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  1. AU="Edelson, Brian T"
  2. AU="Elliott, Bruce M"
  3. AU="Pérez, René"
  4. AU="Lourdes Diaz Rodriguez"
  5. AU="Choi, Kai Chow"
  6. AU="Brandolini, Jury"
  7. AU="Yom, Jina"
  8. AU="Sue Casey"
  9. AU="Arimura, Takashi"
  10. AU="Kizilkilic, Osman"

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  1. Artikel ; Online: New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.

    Lin, Chih-Chung / Edelson, Brian T

    Journal of immunology (Baltimore, Md. : 1950)

    2017  Band 198, Heft 12, Seite(n) 4553–4560

    Abstract: Multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic ... ...

    Abstract Multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic T
    Mesh-Begriff(e) Animals ; Cytokines/immunology ; Cytokines/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Humans ; Interleukin-1beta/antagonists & inhibitors ; Interleukin-1beta/immunology ; Interleukin-1beta/metabolism ; Mice ; Monocytes/immunology ; Multiple Sclerosis/immunology ; Multiple Sclerosis/therapy ; Neutrophils/immunology ; Signal Transduction/immunology ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Helper-Inducer/metabolism
    Chemische Substanzen Cytokines ; Interleukin-1beta
    Sprache Englisch
    Erscheinungsdatum 2017-06-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    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.1700263
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Cutting Edge: STAT4 Promotes Bhlhe40 Induction to Drive Protective IFN-γ from NK Cells during Viral Infection.

    Kim, Hyunu / Abbasi, Aamna / Sharrock, Jessica / Santosa, Endi K / Sheppard, Sam / Lau, Colleen M / Edelson, Brian T / Sun, Joseph C

    Journal of immunology (Baltimore, Md. : 1950)

    2023  Band 211, Heft 10, Seite(n) 1469–1474

    Abstract: NK cells represent a cellular component of the mammalian innate immune system, and they mount rapid responses against viral infection, including the secretion of the potent antiviral effector cytokine IFN-γ. Following mouse CMV infection, Bhlhe40 was the ...

    Abstract NK cells represent a cellular component of the mammalian innate immune system, and they mount rapid responses against viral infection, including the secretion of the potent antiviral effector cytokine IFN-γ. Following mouse CMV infection, Bhlhe40 was the most highly induced transcription factor in NK cells among the basic helix-loop-helix family. Bhlhe40 upregulation in NK cells depended upon IL-12 and IL-18 signals, with the promoter of Bhlhe40 enriched for STAT4 and the permissive histone H3K4me3, and with STAT4-deficient NK cells showing an impairment of Bhlhe40 induction and diminished H3K4me3. Transcriptomic and protein analysis of Bhlhe40-deficient NK cells revealed a defect in IFN-γ production during mouse CMV infection, resulting in diminished protective immunity following viral challenge. Finally, we provide evidence that Bhlhe40 directly promotes IFN-γ by binding throughout the Ifng loci in activated NK cells. Thus, our study reveals how STAT4-mediated control of Bhlhe40 drives protective IFN-γ secretion by NK cells during viral infection.
    Mesh-Begriff(e) Mice ; Animals ; Killer Cells, Natural ; Interferon-gamma ; Cytokines/metabolism ; Interleukin-12/metabolism ; Cytomegalovirus Infections/metabolism ; STAT4 Transcription Factor/metabolism ; Mammals/metabolism ; Homeodomain Proteins/metabolism ; Basic Helix-Loop-Helix Transcription Factors/metabolism
    Chemische Substanzen Interferon-gamma (82115-62-6) ; Cytokines ; Interleukin-12 (187348-17-0) ; STAT4 Transcription Factor ; Bhlhe40 protein, mouse ; Homeodomain Proteins ; Basic Helix-Loop-Helix Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2023-10-13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    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.2300402
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Dendritic cells in Listeria monocytogenes infection.

    Edelson, Brian T

    Advances in immunology

    2012  Band 113, Seite(n) 33–49

    Abstract: Dendritic cells (DCs) represent a unique collection of innate immune cells present throughout the body as distinct subpopulations generally sharing the functions of pathogen recognition, cytokine production, and antigen presentation. A large body of work ...

    Abstract Dendritic cells (DCs) represent a unique collection of innate immune cells present throughout the body as distinct subpopulations generally sharing the functions of pathogen recognition, cytokine production, and antigen presentation. A large body of work in recent years has examined DC functions during infection with Listeria monocytogenes (Lm), particularly in the murine model. Here, I review several aspects of DC biology in this model, with particular emphasis on the role DCs play in the establishment of a productive Lm infection and the role of DCs as cytokine producers and antigen-presenting cells in this system.
    Mesh-Begriff(e) Animals ; Antigen Presentation ; Cytokines/immunology ; Dendritic Cells/immunology ; Dendritic Cells/microbiology ; Disease Models, Animal ; Humans ; Listeria monocytogenes/immunology ; Listeria monocytogenes/pathogenicity ; Listeriosis/immunology ; Listeriosis/microbiology ; Mice
    Chemische Substanzen Cytokines
    Sprache Englisch
    Erscheinungsdatum 2012
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80226-8
    ISSN 1557-8445 ; 0065-2776
    ISSN (online) 1557-8445
    ISSN 0065-2776
    DOI 10.1016/B978-0-12-394590-7.00006-3
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Bhlhe40 Promotes CD4+ T Helper 1 Cell and Suppresses T Follicular Helper Cell Differentiation during Viral Infection.

    Nguyen, Christine / Kudek, Matthew / Zander, Ryan / Niu, Hongshen / Shen, Jian / Bauer, Ashley / Alson, Donia / Khatun, Achia / Chen, Yao / Sun, Jie / Drobyski, William / Edelson, Brian T / Cui, Weiguo

    Journal of immunology (Baltimore, Md. : 1950)

    2024  Band 212, Heft 11, Seite(n) 1829–1842

    Abstract: In response to acute infection, naive CD4+ T cells primarily differentiate into T helper 1 (Th1) or T follicular helper (Tfh) cells that play critical roles in orchestrating cellular or humoral arms of immunity, respectively. However, despite the well ... ...

    Abstract In response to acute infection, naive CD4+ T cells primarily differentiate into T helper 1 (Th1) or T follicular helper (Tfh) cells that play critical roles in orchestrating cellular or humoral arms of immunity, respectively. However, despite the well established role of T-bet and BCL-6 in driving Th1 and Tfh cell lineage commitment, respectively, whether additional transcriptional circuits also underlie the fate bifurcation of Th1 and Tfh cell subsets is not fully understood. In this article, we study how the transcriptional regulator Bhlhe40 dictates the Th1/Tfh differentiation axis in mice. CD4+ T cell-specific deletion of Bhlhe40 abrogates Th1 but augments Tfh differentiation. We also assessed an increase in germinal center B cells and Ab production, suggesting that deletion of Bhlhe40 in CD4+ T cells not only alters Tfh differentiation but also their capacity to provide help to B cells. To identify molecular mechanisms by which Bhlhe40 regulates Th1 versus Tfh lineage choice, we first performed epigenetic profiling in the virus specific Th1 and Tfh cells following LCMV infection, which revealed distinct promoter and enhancer activities between the two helper cell lineages. Furthermore, we identified that Bhlhe40 directly binds to cis-regulatory elements of Th1-related genes such as Tbx21 and Cxcr6 to activate their expression while simultaneously binding to regions of Tfh-related genes such as Bcl6 and Cxcr5 to repress their expression. Collectively, our data suggest that Bhlhe40 functions as a transcription activator to promote Th1 cell differentiation and a transcription repressor to suppress Tfh cell differentiation.
    Mesh-Begriff(e) Animals ; Mice ; Cell Differentiation/immunology ; Cell Differentiation/genetics ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; T Follicular Helper Cells/immunology ; Th1 Cells/immunology ; Mice, Knockout ; Mice, Inbred C57BL ; B-Lymphocytes/immunology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic Choriomeningitis/virology ; Germinal Center/immunology ; Proto-Oncogene Proteins c-bcl-6/genetics ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Lymphocytic choriomeningitis virus/immunology ; Receptors, CXCR5/genetics ; Receptors, CXCR5/metabolism ; Homeodomain Proteins
    Chemische Substanzen Bhlhe40 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2024-04-15
    Erscheinungsland United States
    Dokumenttyp Journal Article
    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.2300355
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Transcription Factor Bhlhe40 in Immunity and Autoimmunity.

    Cook, Melissa E / Jarjour, Nicholas N / Lin, Chih-Chung / Edelson, Brian T

    Trends in immunology

    2020  Band 41, Heft 11, Seite(n) 1023–1036

    Abstract: The basic helix-loop-helix transcription factor (TF) Bhlhe40 is emerging as a key regulator of immunity during infection, autoimmunity, and inflammatory conditions. We describe the roles of Bhlhe40 in the circulating and tissue-resident arms of the ... ...

    Abstract The basic helix-loop-helix transcription factor (TF) Bhlhe40 is emerging as a key regulator of immunity during infection, autoimmunity, and inflammatory conditions. We describe the roles of Bhlhe40 in the circulating and tissue-resident arms of the immune system, with emphasis on recent work on the regulation of cytokine production and proliferation. We explore the mechanisms behind these functions in mouse models and human cells, including interactions with other TFs, and propose that Bhlhe40 is a central mediator of both inflammation and pathogen control, as well as a crucial regulator of a growing number of tissue-resident leukocyte populations. Finally, we suggest areas for further study that may advance our understanding of immunity and disease.
    Mesh-Begriff(e) Animals ; Autoimmunity/genetics ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/immunology ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Gene Expression Regulation ; Homeodomain Proteins/immunology ; Humans ; Immunity/genetics ; Transcription Factors/genetics
    Chemische Substanzen BHLHE40 protein, human ; Basic Helix-Loop-Helix Transcription Factors ; Homeodomain Proteins ; Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2020-10-07
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2020.09.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Antigen-guided depletion of anti-HLA antibody-producing cells by HLA-Fc fusion proteins.

    Webber, Ashlee M / Bradstreet, Tara R / Wang, Xiaoli / Guo, Hongjie / Nelson, Christopher A / Fremont, Daved H / Edelson, Brian T / Liu, Chang

    Blood

    2022  Band 140, Heft 16, Seite(n) 1803–1815

    Abstract: Platelet transfusion and transplantation of allogeneic stem cells and solid organs are life-saving therapies. Unwanted alloantibodies to nonself human leukocyte antigens (HLAs) on donor cells increase the immunological barrier to these therapies and are ... ...

    Abstract Platelet transfusion and transplantation of allogeneic stem cells and solid organs are life-saving therapies. Unwanted alloantibodies to nonself human leukocyte antigens (HLAs) on donor cells increase the immunological barrier to these therapies and are important causes of platelet transfusion refractoriness and graft rejection. Although the specificities of anti-HLA antibodies can be determined at the allelic level, traditional treatments for antibody-mediated rejection nonselectively suppress humoral immunity and are not universally successful. We designed HLA-Fc fusion proteins with a bivalent targeting module derived from extracellular domains of HLA and an Fc effector module from mouse IgG2a. We found that HLA-Fc with A2 (A2Fc) and B7 (B7Fc) antigens lowered HLA-A2- and HLA-B7-specific reactivities, respectively, in sera from HLA-sensitized patients. A2Fc and B7Fc bound to B-cell hybridomas bearing surface immunoglobulins with cognate specificities and triggered antigen-specific and Fc-dependent cytotoxicity in vitro. In immunodeficient mice carrying HLA-A2-specific hybridoma cells, A2Fc treatment lowered circulating anti-HLA-A2 levels, abolished the outgrowth of hybridoma cells, and prolonged survival compared with control groups. In an in vivo anti-HLA-A2-mediated platelet transfusion refractoriness model, A2Fc treatment mitigated refractoriness. These results support HLA-Fc being a novel strategy for antigen-specific humoral suppression to improve transfusion and transplantation outcomes. With the long-term goal of targeting HLA-specific memory B cells for desensitization, further studies of HLA-Fc's efficacy in immune-competent animal models are warranted.
    Mesh-Begriff(e) Humans ; Mice ; Animals ; Isoantibodies ; HLA-B7 Antigen ; HLA Antigens ; Graft Rejection ; Antilymphocyte Serum ; HLA-A2 Antigen ; Antibody-Producing Cells ; Thrombocytopenia ; Immunoglobulin G ; Receptors, Antigen, B-Cell
    Chemische Substanzen Isoantibodies ; HLA-B7 Antigen ; HLA Antigens ; Antilymphocyte Serum ; HLA-A2 Antigen ; Immunoglobulin G ; Receptors, Antigen, B-Cell
    Sprache Englisch
    Erscheinungsdatum 2022-09-02
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2022016376
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: BHLHE40 Regulates Myeloid Cell Polarization through IL-10-Dependent and -Independent Mechanisms.

    Hendrix, Skyler V / Mreyoud, Yassin / McNehlan, Michael E / Smirnov, Asya / Chavez, Sthefany M / Hie, Brian / Chamberland, Megan M / Bradstreet, Tara R / Webber, Ashlee M / Kreamalmeyer, Darren / Taneja, Reshma / Bryson, Bryan D / Edelson, Brian T / Stallings, Christina L

    Journal of immunology (Baltimore, Md. : 1950)

    2024  Band 212, Heft 11, Seite(n) 1766–1781

    Abstract: Better understanding of the host responses to Mycobacterium tuberculosis infections is required to prevent tuberculosis and develop new therapeutic interventions. The host transcription factor BHLHE40 is essential for controlling M. tuberculosis ... ...

    Abstract Better understanding of the host responses to Mycobacterium tuberculosis infections is required to prevent tuberculosis and develop new therapeutic interventions. The host transcription factor BHLHE40 is essential for controlling M. tuberculosis infection, in part by repressing Il10 expression, where excess IL-10 contributes to the early susceptibility of Bhlhe40-/- mice to M. tuberculosis infection. Deletion of Bhlhe40 in lung macrophages and dendritic cells is sufficient to increase the susceptibility of mice to M. tuberculosis infection, but how BHLHE40 impacts macrophage and dendritic cell responses to M. tuberculosis is unknown. In this study, we report that BHLHE40 is required in myeloid cells exposed to GM-CSF, an abundant cytokine in the lung, to promote the expression of genes associated with a proinflammatory state and better control of M. tuberculosis infection. Loss of Bhlhe40 expression in murine bone marrow-derived myeloid cells cultured in the presence of GM-CSF results in lower levels of proinflammatory associated signaling molecules IL-1β, IL-6, IL-12, TNF-α, inducible NO synthase, IL-2, KC, and RANTES, as well as higher levels of the anti-inflammatory-associated molecules MCP-1 and IL-10 following exposure to heat-killed M. tuberculosis. Deletion of Il10 in Bhlhe40-/- myeloid cells restored some, but not all, proinflammatory signals, demonstrating that BHLHE40 promotes proinflammatory responses via both IL-10-dependent and -independent mechanisms. In addition, we show that macrophages and neutrophils within the lungs of M. tuberculosis-infected Bhlhe40-/- mice exhibit defects in inducible NO synthase production compared with infected wild-type mice, supporting that BHLHE40 promotes proinflammatory responses in innate immune cells, which may contribute to the essential role for BHLHE40 during M. tuberculosis infection in vivo.
    Mesh-Begriff(e) Animals ; Mice ; Interleukin-10/immunology ; Interleukin-10/genetics ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/immunology ; Mice, Knockout ; Myeloid Cells/immunology ; Mycobacterium tuberculosis/immunology ; Macrophages/immunology ; Homeodomain Proteins/genetics ; Mice, Inbred C57BL ; Granulocyte-Macrophage Colony-Stimulating Factor ; Dendritic Cells/immunology ; Lung/immunology ; Tuberculosis/immunology ; Cell Polarity ; Cells, Cultured
    Chemische Substanzen Bhlhe40 protein, mouse ; IL10 protein, mouse
    Sprache Englisch
    Erscheinungsdatum 2024-04-29
    Erscheinungsland United States
    Dokumenttyp Journal Article
    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.2200819
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: BHLHE40 Mediates Cross-Talk between Pathogenic TH17 Cells and Myeloid Cells during Experimental Autoimmune Encephalomyelitis.

    Cook, Melissa E / Shchukina, Irina / Lin, Chih-Chung / Bradstreet, Tara R / Schwarzkopf, Elizabeth A / Jarjour, Nicholas N / Webber, Ashlee M / Zaitsev, Konstantin / Artyomov, Maxim N / Edelson, Brian T

    ImmunoHorizons

    2023  Band 7, Heft 11, Seite(n) 737–746

    Abstract: TH17 cells are implicated in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). We previously reported that the transcription factor basic helix-loop-helix family member e40 (BHLHE40) marks cytokine-producing ... ...

    Abstract TH17 cells are implicated in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). We previously reported that the transcription factor basic helix-loop-helix family member e40 (BHLHE40) marks cytokine-producing pathogenic TH cells during EAE, and that its expression in T cells is required for clinical disease. In this study, using dual reporter mice, we show BHLHE40 expression within TH1/17 and ex-TH17 cells following EAE induction. Il17a-Cre-mediated deletion of BHLHE40 in TH cells led to less severe EAE with reduced TH cell cytokine production. Characterization of the leukocytes in the CNS during EAE by single-cell RNA sequencing identified differences in the infiltrating myeloid cells when BHLHE40 was present or absent in TH17 cells. Our studies highlight the importance of BHLHE40 in promoting TH17 cell encephalitogenicity and instructing myeloid cell responses during active EAE.
    Mesh-Begriff(e) Animals ; Mice ; Cross Reactions ; Cytokines ; Encephalomyelitis, Autoimmune, Experimental ; Myeloid Cells ; Th17 Cells ; Basic Helix-Loop-Helix Transcription Factors/metabolism
    Chemische Substanzen Cytokines ; Bhlhe40 protein, mouse ; Basic Helix-Loop-Helix Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2023-11-07
    Erscheinungsland United States
    Dokumenttyp 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.
    ISSN 2573-7732
    ISSN (online) 2573-7732
    DOI 10.4049/immunohorizons.2300042
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Steady-state memory-phenotype conventional CD4

    Cho, Min-Ji / Lee, Hong-Gyun / Yoon, Jae-Won / Kim, Gil-Ran / Koo, Ja-Hyun / Taneja, Reshma / Edelson, Brian T / Lee, You Jeong / Choi, Je-Min

    Experimental & molecular medicine

    2023  Band 55, Heft 5, Seite(n) 1033–1045

    Abstract: Memory-phenotype (MP) ... ...

    Abstract Memory-phenotype (MP) CD4
    Mesh-Begriff(e) Mice ; Animals ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Immunity, Innate ; Neuroinflammatory Diseases ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Th17 Cells ; Interleukin-23 ; Phenotype ; Receptors, Antigen, T-Cell/metabolism ; CD4-Positive T-Lymphocytes ; Mice, Inbred C57BL ; Homeodomain Proteins/genetics ; Basic Helix-Loop-Helix Transcription Factors/genetics
    Chemische Substanzen Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; Interleukin-23 ; Receptors, Antigen, T-Cell ; Bhlhe40 protein, mouse ; Homeodomain Proteins ; Basic Helix-Loop-Helix Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2023-05-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1328915-9
    ISSN 2092-6413 ; 1226-3613 ; 0378-8512
    ISSN (online) 2092-6413
    ISSN 1226-3613 ; 0378-8512
    DOI 10.1038/s12276-023-00995-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Mesothelium-Derived Factors Shape GATA6-Positive Large Cavity Macrophages.

    Lai, Chin-Wen / Bagadia, Prachi / Barisas, Derek A G / Jarjour, Nicholas N / Wong, Rachel / Ohara, Takahiro / Muegge, Brian D / Lu, Qiuhe / Xiong, Shanshan / Edelson, Brian T / Murphy, Kenneth M / Stappenbeck, Thaddeus S

    Journal of immunology (Baltimore, Md. : 1950)

    2022  Band 209, Heft 4, Seite(n) 742–750

    Abstract: The local microenvironment shapes macrophage differentiation in each tissue. We hypothesized that in the peritoneum, local factors in addition to retinoic acid can support GATA6-driven differentiation and function of peritoneal large cavity macrophages ( ... ...

    Abstract The local microenvironment shapes macrophage differentiation in each tissue. We hypothesized that in the peritoneum, local factors in addition to retinoic acid can support GATA6-driven differentiation and function of peritoneal large cavity macrophages (LCMs). We found that soluble proteins produced by mesothelial cells lining the peritoneal cavity maintained GATA6 expression in cultured LCMs. Analysis of global gene expression of isolated mesothelial cells highlighted mesothelin (Msln) and its binding partner mucin 16 (Muc16) as candidate secreted ligands that potentially regulate GATA6 expression in peritoneal LCMs. Mice deficient for either of these molecules showed diminished GATA6 expression in peritoneal and pleural LCMs that was most prominent in aged mice. The more robust phenotype in older mice suggested that monocyte-derived macrophages were the target of Msln and Muc16. Cell transfer and bone marrow chimera experiments supported this hypothesis. We found that lethally irradiated Msln-/- and Muc16-/- mice reconstituted with wild-type bone marrow had lower levels of GATA6 expression in peritoneal and pleural LCMs. Similarly, during the resolution of zymosan-induced inflammation, repopulated peritoneal LCMs lacking expression of Msln or Muc16 expressed diminished GATA6. These data support a role for mesothelial cell-produced Msln and Muc16 in local macrophage differentiation within large cavity spaces such as the peritoneum. The effect appears to be most prominent on monocyte-derived macrophages that enter into this location as the host ages and also in response to infection.
    Mesh-Begriff(e) Mice ; Animals ; Macrophages ; Macrophages, Peritoneal ; Peritoneal Cavity ; Peritoneum ; Epithelium
    Sprache Englisch
    Erscheinungsdatum 2022-03-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    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.2200278
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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