Chronic inflammation degrades CD4 T cell immunity to prior vaccines in treated HIV infection

Melissa Kießling, John J. Cole, Sabrina Kübel, Paulina Klein, Klaus Korn, Amy R. Henry, Farida Laboune, Slim Fourati, Ellen Harrer, Thomas Harrer, Daniel C. Douek, Klaus Überla and Krystelle Nganou-Makamdop ()
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Melissa Kießling: Friedrich-Alexander-Universität Erlangen-Nürnberg
John J. Cole: School of Infection & Immunity, University of Glasgow
Sabrina Kübel: Friedrich-Alexander-Universität Erlangen-Nürnberg
Paulina Klein: Friedrich-Alexander-Universität Erlangen-Nürnberg
Klaus Korn: Friedrich-Alexander-Universität Erlangen-Nürnberg
Amy R. Henry: Human Immunology Section, Vaccine Research Center, National Institutes of Health
Farida Laboune: Human Immunology Section, Vaccine Research Center, National Institutes of Health
Slim Fourati: Department of Medicine, Northwestern University, Feinberg School of Medicine
Ellen Harrer: Infectious Disease and Immunodeficiency Section, Department of Internal Medicine 3, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Thomas Harrer: Infectious Disease and Immunodeficiency Section, Department of Internal Medicine 3, Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg
Daniel C. Douek: Human Immunology Section, Vaccine Research Center, National Institutes of Health
Klaus Überla: Friedrich-Alexander-Universität Erlangen-Nürnberg
Krystelle Nganou-Makamdop: Friedrich-Alexander-Universität Erlangen-Nürnberg

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract To date, our understanding of how HIV infection impacts vaccine-induced cellular immunity is limited. Here, we investigate inflammation, immune activation and antigen-specific T cell responses in HIV-uninfected and antiretroviral-treated HIV-infected people. Our findings highlight lower recall responses of antigen-specific CD4 T cells that correlate with high plasma cytokines levels, T cell hyperactivation and an altered composition of the T subsets enriched with more differentiated cells in the HIV-infected group. Transcriptomic analysis reveals that antigen-specific CD4 T cells of the HIV-infected group have a reduced expression of gene sets previously reported to correlate with vaccine-induced pathogen-specific protective immunity and further identifies a consistent impairment of the IFNα and IFNγ response pathways as mechanism for the functional loss of recall CD4 T cell responses in antiretroviral-treated people. Lastly, in vitro treatment with drugs that reduce inflammation results in higher memory CD4 T cell IFNγ responses. Together, our findings suggest that vaccine-induced cellular immunity may benefit from strategies to counteract inflammation in HIV infection.

Date: 2024
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DOI: 10.1038/s41467-024-54605-3

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