Lung influenza virus-specific memory CD4 T cell location and optimal cytokine production are dependent on interactions with lung antigen-presenting cells.

Influenza A virus (IAV) infection leads to the formation of mucosal memory CD4 T cells that can protect the host. An in-depth understanding of the signals that shape memory cell development is required for more effective vaccine design. We have examined the formation of memory CD4 T cells in the lung following IAV infection of mice, characterizing changes to the lung landscape and immune cell composition.

Triphasic production of IFN by innate and adaptive lymphocytes following influenza A virus infection.

Interferon gamma (IFN) is a potent antiviral cytokine that can be produced by many innate and adaptive immune cells during infection. Currently, our understanding of which cells produce IFN and where they are located at different stages of an infection is limited. We have used reporter mice to investigate expression of mRNA in the lung and secondary lymphoid organs during and following influenza A virus (IAV) infection.

BTN3A3 evasion promotes the zoonotic potential of influenza A viruses.

Spillover events of avian influenza A viruses (IAVs) to humans could represent the first step in a future pandemic. Several factors that limit the transmission and replication of avian IAVs in mammals have been identified. There are several gaps in our understanding to predict which virus lineages are more likely to cross the species barrier and cause disease in humans.

Antigen presenting cells: Professionals, amateurs, and spectators in the 'long game' of lung immunity.

The lung is frequently and repeatedly exposed to invading pathogens and thus requires constant immunosurveillance. Professional antigen presenting cells (APCs), including dendritic cells, engulf invading pathogens and present their peptides via major histocompatibility complexes (MHC) I and II, to CD8 or CD4 T cells. Epithelial cells and stromal cells (including fibroblasts) provide more than structural support, they are increasingly recognised as key players in the immune response, acting as non-professional APCs through interactions with antigen experienced T cells that migrate to the lung.