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  1. Article ; Online: Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses.

    Hodge, Suzanne H / Krauss, Maria Z / Kaymak, Irem / King, James I / Howden, Andrew J M / Panic, Gordana / Grencis, Richard K / Swann, Jonathan R / Sinclair, Linda V / Hepworth, Matthew R

    The Journal of experimental medicine

    2022  Volume 220, Issue 3

    Abstract: Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the ... ...

    Abstract Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the diet and invading pathogens-including helminths. Emerging evidence suggests ILC2 are acutely sensitive not only to canonical activating signals but also perturbations in nutrient availability. In the context of helminth infection, we identify amino acid availability as a nutritional cue in regulating ILC2 responses. ILC2 are found to be uniquely preprimed to import amino acids via the large neutral amino acid transporters Slc7a5 and Slc7a8. Cell-intrinsic deletion of these transporters individually impaired ILC2 expansion, while concurrent loss of both transporters markedly impaired the proliferative and cytokine-producing capacity of ILC2. Mechanistically, amino acid uptake determined the magnitude of ILC2 responses in part via tuning of mTOR. These findings implicate essential amino acids as a metabolic requisite for optimal ILC2 responses within mucosal barrier tissues.
    MeSH term(s) Immunity, Innate ; Lymphocytes/metabolism ; Amino Acids/metabolism ; Cytokines/metabolism ; Mucous Membrane/metabolism
    Chemical Substances Amino Acids ; Cytokines
    Language English
    Publishing date 2022-12-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20221073
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Rhythmicity of intestinal IgA responses confers oscillatory commensal microbiota mutualism.

    Penny, Hugo A / Domingues, Rita G / Krauss, Maria Z / Melo-Gonzalez, Felipe / Lawson, Melissa A E / Dickson, Suzanna / Parkinson, James / Hurry, Madeleine / Purse, Catherine / Jegham, Emna / Godinho-Silva, Cristina / Rendas, Miguel / Veiga-Fernandes, Henrique / Bechtold, David A / Grencis, Richard K / Toellner, Kai-Michael / Waisman, Ari / Swann, Jonathan R / Gibbs, Julie E /
    Hepworth, Matthew R

    Science immunology

    2022  Volume 7, Issue 75, Page(s) eabk2541

    Abstract: Interactions between the mammalian host and commensal microbiota are enforced through a range of immune responses that confer metabolic benefits and promote tissue health and homeostasis. Immunoglobulin A (IgA) responses directly determine the ... ...

    Abstract Interactions between the mammalian host and commensal microbiota are enforced through a range of immune responses that confer metabolic benefits and promote tissue health and homeostasis. Immunoglobulin A (IgA) responses directly determine the composition of commensal species that colonize the intestinal tract but require substantial metabolic resources to fuel antibody production by tissue-resident plasma cells. Here, we demonstrate that IgA responses are subject to diurnal regulation over the course of a circadian day. Specifically, the magnitude of IgA secretion, as well as the transcriptome of intestinal IgA
    MeSH term(s) Animals ; Immunoglobulin A, Secretory ; Intestines ; Mammals ; Microbiota ; Periodicity ; Symbiosis
    Chemical Substances Immunoglobulin A, Secretory
    Language English
    Publishing date 2022-09-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2470-9468
    ISSN (online) 2470-9468
    DOI 10.1126/sciimmunol.abk2541
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation.

    Svedberg, Freya R / Brown, Sheila L / Krauss, Maria Z / Campbell, Laura / Sharpe, Catherine / Clausen, Maryam / Howell, Gareth J / Clark, Howard / Madsen, Jens / Evans, Christopher M / Sutherland, Tara E / Ivens, Alasdair C / Thornton, David J / Grencis, Richard K / Hussell, Tracy / Cunoosamy, Danen M / Cook, Peter C / MacDonald, Andrew S

    Nature immunology

    2019  Volume 20, Issue 5, Page(s) 571–580

    Abstract: Fine control of macrophage activation is needed to prevent inflammatory disease, particularly at barrier sites such as the lungs. However, the dominant mechanisms that regulate the activation of pulmonary macrophages during inflammation are poorly ... ...

    Abstract Fine control of macrophage activation is needed to prevent inflammatory disease, particularly at barrier sites such as the lungs. However, the dominant mechanisms that regulate the activation of pulmonary macrophages during inflammation are poorly understood. We found that alveolar macrophages (AlvMs) were much less able to respond to the canonical type 2 cytokine IL-4, which underpins allergic disease and parasitic worm infections, than macrophages from lung tissue or the peritoneal cavity. We found that the hyporesponsiveness of AlvMs to IL-4 depended upon the lung environment but was independent of the host microbiota or the lung extracellular matrix components surfactant protein D (SP-D) and mucin 5b (Muc5b). AlvMs showed severely dysregulated metabolism relative to that of cavity macrophages. After removal from the lungs, AlvMs regained responsiveness to IL-4 in a glycolysis-dependent manner. Thus, impaired glycolysis in the pulmonary niche regulates AlvM responsiveness during type 2 inflammation.
    MeSH term(s) Animals ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Interleukin-4/genetics ; Interleukin-4/immunology ; Interleukin-4/metabolism ; Larva/immunology ; Larva/physiology ; Lung/immunology ; Lung/metabolism ; Lung/pathology ; Macrophage Activation/genetics ; Macrophage Activation/immunology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/metabolism ; Macrophages, Alveolar/parasitology ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mucin-5B/genetics ; Mucin-5B/immunology ; Mucin-5B/metabolism ; Nippostrongylus/immunology ; Nippostrongylus/physiology ; Pulmonary Surfactant-Associated Protein D/genetics ; Pulmonary Surfactant-Associated Protein D/immunology ; Pulmonary Surfactant-Associated Protein D/metabolism ; Strongylida Infections/genetics ; Strongylida Infections/immunology ; Strongylida Infections/parasitology
    Chemical Substances Mucin-5B ; Pulmonary Surfactant-Associated Protein D ; Interleukin-4 (207137-56-2)
    Language English
    Publishing date 2019-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-019-0352-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5294: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 42: Show issues

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  4. Article ; Online: ILC precursors differentiate into metabolically distinct ILC1-like cells during Mycobacterium tuberculosis infection.

    Corral, Dan / Charton, Alison / Krauss, Maria Z / Blanquart, Eve / Levillain, Florence / Lefrançais, Emma / Sneperger, Tamara / Vahlas, Zoï / Girard, Jean-Philippe / Eberl, Gérard / Poquet, Yannick / Guéry, Jean-Charles / Argüello, Rafael J / Belkaid, Yasmine / Mayer-Barber, Katrin D / Hepworth, Matthew R / Neyrolles, Olivier / Hudrisier, Denis

    Cell reports

    2017  Volume 39, Issue 3, Page(s) 110715

    Abstract: Tissue-resident innate lymphoid cells (ILCs) regulate tissue homeostasis, protect against pathogens at mucosal surfaces, and are key players at the interface of innate and adaptive immunity. How ILCs adapt their phenotype and function to environmental ... ...

    Abstract Tissue-resident innate lymphoid cells (ILCs) regulate tissue homeostasis, protect against pathogens at mucosal surfaces, and are key players at the interface of innate and adaptive immunity. How ILCs adapt their phenotype and function to environmental cues within tissues remains to be fully understood. Here, we show that Mycobacterium tuberculosis (Mtb) infection alters the phenotype and function of lung IL-18Rα
    MeSH term(s) Cytokines ; Humans ; Immunity, Innate ; Inflammation ; Lymphocytes ; Tuberculosis
    Chemical Substances Cytokines
    Language English
    Publishing date 2017-01-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110715
    Database MEDical Literature Analysis and Retrieval System OnLINE

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