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MAIT cell activation augments adenovirus vector vaccine immunogenicity

Title: MAIT cell activation augments adenovirus vector vaccine immunogenicity
Authors: Provine, Nicholas M.; Amini, Ali; Garner, Lucy C.; Spencer, Alexandra J.; Dold, Christina; Hutchings, Claire; Silva Reyes, Laura; FitzPatrick, Michael E. B.; Chinnakannan, Senthil; Oguti, Blanche; Raymond, Meriel; Ulaszewska, Marta; Troise, Fulvia; Sharpe, Hannah; Morgan, Sophie B.; Hinks, Timothy S. C.; Lambe, Teresa; Capone, Stefania; Folgori, Antonella; Barnes, Eleanor; Rollier, Christine S.; Pollard, Andrew J.; Klenerman, Paul
Contributors: Wellcome; Medical Research Council; NIHR Biomedical Research Centre; Oxford-UCB Postdoctoral Fellowship; NIHR Oxford Biomedical Research Centre; Oxford-Celgene Doctoral Fellowship
Source: Science ; volume 371, issue 6528, page 521-526 ; ISSN 0036-8075 1095-9203
Publisher Information: American Association for the Advancement of Science (AAAS)
Publication Year: 2021
Description: Vaccines get a help-MAIT Mucosal-associated invariant T (MAIT) cells are a T cell subset important for mucosal homeostasis. These cells recognize derivatives of microbiota-derived vitamin B2 precursors but can also be activated by certain cytokines in the context of viral infections. Provine et al. report that a leading adenoviral vector vaccine, ChAdOx1, activated MAIT cells in immunized mice (see the Perspective by Juno and O'Connor). This activation required interferon-α produced by plasmacytoid dendritic cells as well as monocyte-derived interleukin-18 and tumor necrosis factor. MAIT cell activation positively correlated with vaccine-mediated T cell responses in human subjects, and mice deficient in MAIT cells showed impaired CD8 + T cell immunity to target antigens after vaccination. This work suggests an additional pathway that could be exploited to enhance the efficacy of vaccines. Science , this issue p. 521 ; see also p. 460
Document Type: article in journal/newspaper
Language: English
DOI: 10.1126/science.aax8819
Availability: https://doi.org/10.1126/science.aax8819; https://syndication.highwire.org/content/doi/10.1126/science.aax8819; https://www.science.org/doi/pdf/10.1126/science.aax8819
Accession Number: edsbas.7B2D9C49
Database: BASE