In a paper published in Immunity, the research has for the first time defined the mechanisms that enable resident memory B (BRM) cells to rapidly deliver antibodies at sites infected with the influenza virus.
Tal Arnon, Associate Professor at the Kennedy Institute said: "Resident memory B cells develop in the lungs of influenza-infected hosts. We uncovered a new network of innate-adaptive cell interactions that coordinates the recruitment of BRM cells to infected sites, subsequently leading to the accumulation of plasma cells directly within these regions."
The study used 3D and two-photon microscopy to visualise the BRM cells within the lungs of influenza-virus immune and reinfected subjects. The tissues were rechallenged with the virus and the BRM cells tracked in situ. During the memory phase, prior to reinfection, the cells were sparsely scattered across the alveoli displaying limited migration capabilities. However, within 24hrs after secondary infection, the cells doubled their mean migration speeds, travelled long distances to accumulate at the infected site, and subsequently differentiated into plasma cells.