Lack of B7-2 expression in the germinal centers of aged mice
The humoral immune response is known to be depressed in the aged mouse. This immunodeficiency is associated with an impairment in the formation of germinal centers, the anatomic site of antibody affinity maturation and memory B cell generation. The formation of germinal centers is dependent on the expression of costimulatory molecules. We have investigated the expression of the recently identified costimulatory molecule, B7-2, and another activation marker, GL7, in the germinal centers of aged mice. In contrast to young syngeneic controls, B7-2 and GL7 are not expressed in the germinal centers of aged C57BL/6 mice. Administration of an antibody specific for the B7-2 molecule produces a defective immune response in young mice that is similar to that seen in old animals. Thus, we propose that the absence of differentiation pathways mediated by B7-2 in aged mice defines a major, age-related immunodeficiency.
