During a bout of influenza, B cells interact with other immune cells and then take different paths to defend the body. One path is the B cells that differentiate into lung-resident memory B cells, or lung-BRMs, that are critical for pulmonary immunity. These long-lived, non-circulating lung-BRMs migrate to the lungs from draining lymph nodes and reside there permanently as the first layer of defense that can quickly react to produce antibodies in a future infection.
During a bout of influenza, B cells interact with other immune cells and then take different paths to defend the body. One path is the B cells that differentiate into antibody producing cells. Another path is the B cells that differentiate into lung-resident memory B cells, or lung-BRMs, that are critical for pulmonary immunity.
Understanding the mechanism that creates these lung-BRMs is important for better flu vaccine development. Seasonal influenza kills 290,000 to 650,000 people each year, according to the World Health Organization. Yet flu vaccines are less effective in the elderly -- the most at-risk population -- compared to younger people. Also, there is need for vaccines that are more effective against later variants of a particular virus.
During influenza infection, both Tfh and B cells are present at germinal centers in the lymph nodes that drain the lungs. Class-switched memory B cells that are primed against the influenza virus begin to appear in the lungs at day 10 of the infection, and their numbers peak at Day 30. However, the UAB researchers found that, if mice were deficient in Tfh cells, or if the Tfh cells were blocked by an antibody, the lung-BRMs did not accumulate.
In mechanistic details, the researchers found that intrinsic IFN-γ-STAT1 signaling in B cells in the germinal center of lung-draining lymph nodes promoted expression of the T-bet transcription factor, and T-bet was necessary for differentiation into pre-memory B cells that express the surface marker CXCR3. Subsequently, CXCR3+ pre-memory B cells differentiated into CXCR3+ memory B cells, which exited the mediastinal lymph nodes and homed to the lung to become lung-BRMs.
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