Antigen recognition by Influenza virus-primed lung-resident memory CD4 T cells accelerates regional antigen presentation and recruitment of newly activated T-cells to the lung

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Presentation Time: 02:15 PM - 03:30 PM
Poster Board Number: B128
Abstract ID: 4937

Presenting Author:
Caroline Finn , Post-doctoral Position at Univ. of Central Florida

Abstract:

Tissue-resident memory CD4 T cells (TRM) aid in protection against pathogens through shaping of inflammation at sites of infection. For example, influenza A virus (IAV) primed lung TRM induce acute local inflammatory responses that help to control initial viral until other antiviral T cells activated in secondary lymphoid organs reach the lung. Whether antigen-sensing by lung TRM can impact the efficiency of systemic T cell priming is unclear. To address this, we first generated OVA-specific lung TRM primed by infection with IAV expressing an OVA peptide. We then transferred these cells intranasally to naive mice to reconstitute a TRM compartment in an otherwise unprimed airway environment. We then gave fluorescently-labeled OVA protein intranasally to recall the TRM in the absence of any infection related signals, and compared the dynamics of OVA+ antigen presenting cells to those in mice that did not receive TRM. The TRM were rapidly activated by OVA, which correlated with increased numbers and activation status of OVA-bearing dendritic cells in the draining lymph nodes 20 hours later versus in mice without TRM. This TRM-mediated enhancement of regional antigen presentation accelerated the priming of naïve OVA-specific T cells, resulting in more newly activated effectors reaching the lung more quickly. Our results thus reveal a novel TRM sentinel function that promotes faster recruitment of new systemically-primed T cells to aid in responses against airway antigens.