1636 AUTO - ANTItDIOTYPE ANTIBODY IN AGING

A decline in immune responsiveness with age has been well documented (1-10). It is known that the B cell function of aged mice is relatively more intact than T cell function, at least quantitatively. Qualitative differences in B cell function do exist, including a decreased affinity of antibody produced by cells from old mice (3) and an enhanced tendency to produce autoantibodies (1). In a previous report (11) we have suggested that part of the age-associated decline in the immune response is due to an increased production of auto-antiidiotype antibodies (anti-Id) 1 by old mice (11). A high auto-anti-Id response by aged animals was also suggested by studies of Kl inman (12). Such an increase in auto-anti-Id has been demonstrated in both thymic-independent (13) and thymie-dependent (14) responses. We describe here a series of experiments that analyze the cellular basis for the increased production of auto-antiId during the immune response of aged mice to trinitrophenylated-lysyl-Ficoll (TNPF). We sought to determine whether the elevated production of auto-anti-Id by old mice is stable upon transfer of spleen cells to irradiated recipients, and whether B or T cells were primarily responsible for this phenomenon. The results to be reported support the view that this age-related alteration in the immune response reflects a change in the peripheral mature B cell population rather than a change in the immature B cell population in the bone marrow, and that peripheral T cells play an important role in determining this property of peripheral B cells.