학술논문

Maintenance of Functional CD57+ Cytolytic CD4+ T Cells in HIV+ Elite Controllers.
Document Type
Academic Journal
Author
Phetsouphanh C; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.; Aldridge D; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.; Marchi E; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.; Munier CML; Department of Medicine, University of New South Wales, Sydney, NSW, Australia.; Meyerowitz J; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.; Murray L; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.; Van Vuuren C; Military Hospital, Bloemfontein, South Africa.; Goedhals D; National Health Laboratory Service, Division of Virology, University of the Free State, Bloemfontein, South Africa.; Fidler S; Imperial College London, London, United Kingdom.; Kelleher A; Department of Medicine, University of New South Wales, Sydney, NSW, Australia.; Klenerman P; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.; Frater J; Peter Medawar Building for Pathogen Research, University of Oxford, Oxford, United Kingdom.
Source
Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
Subject
Language
English
Abstract
Cytolytic CD4+ T cells play a prominent role in chronic viral infection. CD4+ CTLs clones specific for HIV-1 Nef and Gag are capable of killing HIV-1 infected CD4+ T cells and macrophages. Additionally, HIV-specific cytolytic CD4+ T cell responses in acute HIV infection are predictive of disease progression. CD57 expression on CD4s identifies cytolytic cells. These cells were dramatically increased in chronic HIV infection. CD57 expression correlated with cytolytic granules, granzyme B and perforin expression. They express lower CCR5 compared to CD57- cells, have less HIV total DNA, and were a minor component of the HIV reservoir. A small percentage of CD57+ CD4+ CTLs from EC were HIV-specific, could upregulate IFNγ with Gag peptide stimulation, express cytolytic granule markers and maintain Tbet high Eomes+ transcription factor phenotype. This was not observed in viraemic controllers. The maintenance of HIV-specific CD4 cytolytic function in Elite controllers together with CD8 CTLs may be important for the control of HIV viraemia and of potential relevance to cure strategies.