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  1. Article ; Online: Protocols for Studying Murine ILC Development.

    Stier, Matthew T / Peebles, R Stokes

    Methods in molecular biology (Clifton, N.J.)

    2020  Volume 2121, Page(s) 7–22

    Abstract: Understanding the origins and developmental trajectory of innate lymphoid cell (ILC) progenitors has been of substantial interest to the fields of ILC biology and immunology. While mature ILC are rare lymphocytes, ILC progenitors represent an even ... ...

    Abstract Understanding the origins and developmental trajectory of innate lymphoid cell (ILC) progenitors has been of substantial interest to the fields of ILC biology and immunology. While mature ILC are rare lymphocytes, ILC progenitors represent an even smaller fraction of cells, providing additional challenges in studying them. Moreover, though the approaches to studying these cells are conceptually straightforward, the technical nuances that underlie them can substantially affect the quality of the data. Herein, we provide a detailed protocol for assessing the frequency of ILC progenitors in the bone marrow, their phenotype, and their potential to develop into mature ILC. These methods make up the foundation of in vivo investigations into ILC development, and we hope these thorough protocols and associated notes facilitate additional, high-quality inquiries into this fascinating field.
    MeSH term(s) Adoptive Transfer/methods ; Animals ; Bone Marrow ; Bone Marrow Cells/cytology ; Cell Lineage ; Female ; Flow Cytometry ; Killer Cells, Natural/cytology ; Killer Cells, Natural/immunology ; Liver/cytology ; Liver/immunology ; Lymphocytes/cytology ; Lymphocytes/immunology ; Lymphoid Progenitor Cells/cytology ; Lymphoid Progenitor Cells/immunology ; Lymphoid Progenitor Cells/metabolism ; Lymphopoiesis/immunology ; Mice ; Mice, Inbred BALB C
    Language English
    Publishing date 2020-03-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-0338-3_2
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  2. Article ; Online: Host and Viral Determinants of Respiratory Syncytial Virus-induced Airway Mucus.

    Stier, Matthew T / Peebles, R Stokes

    Annals of the American Thoracic Society

    2018  Volume 15, Issue Suppl 3, Page(s) S205–S209

    Abstract: Respiratory syncytial virus (RSV) is a leading cause of hospitalization of infants worldwide each year. Both host and viral factors host factors predispose a subset of what appear to be healthy infants to severe RSV-induced disease. In this review, we ... ...

    Abstract Respiratory syncytial virus (RSV) is a leading cause of hospitalization of infants worldwide each year. Both host and viral factors host factors predispose a subset of what appear to be healthy infants to severe RSV-induced disease. In this review, we outline many genetic and immunologic factors that contribute to airway obstruction that contributes to the severity of RSV infection.
    MeSH term(s) Humans ; Infant ; Mucins/metabolism ; Mucus/physiology ; Respiratory Syncytial Virus Infections/etiology ; Respiratory Syncytial Virus Infections/metabolism ; Respiratory Syncytial Virus Infections/pathology ; Respiratory Syncytial Virus, Human/pathogenicity
    Chemical Substances Mucins
    Language English
    Publishing date 2018-11-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2717461-X
    ISSN 2325-6621 ; 1943-5665 ; 2325-6621
    ISSN (online) 2325-6621 ; 1943-5665
    ISSN 2325-6621
    DOI 10.1513/AnnalsATS.201806-380AW
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  3. Article ; Online: Innate lymphoid cells and allergic disease.

    Stier, Matthew T / Peebles, R Stokes

    Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology

    2017  Volume 119, Issue 6, Page(s) 480–488

    MeSH term(s) Animals ; Cell Differentiation ; Cellular Microenvironment ; Cytokines/metabolism ; Homeostasis ; Humans ; Hypersensitivity/immunology ; Immunity, Innate ; Lymphocytes/immunology ; Th2 Cells/immunology
    Chemical Substances Cytokines
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1228189-x
    ISSN 1534-4436 ; 0003-4738 ; 1081-1206
    ISSN (online) 1534-4436
    ISSN 0003-4738 ; 1081-1206
    DOI 10.1016/j.anai.2017.08.290
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  4. Article ; Online: Immune characterization of a xenogeneic human lung cross-circulation support system.

    Wu, Wei K / Stier, Matthew T / Stokes, John W / Ukita, Rei / Patel, Yatrik J / Cortelli, Michael / Landstreet, Stuart R / Talackine, Jennifer R / Cardwell, Nancy L / Simonds, Elizabeth M / Mentz, Meredith / Lowe, Cindy / Benson, Clayne / Demarest, Caitlin T / Alexopoulos, Sophoclis P / Shaver, Ciara M / Bacchetta, Matthew

    Science advances

    2023  Volume 9, Issue 13, Page(s) eade7647

    Abstract: Improved approaches to expanding the pool of donor lungs suitable for transplantation are critically needed for the growing population with end-stage lung disease. Cross-circulation (XC) of whole blood between swine and explanted human lungs has ... ...

    Abstract Improved approaches to expanding the pool of donor lungs suitable for transplantation are critically needed for the growing population with end-stage lung disease. Cross-circulation (XC) of whole blood between swine and explanted human lungs has previously been reported to enable the extracorporeal recovery of donor lungs that declined for transplantation due to acute, reversible injuries. However, immunologic interactions of this xenogeneic platform have not been characterized, thus limiting potential translational applications. Using flow cytometry and immunohistochemistry, we demonstrate that porcine immune cell and immunoglobulin infiltration occurs in this xenogeneic XC system, in the context of calcineurin-based immunosuppression and complement depletion. Despite this, xenogeneic XC supported the viability, tissue integrity, and physiologic improvement of human donor lungs over 24 hours of xeno-support. These findings provide targets for future immunomodulatory strategies to minimize immunologic interactions on this organ support biotechnology.
    MeSH term(s) Humans ; Swine ; Animals ; Lung ; Lung Transplantation ; Immunosuppression Therapy
    Language English
    Publishing date 2023-03-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.ade7647
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  5. Article ; Online: Polymorphisms in Ly6 genes in Msq1 encoding susceptibility to mouse adenovirus type 1.

    Stier, Matthew T / Spindler, Katherine R

    Mammalian genome : official journal of the International Mammalian Genome Society

    2011  Volume 23, Issue 3-4, Page(s) 250–258

    Abstract: Strain-specific differences in susceptibility to mouse adenovirus type 1 (MAV-1) are linked to the quantitative trait locus Msq1 on mouse chromosome 15. This region contains 14 Ly6 or Ly6-related genes, many of which are known to be expressed on the ... ...

    Abstract Strain-specific differences in susceptibility to mouse adenovirus type 1 (MAV-1) are linked to the quantitative trait locus Msq1 on mouse chromosome 15. This region contains 14 Ly6 or Ly6-related genes, many of which are known to be expressed on the surface of immune cells, suggesting a possible role in host defense. We analyzed these genes for polymorphisms between MAV-1-susceptible and MAV-1-resistant inbred mouse strains. Sequencing of cDNAs identified 12 coding-region polymorphisms in 2010109I03Rik, Ly6e, Ly6a, Ly6c1, and Ly6c2, six of which were nonsynonymous and five of which were previously unlisted in dbSNP Build 132. We also clarified sequence discrepancies in GenBank for the coding regions of I830127L07Rik and Ly6g. Additionally, Southern blotting revealed size polymorphisms within the DNA regions of Ly6e, Ly6a, and Ly6g. Collectively, these genetic variations have implications for the structure, function, and/or expression of Ly6 and Ly6-related genes that may contribute to the observed strain-specific differences in susceptibility to MAV-1.
    MeSH term(s) Adenoviridae/physiology ; Adenoviridae Infections/genetics ; Adenoviridae Infections/veterinary ; Adenoviridae Infections/virology ; Amino Acid Sequence ; Animals ; Antigens, Ly/chemistry ; Antigens, Ly/genetics ; Chromosomes, Mammalian/genetics ; Female ; Genetic Predisposition to Disease ; Male ; Mice/genetics ; Mice/virology ; Mice, Inbred Strains ; Molecular Sequence Data ; Polymorphism, Genetic ; Rodent Diseases/genetics ; Rodent Diseases/virology ; Sequence Alignment
    Chemical Substances Antigens, Ly ; Ly6 protein, mouse
    Language English
    Publishing date 2011-11-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1058547-3
    ISSN 1432-1777 ; 0938-8990
    ISSN (online) 1432-1777
    ISSN 0938-8990
    DOI 10.1007/s00335-011-9368-9
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  6. Article: Polymorphisms in Ly6 genes in Msq1 encoding susceptibility to mouse adenovirus type 1

    Stier, Matthew T / Spindler, Katherine R

    Mammalian genome. 2012 Apr., v. 23, no. 3-4

    2012  

    Abstract: Strain-specific differences in susceptibility to mouse adenovirus type 1 (MAV-1) are linked to the quantitative trait locus Msq1 on mouse chromosome 15. This region contains 14 Ly6 or Ly6-related genes, many of which are known to be expressed on the ... ...

    Abstract Strain-specific differences in susceptibility to mouse adenovirus type 1 (MAV-1) are linked to the quantitative trait locus Msq1 on mouse chromosome 15. This region contains 14 Ly6 or Ly6-related genes, many of which are known to be expressed on the surface of immune cells, suggesting a possible role in host defense. We analyzed these genes for polymorphisms between MAV-1-susceptible and MAV-1-resistant inbred mouse strains. Sequencing of cDNAs identified 12 coding-region polymorphisms in 2010109I03Rik, Ly6e, Ly6a, Ly6c1, and Ly6c2, six of which were nonsynonymous and five of which were previously unlisted in dbSNP Build 132. We also clarified sequence discrepancies in GenBank for the coding regions of I830127L07Rik and Ly6g. Additionally, Southern blotting revealed size polymorphisms within the DNA regions of Ly6e, Ly6a, and Ly6g. Collectively, these genetic variations have implications for the structure, function, and/or expression of Ly6 and Ly6-related genes that may contribute to the observed strain-specific differences in susceptibility to MAV-1.
    Keywords Southern blotting ; chromosomes ; complementary DNA ; genes ; genetic variation ; mice ; quantitative trait loci
    Language English
    Dates of publication 2012-04
    Size p. 250-258.
    Publishing place Springer-Verlag
    Document type Article
    ZDB-ID 1058547-3
    ISSN 1432-1777 ; 0938-8990
    ISSN (online) 1432-1777
    ISSN 0938-8990
    DOI 10.1007/s00335-011-9368-9
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  7. Article ; Online: Group 2 Innate Lymphoid Cells Coordinate Damage Response in the Stomach.

    Meyer, Anne R / Engevik, Amy C / Madorsky, Toni / Belmont, Erika / Stier, Matthew T / Norlander, Allison E / Pilkinton, Mark A / McDonnell, Wyatt J / Weis, Jared A / Jang, Bogun / Mallal, Simon A / Peebles, R Stokes / Goldenring, James R

    Gastroenterology

    2020  Volume 159, Issue 6, Page(s) 2077–2091.e8

    Abstract: Background & aims: Severe injury to the lining of the stomach leads to changes in the epithelium (reprogramming) that protect and promote repair of the tissue, including development of spasmolytic polypeptide-expressing metaplasia (SPEM) and tuft and ... ...

    Abstract Background & aims: Severe injury to the lining of the stomach leads to changes in the epithelium (reprogramming) that protect and promote repair of the tissue, including development of spasmolytic polypeptide-expressing metaplasia (SPEM) and tuft and foveolar cell hyperplasia. Acute gastric damage elicits a type-2 inflammatory response that includes production of type-2 cytokines and infiltration by eosinophils and alternatively activated macrophages. Stomachs of mice that lack interleukin 33 (IL33) or interleukin 13 (IL13) did not undergo epithelial reprogramming after drug-induced injury. We investigated the role of group 2 innate lymphoid cells (ILC2s) in gastric epithelial repair.
    Methods: Acute gastric injury was induced in C57BL/6J mice (wild-type and RAG1 knockout) by administration of L635. We isolated ILC2s by flow cytometry from stomachs of mice that were and were not given L635 and performed single-cell RNA sequencing. ILC2s were depleted from wild-type and RAG1-knockout mice by administration of anti-CD90.2. We assessed gastric cell lineages, markers of metaplasia, inflammation, and proliferation. Gastric tissue microarrays from patients with gastric adenocarcinoma were analyzed by immunostaining.
    Results: There was a significant increase in the number of GATA3-positive ILC2s in stomach tissues from wild-type mice after L635-induced damage, but not in stomach tissues from IL33-knockout mice. We characterized a marker signature of gastric mucosal ILC2s and identified a transcription profile of metaplasia-associated ILC2s, which included changes in expression of Il5, Il13, Csf2, Pd1, and Ramp3; these changes were validated by quantitative polymerase chain reaction and immunocytochemistry. Depletion of ILC2s from mice blocked development of metaplasia after L635-induced injury in wild-type and RAG1-knockout mice and prevented foveolar and tuft cell hyperplasia and infiltration or activation of macrophages after injury. Numbers of ILC2s were increased in stomach tissues from patients with SPEM compared with patients with normal corpus mucosa.
    Conclusions: In analyses of stomach tissues from mice with gastric tissue damage and patients with SPEM, we found evidence of type 2 inflammation and increased numbers of ILC2s. Our results suggest that ILC2s coordinate the metaplastic response to severe gastric injury.
    MeSH term(s) Animals ; Disease Models, Animal ; Gastric Mucosa/drug effects ; Gastric Mucosa/immunology ; Gastric Mucosa/pathology ; Humans ; Immunity, Innate ; Interleukin-33/genetics ; Lymphocyte Subsets/immunology ; Metaplasia/chemically induced ; Metaplasia/genetics ; Metaplasia/immunology ; Mice ; Mice, Knockout
    Chemical Substances Il33 protein, mouse ; Interleukin-33
    Language English
    Publishing date 2020-09-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2020.08.051
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  8. Article ; Online: IL-33 Is a Cell-Intrinsic Regulator of Fitness during Early B Cell Development.

    Stier, Matthew T / Mitra, Ramkrishna / Nyhoff, Lindsay E / Goleniewska, Kasia / Zhang, Jian / Puccetti, Matthew V / Casanova, Holly C / Seegmiller, Adam C / Newcomb, Dawn C / Kendall, Peggy L / Eischen, Christine M / Peebles, R Stokes

    Journal of immunology (Baltimore, Md. : 1950)

    2019  Volume 203, Issue 6, Page(s) 1457–1467

    Abstract: IL-33 is an IL-1 family member protein that is a potent driver of inflammatory responses in both allergic and nonallergic disease. This proinflammatory effect is mediated primarily by extracellular release of IL-33 from stromal cells and binding of the C- ...

    Abstract IL-33 is an IL-1 family member protein that is a potent driver of inflammatory responses in both allergic and nonallergic disease. This proinflammatory effect is mediated primarily by extracellular release of IL-33 from stromal cells and binding of the C-terminal domain of IL-33 to its receptor ST2 on targets such as CD4
    MeSH term(s) Adult ; Animals ; B-Lymphocytes/immunology ; DNA Replication/immunology ; Female ; Humans ; Interleukin-33/immunology ; Leukemia, Lymphocytic, Chronic, B-Cell/immunology ; Male ; Mast Cells/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; RNA, Messenger/immunology ; Signal Transduction/immunology ; Th2 Cells/immunology ; Tumor Suppressor Protein p53/immunology
    Chemical Substances IL33 protein, human ; Il33 protein, mouse ; Interleukin-33 ; RNA, Messenger ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2019-08-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1900408
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  9. Article ; Online: Glucagon-like peptide 1 signaling inhibits allergen-induced lung IL-33 release and reduces group 2 innate lymphoid cell cytokine production in vivo.

    Toki, Shinji / Goleniewska, Kasia / Reiss, Sara / Zhang, Jian / Bloodworth, Melissa H / Stier, Matthew T / Zhou, Weisong / Newcomb, Dawn C / Ware, Lorraine B / Stanwood, Gregg D / Galli, Aurelio / Boyd, Kelli L / Niswender, Kevin D / Peebles, R Stokes

    The Journal of allergy and clinical immunology

    2018  Volume 142, Issue 5, Page(s) 1515–1528.e8

    Abstract: Background: IL-33 is one of the most consistently associated gene candidates for asthma identified by using a genome-wide association study. Studies in mice and in human cells have confirmed the importance of IL-33 in inducing type 2 cytokine production ...

    Abstract Background: IL-33 is one of the most consistently associated gene candidates for asthma identified by using a genome-wide association study. Studies in mice and in human cells have confirmed the importance of IL-33 in inducing type 2 cytokine production from both group 2 innate lymphoid cells (ILC2s) and T
    Objective: We sought to determine the effect of glucagon-like peptide 1 receptor (GLP-1R) signaling on aeroallergen-induced airway IL-33 production and release and on innate type 2 airway inflammation.
    Methods: BALB/c mice were challenged intranasally with Alternaria extract for 4 consecutive days. GLP-1R agonist or vehicle was administered starting either 2 days before the first Alternaria extract challenge or 1 day after the first Alternaria extract challenge.
    Results: GLP-1R agonist treatment starting 2 days before the first Alternaria extract challenge decreased IL-33 release in the bronchoalveolar lavage fluid and dual oxidase 1 (Duox1) mRNA expression 1 hour after the first Alternaria extract challenge and IL-33 expression in lung epithelial cells 24 hours after the last Alternaria extract challenge. Furthermore, GLP-1R agonist significantly decreased the number of ILC2s expressing IL-5 and IL-13, lung protein expression of type 2 cytokines and chemokines, the number of perivascular eosinophils, mucus production, and airway responsiveness compared with vehicle treatment. GLP-1R agonist treatment starting 1 day after the first Alternaria extract challenge also significantly decreased eosinophilia and type 2 cytokine and chemokine expression in the airway after 4 days of Alternaria extract challenge.
    Conclusion: These results reveal that GLP-1R signaling might be a therapy to reduce IL-33 release and inhibit the ILC2 response to protease-containing aeroallergens, such as Alternaria.
    MeSH term(s) Allergens/immunology ; Alternaria/immunology ; Animals ; Asthma/immunology ; Cytokines/immunology ; Dermatophagoides pteronyssinus/immunology ; Eosinophilia/immunology ; Female ; Glucagon-Like Peptide 1/immunology ; Glucagon-Like Peptide-1 Receptor/agonists ; Glucagon-Like Peptide-1 Receptor/immunology ; Immunity, Innate ; Interleukin-33/immunology ; Lung/cytology ; Lung/immunology ; Lymphocytes/immunology ; Mice, Inbred BALB C ; Mice, Transgenic ; Mucus/immunology ; Signal Transduction
    Chemical Substances Allergens ; Cytokines ; Glp1r protein, mouse ; Glucagon-Like Peptide-1 Receptor ; Il33 protein, mouse ; Interleukin-33 ; Glucagon-Like Peptide 1 (89750-14-1)
    Language English
    Publishing date 2018-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2017.11.043
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  10. Article ; Online: Matrix Metalloproteinase Activity in Infections by an Encephalitic Virus, Mouse Adenovirus Type 1.

    Ashley, Shanna L / Pretto, Carla D / Stier, Matthew T / Kadiyala, Padma / Castro-Jorge, Luiza / Hsu, Tien-Huei / Doherty, Robert / Carnahan, Kelly E / Castro, Maria G / Lowenstein, Pedro R / Spindler, Katherine R

    Journal of virology

    2017  Volume 91, Issue 6

    Abstract: Mouse adenovirus type 1 (MAV-1) infection causes encephalitis in susceptible strains of mice and alters the permeability of infected brains to small molecules, which indicates disruption of the blood-brain barrier (BBB). Under pathological conditions, ... ...

    Abstract Mouse adenovirus type 1 (MAV-1) infection causes encephalitis in susceptible strains of mice and alters the permeability of infected brains to small molecules, which indicates disruption of the blood-brain barrier (BBB). Under pathological conditions, matrix metalloproteinases (MMPs) can disrupt the BBB through their proteolytic activity on basement membrane and tight junction proteins. We examined whether MAV-1 infection alters MMP activity
    MeSH term(s) Adenoviridae Infections/pathology ; Adenoviridae Infections/virology ; Animals ; Astrocytes/enzymology ; Astrocytes/virology ; Brain/pathology ; Cells, Cultured ; Disease Models, Animal ; Encephalitis, Viral/pathology ; Encephalitis, Viral/virology ; Endothelial Cells/enzymology ; Endothelial Cells/virology ; Mastadenovirus/pathogenicity ; Matrix Metalloproteinase 2/analysis ; Matrix Metalloproteinase 9/analysis ; Mice ; Microglia/enzymology ; Microglia/virology
    Chemical Substances Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Mmp2 protein, mouse (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35)
    Language English
    Publishing date 2017-03-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.01412-16
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