B cell activation and antibody production are known to be impaired with age in both mice and humans, but it was not clear whether this defect is intrinsic to B cells or is a by-product of declining CD4 T cell helper functions.
Eaton and colleagues transferred young or old CD4 T cells into mice lacking their own CD4 T cells to determine which cells are responsible for the age-related decline in B cell function. They show that B cell activation and antibody production can be restored in old mice if they are infused with young CD4 T cells prior to immunization. On the flip side, young mice infused with old CD4 T cells developed antibody defects, even though their B cells were young. In other words, old B cells function like young ones if provided with signals from young helper T cells. While the mechanism is not completely clear, the authors show that old T cells can travel to the right location in the spleen of the mice, but have fewer of the surface proteins that send stimulatory signals to B cells.
Journal of Experimental Medicine