AustralieFrV1, Main, Exploration, bibRecord, 000862

MAIT cells launch a rapid, robust and distinct hyperinflammatory response to bacterial superantigens and quickly acquire an anergic phenotype that impedes their cognate antimicrobial function: Defining a novel mechanism of superantigen-induced immunopathology and immunosuppression

Identifieur interne : 000862 ( Main/Exploration ); précédent : 000861; suivant : 000863

MAIT cells launch a rapid, robust and distinct hyperinflammatory response to bacterial superantigens and quickly acquire an anergic phenotype that impedes their cognate antimicrobial function: Defining a novel mechanism of superantigen-induced immunopathology and immunosuppression

Auteurs : Christopher R. Shaler [Canada] ; Joshua Choi [Canada] ; Patrick T. Rudak [Canada] ; Arash Memarnejadian [Canada] ; Peter A. Szabo [Canada] ; Mauro E. Tun-Abraham [Canada] ; Jamie Rossjohn [Australie, Royaume-Uni] ; Alexandra J. Corbett [Australie] ; James Mccluskey [Australie] ; John K. Mccormick [Canada] ; Olivier Lantz [France] ; Roberto Hernandez-Alejandro [Canada, États-Unis] ; S. M. Mansour Haeryfar [Canada]

Source :

PLoS Biology [ 1544-9173 ] ; 2017.

RBID : PMC:5478099

Descripteurs français

English descriptors

KwdEn :
- Animals, Antigens, Bacterial (metabolism), Antigens, Bacterial (toxicity), Bone Marrow Cells (cytology), Bone Marrow Cells (drug effects), Bone Marrow Cells (immunology), Bone Marrow Cells (metabolism), Cell Line, Cells, Cultured, Clonal Anergy (drug effects), Crosses, Genetic, Enterotoxins (secretion), Enterotoxins (toxicity), Female, Humans, Hybridomas, Immunity, Innate, Leukocytes, Mononuclear (cytology), Leukocytes, Mononuclear (drug effects), Leukocytes, Mononuclear (immunology), Leukocytes, Mononuclear (metabolism), Lymphocyte Activation (drug effects), Mice, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Mice, Transgenic, Models, Immunological, Mucosal-Associated Invariant T Cells (cytology), Mucosal-Associated Invariant T Cells (drug effects), Mucosal-Associated Invariant T Cells (immunology), Mucosal-Associated Invariant T Cells (metabolism), Specific Pathogen-Free Organisms, Staphylococcus aureus (immunology), Staphylococcus aureus (metabolism), Streptococcus pyogenes (immunology), Streptococcus pyogenes (metabolism), Superantigens (metabolism), Superantigens (toxicity), Transplantation Chimera (blood), Transplantation Chimera (immunology), Transplantation Chimera (metabolism).
MESH :
- chemical , metabolism : Antigens, Bacterial, Superantigens.
- chemical , secretion : Enterotoxins.
- chemical , toxicity : Antigens, Bacterial, Enterotoxins, Superantigens.
- blood : Transplantation Chimera.
- cytology : Bone Marrow Cells, Leukocytes, Mononuclear, Mucosal-Associated Invariant T Cells.
- drug effects : Bone Marrow Cells, Clonal Anergy, Leukocytes, Mononuclear, Lymphocyte Activation, Mucosal-Associated Invariant T Cells.
- immunology : Bone Marrow Cells, Leukocytes, Mononuclear, Mucosal-Associated Invariant T Cells, Staphylococcus aureus, Streptococcus pyogenes, Transplantation Chimera.
- metabolism : Bone Marrow Cells, Leukocytes, Mononuclear, Mucosal-Associated Invariant T Cells, Staphylococcus aureus, Streptococcus pyogenes, Transplantation Chimera.
- Animals, Cell Line, Cells, Cultured, Crosses, Genetic, Female, Humans, Hybridomas, Immunity, Innate, Mice, Mice, Inbred NOD, Mice, Knockout, Mice, SCID, Mice, Transgenic, Models, Immunological, Specific Pathogen-Free Organisms.

Abstract

Superantigens (SAgs) are potent exotoxins secreted by Staphylococcus aureus and Streptococcus pyogenes. They target a large fraction of T cell pools to set in motion a “cytokine storm” with severe and sometimes life-threatening consequences typically encountered in toxic shock syndrome (TSS). Given the rapidity with which TSS develops, designing timely and truly targeted therapies for this syndrome requires identification of key mediators of the cytokine storm’s initial wave. Equally important, early host responses to SAgs can be accompanied or followed by a state of immunosuppression, which in turn jeopardizes the host’s ability to combat and clear infections. Unlike in mouse models, the mechanisms underlying SAg-associated immunosuppression in humans are ill-defined. In this work, we have identified a population of innate-like T cells, called mucosa-associated invariant T (MAIT) cells, as the most powerful source of pro-inflammatory cytokines after exposure to SAgs. We have utilized primary human peripheral blood and hepatic mononuclear cells, mouse MAIT hybridoma lines, HLA-DR4-transgenic mice, MAIT^highHLA-DR4⁺ bone marrow chimeras, and humanized NOD-scid IL-2Rγ^null mice to demonstrate for the first time that: i) mouse and human MAIT cells are hyperresponsive to SAgs, typified by staphylococcal enterotoxin B (SEB); ii) the human MAIT cell response to SEB is rapid and far greater in magnitude than that launched by unfractionated conventional T, invariant natural killer T (iNKT) or γδ T cells, and is characterized by production of interferon (IFN)-γ, tumor necrosis factor (TNF)-α and interleukin (IL)-2, but not IL-17A; iii) high-affinity MHC class II interaction with SAgs, but not MHC-related protein 1 (MR1) participation, is required for MAIT cell activation; iv) MAIT cell responses to SEB can occur in a T cell receptor (TCR) Vβ–specific manner but are largely contributed by IL-12 and IL-18; v) as MAIT cells are primed by SAgs, they also begin to develop a molecular signature consistent with exhaustion and failure to participate in antimicrobial defense. Accordingly, they upregulate lymphocyte-activation gene 3 (LAG-3), T cell immunoglobulin and mucin-3 (TIM-3), and/or programmed cell death-1 (PD-1), and acquire an anergic phenotype that interferes with their cognate function against Klebsiella pneumoniae and Escherichia coli; vi) MAIT cell hyperactivation and anergy co-utilize a signaling pathway that is governed by p38 and MEK1/2. Collectively, our findings demonstrate a pathogenic, rather than protective, role for MAIT cells during infection. Furthermore, we propose a novel mechanism of SAg-associated immunosuppression in humans. MAIT cells may therefore provide an attractive therapeutic target for the management of both early and late phases of severe SAg-mediated illnesses.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5478099

DOI: 10.1371/journal.pbio.2001930
PubMed: 28632753
PubMed Central: 5478099

Affiliations:

Le document en format XML

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<author><name sortKey="Hernandez Alejandro, Roberto" sort="Hernandez Alejandro, Roberto" uniqKey="Hernandez Alejandro R" first="Roberto" last="Hernandez-Alejandro">Roberto Hernandez-Alejandro</name>
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<author><name sortKey="Haeryfar, S M Mansour" sort="Haeryfar, S M Mansour" uniqKey="Haeryfar S" first="S. M. Mansour" last="Haeryfar">S. M. Mansour Haeryfar</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">MAIT cells launch a rapid, robust and distinct hyperinflammatory response to bacterial superantigens and quickly acquire an anergic phenotype that impedes their cognate antimicrobial function: Defining a novel mechanism of superantigen-induced immunopathology and immunosuppression</title>
<author><name sortKey="Shaler, Christopher R" sort="Shaler, Christopher R" uniqKey="Shaler C" first="Christopher R." last="Shaler">Christopher R. Shaler</name>
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<author><name sortKey="Choi, Joshua" sort="Choi, Joshua" uniqKey="Choi J" first="Joshua" last="Choi">Joshua Choi</name>
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</nlm:aff>
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<wicri:regionArea>Department of Microbiology and Immunology, Western University, London, Ontario</wicri:regionArea>
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<author><name sortKey="Rudak, Patrick T" sort="Rudak, Patrick T" uniqKey="Rudak P" first="Patrick T." last="Rudak">Patrick T. Rudak</name>
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<author><name sortKey="Memarnejadian, Arash" sort="Memarnejadian, Arash" uniqKey="Memarnejadian A" first="Arash" last="Memarnejadian">Arash Memarnejadian</name>
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<author><name sortKey="Szabo, Peter A" sort="Szabo, Peter A" uniqKey="Szabo P" first="Peter A." last="Szabo">Peter A. Szabo</name>
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</nlm:aff>
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<author><name sortKey="Tun Abraham, Mauro E" sort="Tun Abraham, Mauro E" uniqKey="Tun Abraham M" first="Mauro E." last="Tun-Abraham">Mauro E. Tun-Abraham</name>
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</nlm:aff>
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<author><name sortKey="Rossjohn, Jamie" sort="Rossjohn, Jamie" uniqKey="Rossjohn J" first="Jamie" last="Rossjohn">Jamie Rossjohn</name>
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</nlm:aff>
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria</wicri:regionArea>
<wicri:noRegion>Victoria</wicri:noRegion>
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<affiliation wicri:level="1"><nlm:aff id="aff004"><addr-line>Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia</addr-line>
</nlm:aff>
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<wicri:noRegion>Victoria</wicri:noRegion>
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<affiliation wicri:level="1"><nlm:aff id="aff005"><addr-line>Institute of Infection and Immunity, Cardiff University School of Medicine, Cardiff, United Kingdom</addr-line>
</nlm:aff>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Institute of Infection and Immunity, Cardiff University School of Medicine, Cardiff</wicri:regionArea>
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<author><name sortKey="Corbett, Alexandra J" sort="Corbett, Alexandra J" uniqKey="Corbett A" first="Alexandra J." last="Corbett">Alexandra J. Corbett</name>
<affiliation wicri:level="4"><nlm:aff id="aff006"><addr-line>Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia</addr-line>
</nlm:aff>
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria</wicri:regionArea>
<orgName type="university">Université de Melbourne</orgName>
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<region type="état">Victoria (État)</region>
</placeName>
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<author><name sortKey="Mccluskey, James" sort="Mccluskey, James" uniqKey="Mccluskey J" first="James" last="Mccluskey">James Mccluskey</name>
<affiliation wicri:level="4"><nlm:aff id="aff006"><addr-line>Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia</addr-line>
</nlm:aff>
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria</wicri:regionArea>
<orgName type="university">Université de Melbourne</orgName>
<placeName><settlement type="city">Melbourne</settlement>
<region type="état">Victoria (État)</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Mccormick, John K" sort="Mccormick, John K" uniqKey="Mccormick J" first="John K." last="Mccormick">John K. Mccormick</name>
<affiliation wicri:level="1"><nlm:aff id="aff001"><addr-line>Department of Microbiology and Immunology, Western University, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Microbiology and Immunology, Western University, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff007"><addr-line>Centre for Human Immunology, Western University, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Centre for Human Immunology, Western University, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff008"><addr-line>Lawson Health Research Institute, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Lawson Health Research Institute, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Lantz, Olivier" sort="Lantz, Olivier" uniqKey="Lantz O" first="Olivier" last="Lantz">Olivier Lantz</name>
<affiliation wicri:level="3"><nlm:aff id="aff009"><addr-line>Laboratoire d'Immunologie and INSERM U932, Institut Curie, Paris, France</addr-line>
</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Laboratoire d'Immunologie and INSERM U932, Institut Curie, Paris</wicri:regionArea>
<placeName><region type="region">Île-de-France</region>
<region type="old region">Île-de-France</region>
<settlement type="city">Paris</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Hernandez Alejandro, Roberto" sort="Hernandez Alejandro, Roberto" uniqKey="Hernandez Alejandro R" first="Roberto" last="Hernandez-Alejandro">Roberto Hernandez-Alejandro</name>
<affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>Division of General Surgery, Department of Surgery, Western University, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Division of General Surgery, Department of Surgery, Western University, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="aff010"><addr-line>Division of Transplantation, Department of Surgery, University of Rochester Medical Center, Rochester, New York, United States of America</addr-line>
</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Transplantation, Department of Surgery, University of Rochester Medical Center, Rochester, New York</wicri:regionArea>
<placeName><region type="state">État de New York</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Haeryfar, S M Mansour" sort="Haeryfar, S M Mansour" uniqKey="Haeryfar S" first="S. M. Mansour" last="Haeryfar">S. M. Mansour Haeryfar</name>
<affiliation wicri:level="1"><nlm:aff id="aff001"><addr-line>Department of Microbiology and Immunology, Western University, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Microbiology and Immunology, Western University, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff007"><addr-line>Centre for Human Immunology, Western University, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Centre for Human Immunology, Western University, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff008"><addr-line>Lawson Health Research Institute, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Lawson Health Research Institute, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff011"><addr-line>Division of Clinical Immunology and Allergy, Department of Medicine, Western University, London, Ontario, Canada</addr-line>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Division of Clinical Immunology and Allergy, Department of Medicine, Western University, London, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series><title level="j">PLoS Biology</title>
<idno type="ISSN">1544-9173</idno>
<idno type="eISSN">1545-7885</idno>
<imprint><date when="2017">2017</date>
</imprint>
</series>
</biblStruct>
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</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Antigens, Bacterial (metabolism)</term>
<term>Antigens, Bacterial (toxicity)</term>
<term>Bone Marrow Cells (cytology)</term>
<term>Bone Marrow Cells (drug effects)</term>
<term>Bone Marrow Cells (immunology)</term>
<term>Bone Marrow Cells (metabolism)</term>
<term>Cell Line</term>
<term>Cells, Cultured</term>
<term>Clonal Anergy (drug effects)</term>
<term>Crosses, Genetic</term>
<term>Enterotoxins (secretion)</term>
<term>Enterotoxins (toxicity)</term>
<term>Female</term>
<term>Humans</term>
<term>Hybridomas</term>
<term>Immunity, Innate</term>
<term>Leukocytes, Mononuclear (cytology)</term>
<term>Leukocytes, Mononuclear (drug effects)</term>
<term>Leukocytes, Mononuclear (immunology)</term>
<term>Leukocytes, Mononuclear (metabolism)</term>
<term>Lymphocyte Activation (drug effects)</term>
<term>Mice</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Knockout</term>
<term>Mice, SCID</term>
<term>Mice, Transgenic</term>
<term>Models, Immunological</term>
<term>Mucosal-Associated Invariant T Cells (cytology)</term>
<term>Mucosal-Associated Invariant T Cells (drug effects)</term>
<term>Mucosal-Associated Invariant T Cells (immunology)</term>
<term>Mucosal-Associated Invariant T Cells (metabolism)</term>
<term>Specific Pathogen-Free Organisms</term>
<term>Staphylococcus aureus (immunology)</term>
<term>Staphylococcus aureus (metabolism)</term>
<term>Streptococcus pyogenes (immunology)</term>
<term>Streptococcus pyogenes (metabolism)</term>
<term>Superantigens (metabolism)</term>
<term>Superantigens (toxicity)</term>
<term>Transplantation Chimera (blood)</term>
<term>Transplantation Chimera (immunology)</term>
<term>Transplantation Chimera (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes ()</term>
<term>Agranulocytes ()</term>
<term>Agranulocytes (cytologie)</term>
<term>Agranulocytes (immunologie)</term>
<term>Agranulocytes (métabolisme)</term>
<term>Anergie clonale ()</term>
<term>Animaux</term>
<term>Antigènes bactériens (métabolisme)</term>
<term>Antigènes bactériens (toxicité)</term>
<term>Cellules T invariantes associées aux muqueuses ()</term>
<term>Cellules T invariantes associées aux muqueuses (cytologie)</term>
<term>Cellules T invariantes associées aux muqueuses (immunologie)</term>
<term>Cellules T invariantes associées aux muqueuses (métabolisme)</term>
<term>Cellules cultivées</term>
<term>Cellules de la moelle osseuse ()</term>
<term>Cellules de la moelle osseuse (cytologie)</term>
<term>Cellules de la moelle osseuse (immunologie)</term>
<term>Cellules de la moelle osseuse (métabolisme)</term>
<term>Chimère obtenue par transplantation (immunologie)</term>
<term>Chimère obtenue par transplantation (métabolisme)</term>
<term>Chimère obtenue par transplantation (sang)</term>
<term>Croisements génétiques</term>
<term>Entérotoxines (sécrétion)</term>
<term>Entérotoxines (toxicité)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hybridomes</term>
<term>Immunité innée</term>
<term>Lignée cellulaire</term>
<term>Modèles immunologiques</term>
<term>Organismes exempts d'organismes pathogènes spécifiques</term>
<term>Souris</term>
<term>Souris SCID</term>
<term>Souris de lignée NOD</term>
<term>Souris knockout</term>
<term>Souris transgéniques</term>
<term>Staphylococcus aureus (immunologie)</term>
<term>Staphylococcus aureus (métabolisme)</term>
<term>Streptococcus pyogenes (immunologie)</term>
<term>Streptococcus pyogenes (métabolisme)</term>
<term>Superantigènes (métabolisme)</term>
<term>Superantigènes (toxicité)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Bacterial</term>
<term>Superantigens</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="secretion" xml:lang="en"><term>Enterotoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Antigens, Bacterial</term>
<term>Enterotoxins</term>
<term>Superantigens</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Transplantation Chimera</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Agranulocytes</term>
<term>Cellules T invariantes associées aux muqueuses</term>
<term>Cellules de la moelle osseuse</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Bone Marrow Cells</term>
<term>Leukocytes, Mononuclear</term>
<term>Mucosal-Associated Invariant T Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Bone Marrow Cells</term>
<term>Clonal Anergy</term>
<term>Leukocytes, Mononuclear</term>
<term>Lymphocyte Activation</term>
<term>Mucosal-Associated Invariant T Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Agranulocytes</term>
<term>Cellules T invariantes associées aux muqueuses</term>
<term>Cellules de la moelle osseuse</term>
<term>Chimère obtenue par transplantation</term>
<term>Staphylococcus aureus</term>
<term>Streptococcus pyogenes</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Bone Marrow Cells</term>
<term>Leukocytes, Mononuclear</term>
<term>Mucosal-Associated Invariant T Cells</term>
<term>Staphylococcus aureus</term>
<term>Streptococcus pyogenes</term>
<term>Transplantation Chimera</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Bone Marrow Cells</term>
<term>Leukocytes, Mononuclear</term>
<term>Mucosal-Associated Invariant T Cells</term>
<term>Staphylococcus aureus</term>
<term>Streptococcus pyogenes</term>
<term>Transplantation Chimera</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Agranulocytes</term>
<term>Antigènes bactériens</term>
<term>Cellules T invariantes associées aux muqueuses</term>
<term>Cellules de la moelle osseuse</term>
<term>Chimère obtenue par transplantation</term>
<term>Staphylococcus aureus</term>
<term>Streptococcus pyogenes</term>
<term>Superantigènes</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Chimère obtenue par transplantation</term>
</keywords>
<keywords scheme="MESH" qualifier="sécrétion" xml:lang="fr"><term>Entérotoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Antigènes bactériens</term>
<term>Entérotoxines</term>
<term>Superantigènes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Cells, Cultured</term>
<term>Crosses, Genetic</term>
<term>Female</term>
<term>Humans</term>
<term>Hybridomas</term>
<term>Immunity, Innate</term>
<term>Mice</term>
<term>Mice, Inbred NOD</term>
<term>Mice, Knockout</term>
<term>Mice, SCID</term>
<term>Mice, Transgenic</term>
<term>Models, Immunological</term>
<term>Specific Pathogen-Free Organisms</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Agranulocytes</term>
<term>Anergie clonale</term>
<term>Animaux</term>
<term>Cellules T invariantes associées aux muqueuses</term>
<term>Cellules cultivées</term>
<term>Cellules de la moelle osseuse</term>
<term>Croisements génétiques</term>
<term>Femelle</term>
<term>Humains</term>
<term>Hybridomes</term>
<term>Immunité innée</term>
<term>Lignée cellulaire</term>
<term>Modèles immunologiques</term>
<term>Organismes exempts d'organismes pathogènes spécifiques</term>
<term>Souris</term>
<term>Souris SCID</term>
<term>Souris de lignée NOD</term>
<term>Souris knockout</term>
<term>Souris transgéniques</term>
</keywords>
</textClass>
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</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Superantigens (SAgs) are potent exotoxins secreted by <italic>Staphylococcus aureus</italic>
 and <italic>Streptococcus pyogenes</italic>
. They target a large fraction of T cell pools to set in motion a “cytokine storm” with severe and sometimes life-threatening consequences typically encountered in toxic shock syndrome (TSS). Given the rapidity with which TSS develops, designing timely and truly targeted therapies for this syndrome requires identification of key mediators of the cytokine storm’s initial wave. Equally important, early host responses to SAgs can be accompanied or followed by a state of immunosuppression, which in turn jeopardizes the host’s ability to combat and clear infections. Unlike in mouse models, the mechanisms underlying SAg-associated immunosuppression in humans are ill-defined. In this work, we have identified a population of innate-like T cells, called mucosa-associated invariant T (MAIT) cells, as the most powerful source of pro-inflammatory cytokines after exposure to SAgs. We have utilized primary human peripheral blood and hepatic mononuclear cells, mouse MAIT hybridoma lines, HLA-DR4-transgenic mice, MAIT<sup>high</sup>
HLA-DR4<sup>+</sup>
 bone marrow chimeras, and humanized NOD-<italic>scid</italic>
 IL-2Rγ<sup>null</sup>
 mice to demonstrate for the first time that: <bold>i)</bold>
 mouse and human MAIT cells are hyperresponsive to SAgs, typified by staphylococcal enterotoxin B (SEB); <bold>ii)</bold>
 the human MAIT cell response to SEB is rapid and far greater in magnitude than that launched by unfractionated conventional T, invariant natural killer T (<italic>i</italic>
NKT) or γδ T cells, and is characterized by production of interferon (IFN)-γ, tumor necrosis factor (TNF)-α and interleukin (IL)-2, but not IL-17A; <bold>iii)</bold>
 high-affinity MHC class II interaction with SAgs, but not MHC-related protein 1 (MR1) participation, is required for MAIT cell activation; <bold>iv)</bold>
 MAIT cell responses to SEB can occur in a T cell receptor (TCR) Vβ–specific manner but are largely contributed by IL-12 and IL-18; <bold>v)</bold>
 as MAIT cells are primed by SAgs, they also begin to develop a molecular signature consistent with exhaustion and failure to participate in antimicrobial defense. Accordingly, they upregulate lymphocyte-activation gene 3 (LAG-3), T cell immunoglobulin and mucin-3 (TIM-3), and/or programmed cell death-1 (PD-1), and acquire an anergic phenotype that interferes with their cognate function against <italic>Klebsiella pneumoniae</italic>
 and <italic>Escherichia coli</italic>
; <bold>vi)</bold>
 MAIT cell hyperactivation and anergy co-utilize a signaling pathway that is governed by p38 and MEK1/2. Collectively, our findings demonstrate a pathogenic, rather than protective, role for MAIT cells during infection. Furthermore, we propose a novel mechanism of SAg-associated immunosuppression in humans. MAIT cells may therefore provide an attractive therapeutic target for the management of both early and late phases of severe SAg-mediated illnesses.</p>
</div>
</front>
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<author><name sortKey="Han, J" uniqKey="Han J">J Han</name>
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<author><name sortKey="Kotb, M" uniqKey="Kotb M">M Kotb</name>
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<li>Canada</li>
<li>France</li>
<li>Royaume-Uni</li>
<li>États-Unis</li>
</country>
<region><li>Victoria (État)</li>
<li>État de New York</li>
<li>Île-de-France</li>
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<settlement><li>Melbourne</li>
<li>Paris</li>
</settlement>
<orgName><li>Université de Melbourne</li>
</orgName>
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<tree><country name="Canada"><noRegion><name sortKey="Shaler, Christopher R" sort="Shaler, Christopher R" uniqKey="Shaler C" first="Christopher R." last="Shaler">Christopher R. Shaler</name>
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<name sortKey="Haeryfar, S M Mansour" sort="Haeryfar, S M Mansour" uniqKey="Haeryfar S" first="S. M. Mansour" last="Haeryfar">S. M. Mansour Haeryfar</name>
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<name sortKey="Haeryfar, S M Mansour" sort="Haeryfar, S M Mansour" uniqKey="Haeryfar S" first="S. M. Mansour" last="Haeryfar">S. M. Mansour Haeryfar</name>
<name sortKey="Haeryfar, S M Mansour" sort="Haeryfar, S M Mansour" uniqKey="Haeryfar S" first="S. M. Mansour" last="Haeryfar">S. M. Mansour Haeryfar</name>
<name sortKey="Hernandez Alejandro, Roberto" sort="Hernandez Alejandro, Roberto" uniqKey="Hernandez Alejandro R" first="Roberto" last="Hernandez-Alejandro">Roberto Hernandez-Alejandro</name>
<name sortKey="Mccormick, John K" sort="Mccormick, John K" uniqKey="Mccormick J" first="John K." last="Mccormick">John K. Mccormick</name>
<name sortKey="Mccormick, John K" sort="Mccormick, John K" uniqKey="Mccormick J" first="John K." last="Mccormick">John K. Mccormick</name>
<name sortKey="Mccormick, John K" sort="Mccormick, John K" uniqKey="Mccormick J" first="John K." last="Mccormick">John K. Mccormick</name>
<name sortKey="Memarnejadian, Arash" sort="Memarnejadian, Arash" uniqKey="Memarnejadian A" first="Arash" last="Memarnejadian">Arash Memarnejadian</name>
<name sortKey="Rudak, Patrick T" sort="Rudak, Patrick T" uniqKey="Rudak P" first="Patrick T." last="Rudak">Patrick T. Rudak</name>
<name sortKey="Szabo, Peter A" sort="Szabo, Peter A" uniqKey="Szabo P" first="Peter A." last="Szabo">Peter A. Szabo</name>
<name sortKey="Tun Abraham, Mauro E" sort="Tun Abraham, Mauro E" uniqKey="Tun Abraham M" first="Mauro E." last="Tun-Abraham">Mauro E. Tun-Abraham</name>
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<country name="Australie"><noRegion><name sortKey="Rossjohn, Jamie" sort="Rossjohn, Jamie" uniqKey="Rossjohn J" first="Jamie" last="Rossjohn">Jamie Rossjohn</name>
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<name sortKey="Corbett, Alexandra J" sort="Corbett, Alexandra J" uniqKey="Corbett A" first="Alexandra J." last="Corbett">Alexandra J. Corbett</name>
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Serveur d'exploration sur les relations entre la France et l'Australie

MAIT cells launch a rapid, robust and distinct hyperinflammatory response to bacterial superantigens and quickly acquire an anergic phenotype that impedes their cognate antimicrobial function: Defining a novel mechanism of superantigen-induced immunopathology and immunosuppression

MAIT cells launch a rapid, robust and distinct hyperinflammatory response to bacterial superantigens and quickly acquire an anergic phenotype that impedes their cognate antimicrobial function: Defining a novel mechanism of superantigen-induced immunopathology and immunosuppression

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