tetano
Editor, Senior Moderator
J Immunol
. 2023 Mar 13;ji2200931.
doi: 10.4049/jimmunol.2200931. Online ahead of print.
Cutting Edge: Influenza-Induced CD11alo Airway CD103+ Tissue Resident Memory T Cells Exhibit Compromised IFN-γ Production after In Vivo TCR Stimulation
Stephanie van de Wall[SUP] 1 [/SUP], Sequoia Crooks[SUP] 1 2 [/SUP], Steven M Varga[SUP] 1 2 [/SUP], Vladimir P Badovinac[SUP] 1 2 [/SUP], John T Harty[SUP] 1 2 [/SUP]
Affiliations
Abstract
Although tissue resident memory T cells (TRM) in the lung confer robust protection against secondary influenza infection, their in vivo production of IFN-γ is unknown. In this study, using a mouse model, we evaluated production of IFN-γ by influenza-induced TRM (defined as CD103+) that localize to the airways or lung parenchyma. Airway TRM consist of both CD11ahi and CD11alo populations, with low CD11a expression signifying prolonged airway residence. In vitro, high-dose peptide stimulation evoked IFN-γ from most CD11ahi airway and parenchymal TRM, whereas most CD11alo airway TRM did not produce IFN-γ. In vivo production of IFN-γ was clearly detectable in CD11ahi airway and parenchymal TRM but essentially absent in CD11alo airway TRM, irrespective of airway-instilled peptide concentration or influenza reinfection. The majority of IFN-γ-producing airway TRM in vivo were CD11ahi, suggesting recent airway entry. These results question the contribution of long-term CD11alo airway TRM to influenza immunity and reinforce the importance of defining TRM tissue compartment-specific contributions to protective immunity.
. 2023 Mar 13;ji2200931.
doi: 10.4049/jimmunol.2200931. Online ahead of print.
Cutting Edge: Influenza-Induced CD11alo Airway CD103+ Tissue Resident Memory T Cells Exhibit Compromised IFN-γ Production after In Vivo TCR Stimulation
Stephanie van de Wall[SUP] 1 [/SUP], Sequoia Crooks[SUP] 1 2 [/SUP], Steven M Varga[SUP] 1 2 [/SUP], Vladimir P Badovinac[SUP] 1 2 [/SUP], John T Harty[SUP] 1 2 [/SUP]
Affiliations
- PMID: 36912465
- DOI: 10.4049/jimmunol.2200931
Abstract
Although tissue resident memory T cells (TRM) in the lung confer robust protection against secondary influenza infection, their in vivo production of IFN-γ is unknown. In this study, using a mouse model, we evaluated production of IFN-γ by influenza-induced TRM (defined as CD103+) that localize to the airways or lung parenchyma. Airway TRM consist of both CD11ahi and CD11alo populations, with low CD11a expression signifying prolonged airway residence. In vitro, high-dose peptide stimulation evoked IFN-γ from most CD11ahi airway and parenchymal TRM, whereas most CD11alo airway TRM did not produce IFN-γ. In vivo production of IFN-γ was clearly detectable in CD11ahi airway and parenchymal TRM but essentially absent in CD11alo airway TRM, irrespective of airway-instilled peptide concentration or influenza reinfection. The majority of IFN-γ-producing airway TRM in vivo were CD11ahi, suggesting recent airway entry. These results question the contribution of long-term CD11alo airway TRM to influenza immunity and reinforce the importance of defining TRM tissue compartment-specific contributions to protective immunity.