Please use this identifier to cite or link to this item: https://dora.health.qld.gov.au/qldresearchjspui/handle/1/4757
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dc.contributor.authorKumar, V.en
dc.date.accessioned2022-11-07T23:56:02Z-
dc.date.available2022-11-07T23:56:02Z-
dc.date.issued2018en
dc.identifier.citation97, (6), 2018, p. 379-392en
dc.identifier.otherRISen
dc.identifier.urihttp://dora.health.qld.gov.au/qldresearchjspui/handle/1/4757-
dc.description.abstractSepsis has always been considered as a big challenge for pharmaceutical companies in terms of discovering and designing new therapeutics. The pathogenesis of sepsis involves aberrant activation of innate immune cells (i.e. macrophages, neutrophils etc.) at early stages. However, a stage of immunosuppression is also observed during sepsis even in the patients who have recovered from it. This stage of immunosuppression is observed due to the loss of conventional (i.e. CD4+, CD8+) T cells, Th17 cells and an upregulation of regulatory T cells (Tregs). This process also impacts metabolic processes controlling immune cell metabolism called immunometabolism. The present review is focused on the T cell-mediated immune response, their immunometabolism and targeting T cell immunometabolism during sepsis as future therapeutic approach. The first part of the manuscripts describes an impact of sepsis on conventional T cells, Th17 cells and Tregs along with their impact on sepsis. The subsequent section further describes the immunometabolism of these cells (CD4+, CD8+, Th17, and Tregs) under normal conditions and during sepsis-induced immunosuppression. The article ends with the therapeutic targeting of T cell immunometabolism (both conventional T cells and Tregs) during sepsis as a future immunomodulatory approach for its management.L20007648552018-05-24 <br />2018-11-26 <br />en
dc.language.isoenen
dc.relation.ispartofEuropean Journal of Cell Biologyen
dc.titleT cells and their immunometabolism: A novel way to understanding sepsis immunopathogenesis and future therapeuticsen
dc.typeArticleen
dc.identifier.doi10.1016/j.ejcb.2018.05.001en
dc.subject.keywordsimmunopathogenesisen
dc.subject.keywordsimmunosuppressive treatmenten
dc.subject.keywordsmetabolismen
dc.subject.keywordsnonhumanen
dc.subject.keywordspriority journalen
dc.subject.keywordsregulatory T lymphocyteen
dc.subject.keywordsreviewen
dc.subject.keywordsfuturologyen
dc.subject.keywordsT lymphocyteen
dc.subject.keywordstarget cellen
dc.subject.keywordsTh17 cellen
dc.subject.keywordsCD4+ T lymphocyteCD8+ T lymphocyteen
dc.subject.keywordssepsisen
dc.subject.keywordshomeostasisen
dc.subject.keywordshumanen
dc.subject.keywordsimmune systemen
dc.relation.urlhttps://www.embase.com/search/results?subaction=viewrecord&id=L2000764855&from=exporthttp://dx.doi.org/10.1016/j.ejcb.2018.05.001 |en
dc.identifier.risid881en
dc.description.pages379-392en
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
Appears in Sites:Children's Health Queensland Publications
Queensland Health Publications
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