TGF-β1 signaling inhibit the in vitro apoptotic, infection and stimulatory cell response induced by influenza H1N1 virus infection on A549 cells.

Influenza A virus (IAV) infection induces host cell responses that could derive in inflammatory and apoptotic response. In this respect, in multiple pathological situations, TGF-β1 has shown anti-inflammatory effect, but its role during IAV infection is poorly understood. Interestingly, recent profiling expression studies have suggested that the TGF-β1 pathway could be functionally related to the IAV infection's host response.

Flagellin is a Th1 polarizing factor for human CD4 T cells and induces protection in a murine neonatal vaccination model of rotavirus infection.

Neonates have an increased susceptibility to infections, particularly those caused by intracellular pathogens, leading to high morbidity and mortality rates. This is partly because of a poor response of neonatal CD4 T cells, leading to deficient antibody production and a low production of IFN-γ, resulting in deficient elimination of intracellular pathogens. The poor memory response of human neonates has underpinned the need for improving vaccine formulations.