Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom; The Kirby Institute, University of New South Wales, Sydney, Australia
Prabhjeet Phalora
Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom
Carl-Philipp Hackstein
Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom
John Thornhill
Imperial College London, London, United Kingdom
C Mee Ling Munier
The Kirby Institute, University of New South Wales, Sydney, Australia
Jodi Meyerowitz
Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom
Lyle Murray
Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom
Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
Jeffrey YW Mak
ARC Centre of Excellence in Advanced Molecular Imaging, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia; ARC Centre of Excellence in Advanced Molecular Imaging, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia
David P Fairlie
ARC Centre of Excellence in Advanced Molecular Imaging, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia; ARC Centre of Excellence in Advanced Molecular Imaging, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia
Sarah Fidler
Imperial College London, London, United Kingdom
Anthony D Kelleher
The Kirby Institute, University of New South Wales, Sydney, Australia
Human MAIT cells sit at the interface between innate and adaptive immunity, are polyfunctional and are capable of killing pathogen infected cells via recognition of the Class IB molecule MR1. MAIT cells have recently been shown to possess an antiviral protective role in vivo and we therefore sought to explore this in relation to HIV-1 infection. There was marked activation of MAIT cells in vivo in HIV-1-infected individuals, which decreased following ART. Stimulation of THP1 monocytes with R5 tropic HIVBAL potently activated MAIT cells in vitro. This activation was dependent on IL-12 and IL-18 but was independent of the TCR. Upon activation, MAIT cells were able to upregulate granzyme B, IFNγ and HIV-1 restriction factors CCL3, 4, and 5. Restriction factors produced by MAIT cells inhibited HIV-1 infection of primary PBMCs and immortalized target cells in vitro. These data reveal MAIT cells to be an additional T cell population responding to HIV-1, with a potentially important role in controlling viral replication at mucosal sites.
