CD8 + T Cell Biology in Cytokine Storm Syndromes.

Autor:	Sekine T; Center for Hematology and Regenerative Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden., Galgano D; Center for Hematology and Regenerative Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden., Casoni GP; Center for Hematology and Regenerative Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden., Meeths M; Childhood Cancer Research Unit, Department of Women's and Children's Health, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden.; Clinical Genetics Unit, Department of Molecular Medicine and Surgery, and Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital Solna, Stockholm, Sweden., Cron RQ; Division of Pediatric Rheumatology, University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL, USA., Bryceson YT; Center for Hematology and Regenerative Medicine, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. Yenan.Bryceson@ki.se.; Broegelmann Research Laboratory, Department of Clinical Sciences, University of Bergen, Bergen, Norway. Yenan.Bryceson@ki.se.
Jazyk:	angličtina
Zdroj:	Advances in experimental medicine and biology [Adv Exp Med Biol] 2024; Vol. 1448, pp. 129-144.
DOI:	10.1007/978-3-031-59815-9_10
Abstrakt:	Familial forms of hemophagocytic lymphohistiocytosis (HLH) are caused by loss-of-function mutations in genes encoding perforin as well as those required for release of perforin-containing cytotoxic granule constituent. Perforin is expressed by subsets of CD8 + T cells and NK cells, representing lymphocytes that share mechanism of target cell killing yet display distinct modes of target cell recognition. Here, we highlight recent findings concerning the genetics of familial HLH that implicate CD8 + T cells in the pathogenesis of HLH and discuss mechanistic insights from animal models as well as patients that reveal how CD8 + T cells may contribute to or drive disease, at least in part through release of IFN-γ. Intriguingly, CD8 + T cells and NK cells may act differentially in severe hyperinflammatory diseases such as HLH. We also discuss how CD8 + T cells may promote or drive pathology in other cytokine release syndromes (CSS). Moreover, we review the molecular mechanisms underpinning CD8 + T cell-mediated lymphocyte cytotoxicity, key to the development of familial HLH. Together, recent insights to the pathophysiology of CSS in general and HLH in particular are providing promising new therapeutic targets. (© 2024. The Author(s), under exclusive license to Springer Nature Switzerland AG.)
Databáze:	MEDLINE
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