The vertebrate immune system has evolved to protect the animal from the disturbances caused by invading pathogens. Given the great diversity of pathogens, the repertoire of antigen-specific T-cells must be equally diverse if all possible invading microorganisms are to be eliminated. However, the generation of an immense T-cell repertoire increases the likelihood of autoreactive T-cell development.

The immune system has developed mechanisms for eliminating autoreactive T cells or rendering them non-functional, to limit self-tissue damage whilst maintaining T-cell diversity. Tolerance to tissue antigens is achieved through a combination of events that occur in the thymus and in peripheral lymphoid organs aimed at eliminating or inactivating potentially dangerous, autoreactive T cells. The thymus plays a key role in eliminating dangerous self-specific T cells. However, many tissue proteins are not produced in large enough quantities in the thymus to induce clonal deletion or tolerization. For this reason, several mechanisms of T-cell tolerization have evolved in peripheral lymphoid organs, such as spleen and lymph nodes, where autoreactive T cells actively recognizing an antigen may become non-functional or may be deleted. The purpose of this study is to investigate the role of dendritic cells, special leukocytes capable of alerting the immune system to the presence of infections and responsible for the activation and control of both innate and adaptive immune responses, in the maintenance of peripheral T cell tolerance in young and aged mouse models.