mechanistically, <em>Git2</em> gene knockout dramatically increased the recruitment of MDSCs in the intestine, and <em>in vivo</em> depletion of MDSCs almost completely abrogated the protective effect of <em>Git2</em> deficiency on NEC. Moreover, <em>Git2</em> deficiency induced MDSCs intestinal accumulation mainly relied on CXCL1/CXCL12 signaling, as evidenced by the significant increment of CXCL1 and CXCL12 levels in intestinal epithelium of <em>Git2</em>^-/- mice and dramatically decrease of MDSCs accumulation in intestine as well as increase of NEC severity upon treatment of CXCL1/CXCL12 pathway inhibitors. In addition, <em>Git2</em> deficiency induced up-regulation of CXCL1 and CXCL12 is at least partially mediated through activating NF-κB signaling. Thus, our findings suggest that GIT2 is involved in the pathogenesis of NEC, and targeting GIT2 may be a potential preventive and therapeutic approach for NEC.</div></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792938","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":"Inducible pluripotent stem cells to study human mast cell trajectories","authors":"Gila Idelman ,&nbsp;Christian F. Rizza ,&nbsp;Sahiti Marella ,&nbsp;Ankit Sharma ,&nbsp;Somdutta Chakraborty ,&nbsp;Hock L. Tay ,&nbsp;Sunil Tomar ,&nbsp;Varsha Ganesan ,&nbsp;Charles F. Schuler IV ,&nbsp;James R. Baker ,&nbsp;Simon P. Hogan","doi":"10.1016/j.mucimm.2024.07.003","DOIUrl":"10.1016/j.mucimm.2024.07.003","url":null,"abstract":"&lt;div&gt;&lt;div&gt;Mast cells (MCs) are derived from CD34&lt;sup&gt;+&lt;/sup&gt; hematopoietic progenitors, consist of different subtypes, and are involved in several inflammatory conditions. However, our understanding of human MC developmental trajectories and subtypes has been limited by a scarcity of suitable cellular model systems. Herein, we developed an &lt;em&gt;in vitro&lt;/em&gt; model of human MC differentiation from induced pluripotent stem cells (iPSC) to study human MC differentiation trajectories. Flow cytometry characterization of hemopoietic cells derived from the myeloid cells-forming complex (MCFC) revealed an initial increase in Lin&lt;sup&gt;-&lt;/sup&gt; CD34&lt;sup&gt;+&lt;/sup&gt; hematopoietic progenitors within Weeks 1–3, followed by an increase in CD34&lt;sup&gt;-&lt;/sup&gt; CD45RA&lt;sup&gt;-&lt;/sup&gt; SSC&lt;sup&gt;l&lt;/sup&gt;&lt;sup&gt;ow&lt;/sup&gt; and SSC&lt;sup&gt;high&lt;/sup&gt; hematopoietic cells. The Lin&lt;sup&gt;-&lt;/sup&gt; CD34&lt;sup&gt;+&lt;/sup&gt; hematopoietic progenitors consisted of SSC&lt;sup&gt;low&lt;/sup&gt; CD45RA&lt;sup&gt;-&lt;/sup&gt; CD123&lt;sup&gt;±&lt;/sup&gt; c-Kit&lt;sup&gt;+&lt;/sup&gt; FcεRI&lt;sup&gt;+&lt;/sup&gt; populations that were β7-integrin&lt;sup&gt;high&lt;/sup&gt; CD203c&lt;sup&gt;+&lt;/sup&gt; and β7-integrin&lt;sup&gt;high&lt;/sup&gt; CD203c&lt;sup&gt;-&lt;/sup&gt; cells consistent with CMP&lt;sup&gt;Fc&lt;/sup&gt;&lt;sup&gt;ε&lt;/sup&gt;&lt;sup&gt;RI+&lt;/sup&gt; cells. Flow cytometry and cytologic analyses of the CD34&lt;sup&gt;-&lt;/sup&gt; Lin&lt;sup&gt;-&lt;/sup&gt; (SSC&lt;sup&gt;low&lt;/sup&gt;) population revealed hypogranular cell populations, predominantly characterized by CD45RA&lt;sup&gt;-&lt;/sup&gt; CD123&lt;sup&gt;±&lt;/sup&gt; c-Kit&lt;sup&gt;+&lt;/sup&gt; FcεRI&lt;sup&gt;-&lt;/sup&gt; β7-integrin&lt;sup&gt;low&lt;/sup&gt; and CD45RA&lt;sup&gt;-&lt;/sup&gt; CD123&lt;sup&gt;±&lt;/sup&gt; c-Kit&lt;sup&gt;-&lt;/sup&gt; FcεRI&lt;sup&gt;+&lt;/sup&gt; β7-integrin&lt;sup&gt;Mid&lt;/sup&gt; cells. Analyses of hypergranular SSC&lt;sup&gt;high&lt;/sup&gt; cells identified Lin&lt;sup&gt;-&lt;/sup&gt; CD34&lt;sup&gt;-&lt;/sup&gt; CD45RA&lt;sup&gt;-&lt;/sup&gt; c-Kit&lt;sup&gt;+&lt;/sup&gt; FcεRI&lt;sup&gt;-&lt;/sup&gt; and Lin&lt;sup&gt;-&lt;/sup&gt; CD34&lt;sup&gt;-&lt;/sup&gt; CD45RA&lt;sup&gt;-&lt;/sup&gt; c-Kit&lt;sup&gt;+&lt;/sup&gt; FcεRI&lt;sup&gt;+&lt;/sup&gt; cells. scRNA-seq analysis of the cells harvested at week 4 of the MCFC culture revealed the presence of monocyte and granulocyte progenitors (n = 547 cells, 26.7 %), Erythrocyte / unknown (n = 85, 4.1 %), neutrophils / myelocytes (n = 211 cells, 10.2 %), mast cell progenitor 1 (n = 599, 29.1 %), mast cell progenitor 2 (n = 152, 7.4 %), committed mast cell precursor (n = 113, 5.5 %), and MCs (n = 353, 17.1 %). In silico analyses of the MC precursor and mature MC populations revealed transcriptionally distinct MC precursor subtype and mature MC states (CMA1&lt;sup&gt;+&lt;/sup&gt; and CMA1&lt;sup&gt;-&lt;/sup&gt; subtypes). Culturing MC precursor populations in MC maturation media (mast cell media II) led to homogenous mature MC populations as evidenced by high expression of high-affinity IgE receptor, metachromatic granules, presence of MC granule proteins (Tryptase and Chymase) and activation following substance P stimulation and FcεRI crosslinking. This human iPSC-based approach generates MC precursors and phenotypically mature and functional MC populations. This system will be a useful model to generate human MC populations and broaden our understanding of MC biology and transcr","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748611","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}