Epidemiologic studies show an association between both neonatal RSV infection as well as maternal asthma and subsequent asthma development. However, the immunological mechanisms underlying this association remain elusive. We aim to bridge this gap and elucidate the mechanisms whereby severe RSV infection in early life renders the host more susceptible to allergic asthma.

Recent work from our lab has shown that during viral infection in adult mice, inf-cDC2s arise which acquire antigens via Fc receptors, binding immune complexes, and are superior in boosting CD4 Th cell immunity. We hypothesized that these inf-cDC2s also arise upon neonatal RSV infection, thereby lowering the threshold for allergic sensitization. When the mother is allergic on top, allergen specific antibodies will be transferred and immune complexes can be formed. Indeed, we see more antigen uptake by dendritic cells upon viral infection and even more when the mice are born to an allergic mother. When the mother cannot transfer antibodies, the antigen uptake drops significantly. Additionally, viral infection increases allergen specific T cell proliferation compared to mock infected mice. Again, this is more pronounced when antigen can be presented as an immune complex and happens in an Fc receptor dependent manner.

These results might be a first step to explain the epidemiologic observations linking allergic sensitization and asthma development to neonatal viral infection and maternal asthmatic status.