Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pbio.2003167
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dc.titleBacterial deception of MAIT cells in a cloud of superantigen and cytokines
dc.contributor.authorSandberg J.K.
dc.contributor.authorNorrby-Teglund A.
dc.contributor.authorLeeansyah E.
dc.date.accessioned2019-11-08T06:43:57Z
dc.date.available2019-11-08T06:43:57Z
dc.date.issued2017
dc.identifier.citationSandberg J.K., Norrby-Teglund A., Leeansyah E. (2017). Bacterial deception of MAIT cells in a cloud of superantigen and cytokines. PLoS Biology 15 (7) : e2003167. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pbio.2003167
dc.identifier.issn15449173
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/161892
dc.description.abstractThe bacterium Staphylococcus aureus is an important cause of the life-threatening condition toxic shock syndrome in humans. Bacterial toxins known as superantigens (SAgs) generate this illness by acting as broad activators of a substantial fraction of all T lymphocytes, bypassing the normally highly stringent T-cell receptor antigen specificity to cause a systemic inflammatory cytokine storm in the host. In a new study, Shaler et al. found that immune cells called mucosa-associated invariant T (MAIT) cells make an unexpectedly large contribution to the SAg response in a largely T-cell receptor?independent, cytokine-driven manner. Subsequent to such activation, the MAIT cells remain unresponsive to stimulation with bacterial antigen. Thus, S. aureus hijacks MAIT cells in the cytokine storm and leaves them functionally impaired. This work provides new insight into the role of MAIT cells in antibacterial immunity and opens new avenues of investigation to understand and possibly treat bacterial toxic shock and sepsis. ? 2017 Sandberg et al.
dc.sourceUnpaywall
dc.subjectbacterial antigen
dc.subjectcytokine
dc.subjectgamma interferon
dc.subjecthepatitis A virus cellular receptor 2
dc.subjectinterleukin 12
dc.subjectinterleukin 15
dc.subjectinterleukin 17
dc.subjectinterleukin 18
dc.subjectlymphocyte activation gene 3
dc.subjectmajor histocompatibility antigen class 1
dc.subjectmajor histocompatibility complex class Ib related protein 1
dc.subjectsuperantigen
dc.subjecttumor necrosis factor
dc.subjectunclassified drug
dc.subjectvitamin B group
dc.subjectcytokine
dc.subjectsuperantigen
dc.subjectbacterial immunity
dc.subjectcytokine storm
dc.subjecthuman
dc.subjectmucosal-associated invariant T cell
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectReview
dc.subjectsepsis
dc.subjectStaphylococcus aureus
dc.subjectStreptococcus pyogenes
dc.subjecttoxic shock syndrome
dc.subjectanimal
dc.subjectbiological model
dc.subjectcellular immunity
dc.subjectclonal anergy
dc.subjectimmunology
dc.subjectlymphocyte activation
dc.subjectmetabolism
dc.subjectmicrobiology
dc.subjectmucosal-associated invariant T cell
dc.subjectStaphylococcus aureus
dc.subjectT lymphocyte
dc.subjectAnimals
dc.subjectClonal Anergy
dc.subjectCytokines
dc.subjectHumans
dc.subjectImmunity, Cellular
dc.subjectLymphocyte Activation
dc.subjectModels, Immunological
dc.subjectMucosal-Associated Invariant T Cells
dc.subjectStaphylococcus aureus
dc.subjectSuperantigens
dc.subjectT-Lymphocytes
dc.typeReview
dc.contributor.departmentDEAN'S OFFICE (DUKE-NUS MEDICAL SCHOOL)
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1371/journal.pbio.2003167
dc.description.sourcetitlePLoS Biology
dc.description.volume15
dc.description.issue7
dc.description.pagee2003167
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