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Type I interferons and MAVS signaling are necessary for tissue resident memory CD8+ T cell responses to RSV infection

Varese, Augusto ; Nakawesi, Joy ; Farias, Ana ; Kirsebom, Freja C M ; Paulsen, Michelle ; Nuriev, Rinat ; Johansson, Cecilia Subbarao, Kanta

PLoS pathogens, 2022-02, Vol.18 (2), p.e1010272 [Periódico revisado por pares]

United States: Public Library of Science

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Título:
Type I interferons and MAVS signaling are necessary for tissue resident memory CD8+ T cell responses to RSV infection
Autor: Varese, Augusto ; Nakawesi, Joy ; Farias, Ana ; Kirsebom, Freja C M ; Paulsen, Michelle ; Nuriev, Rinat ; Johansson, Cecilia
Subbarao, Kanta
Assuntos: Adaptor Proteins, Signal Transducing - immunology ; Animal models ; Animals ; Antigens ; Biology and life sciences ; Bronchopneumonia ; CD8 antigen ; CD8-Positive T-Lymphocytes - immunology ; Children ; Granzyme B ; Granzymes - immunology ; Granzymes - metabolism ; Immune response ; Immune system ; Immunity, Innate ; Immunologic Memory ; Immunological memory ; Infections ; Influenza ; Innate immunity ; Interferon Type I - immunology ; Interferon Type I - metabolism ; Lung - immunology ; Lungs ; Lymphocytes ; Lymphocytes T ; Medicine and health sciences ; Memory cells ; Memory T Cells - immunology ; Mice ; Mice, Inbred C57BL ; MyD88 protein ; Neutrophils ; Pathogens ; Research and Analysis Methods ; Respiratory syncytial virus ; Respiratory Syncytial Virus Infections - immunology ; Respiratory Syncytial Virus Infections - virology ; Respiratory Syncytial Viruses - immunology ; Signal Transduction ; Vaccines ; Viral infections ; Viruses ; α-Interferon ; γ-Interferon
É parte de: PLoS pathogens, 2022-02, Vol.18 (2), p.e1010272
Notas: new_version
Current address: Instituto de Investigaciones Biomédicas en Retrovirus y SIDA (INBIRS), Facultad de Medicina Universidad de Buenos Aires, Buenos Aires, Argentina
The authors have declared that no competing interests exist.
Descrição: Respiratory syncytial virus (RSV) can cause bronchiolitis and viral pneumonia in young children and the elderly. Lack of vaccines and recurrence of RSV infection indicate the difficulty in eliciting protective memory immune responses. Tissue resident memory T cells (TRM) can confer protection from pathogen re-infection and, in human experimental RSV infection, the presence of lung CD8+ TRM cells correlates with a better outcome. However, the requirements for generating and maintaining lung TRM cells during RSV infection are not fully understood. Here, we use mouse models to assess the impact of innate immune response determinants in the generation and subsequent expansion of the TRM cell pool during RSV infection. We show that CD8+ TRM cells expand independently from systemic CD8+ T cells after RSV re-infection. Re-infected MAVS and MyD88/TRIF deficient mice, lacking key components involved in innate immune recognition of RSV and induction of type I interferons (IFN-α/β), display impaired expansion of CD8+ TRM cells and reduction in antigen specific production of granzyme B and IFN-γ. IFN-α treatment of MAVS deficient mice during primary RSV infection restored TRM cell expansion upon re-challenge but failed to recover TRM cell functionality. Our data reveal how innate immunity, including the axis controlling type I IFN induction, instructs and regulates CD8+ TRM cell responses to RSV infection, suggesting possible mechanisms for therapeutic intervention.
Editor: United States: Public Library of Science
Idioma: Inglês

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Type I interferons and MAVS signaling are necessary for tissue resident memory CD8+ T cell responses to RSV infection

Varese, Augusto ; Nakawesi, Joy ; Farias, Ana ; Kirsebom, Freja C M ; Paulsen, Michelle ; Nuriev, Rinat ; Johansson, Cecilia Subbarao, Kanta

United States: Public Library of Science

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