STING activation promotes autologous type I interferon-dependent development of type 1 regulatory T cells during malaria.

Autor:	Wang Y; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; Griffith University, School of Environment and Science, Nathan, Australia., De Labastida Rivera F; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Edwards CL; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; University of Queensland, School of Medicine, Brisbane, Australia., Frame TC; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; University of Queensland, School of Medicine, Brisbane, Australia., Engel JA; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Bukali L; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; University of Queensland, School of Medicine, Brisbane, Australia., Na J; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; University of Queensland, School of Medicine, Brisbane, Australia., Ng SS; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; Institute of Experimental Oncology, University Hospital Bonn, Bonn, Germany., Corvino D; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; Institute of Experimental Oncology, University Hospital Bonn, Bonn, Germany., Montes de Oca M; York Biomedical Research Institute, Hull York Medical School, University of York, York, United Kingdom., Bunn PT; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Soon MS; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Andrew D; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Loughland JR; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Zhang J; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Amante FH; QIMR Berghofer Medical Research Institute, Brisbane, Australia., Barber BE; QIMR Berghofer Medical Research Institute, Brisbane, Australia., McCarthy JS; Victorian Infectious Diseases Services, Doherty Institute, University of Melbourne, Melbourne, Australia., Lopez JA; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; Griffith University, School of Environment and Science, Nathan, Australia., Boyle MJ; QIMR Berghofer Medical Research Institute, Brisbane, Australia.; Life Sciences Division, Burnet Institute, Melbourne, Australia., Engwerda CR; QIMR Berghofer Medical Research Institute, Brisbane, Australia.
Jazyk:	angličtina
Zdroj:	The Journal of clinical investigation [J Clin Invest] 2023 Oct 02; Vol. 133 (19). Date of Electronic Publication: 2023 Oct 02.
DOI:	10.1172/JCI169417
Abstrakt:	The development of highly effective malaria vaccines and improvement of drug-treatment protocols to boost antiparasitic immunity are critical for malaria elimination. However, the rapid establishment of parasite-specific immune regulatory networks following exposure to malaria parasites hampers these efforts. Here, we identified stimulator of interferon genes (STING) as a critical mediator of type I interferon production by CD4+ T cells during blood-stage Plasmodium falciparum infection. The activation of STING in CD4+ T cells by cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) stimulated IFNB gene transcription, which promoted development of IL-10- and IFN-γ-coproducing CD4+ T (type I regulatory [Tr1]) cells. The critical role for type I IFN signaling for Tr1 cell development was confirmed in vivo using a preclinical malaria model. CD4+ T cell sensitivity to STING phosphorylation was increased in healthy volunteers following P. falciparum infection, particularly in Tr1 cells. These findings identified STING expressed by CD4+ T cells as an important mediator of type I IFN production and Tr1 cell development and activation during malaria.
Databáze:	MEDLINE
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