Role of Fc receptors in lymphocyte activation: deficiency in T- and B-lymphocytes from aged animals.

Fc fragments derived from human immunoglobulin possess the ability to induce B-cell proliferation, polyclonal antibody responses, and augment cell-mediated and T-dependent humoral responses. However, aged animals display much lower responses to Fc fragment stimulation. Proliferation and polyclonal antibody synthesis are reduced two-five-fold in aged animals compared to the young-adult responses. Furthermore, Fc fragments are unable to potentiate plaque-forming cell (PFC) development in aged animals. Aged B-lymphocytes are deficient in responding to Fc fragments, as their admixture with young-adult T-cells does not restore polyclonal antibody formation. T-cells from aged animals are also ineffective in promoting the polyclonal response when mixed with young-adult B-cells. The T-cell lesion has been further defined as a deficiency in production of an Fc fragment induced T-cell-replacing factor [(Fc)TRF]. The inability of Fc fragments to potentiate anti-SRBC responses in aged animals is also due to a T-cell defect which can be corrected by supplementation with interleukin-2 (IL-2).