A Bidirectional Relationship Between Cellular Senescence and Immune System Aging

The pace of age-related loss of function and consequent mortality accelerates over time, picking up particularly rapidly in later life. This is characteristic of systems in which multiple processes feed into each other. A causes B, but B also makes A worse. In the biology of aging there are many more than two processes at work, but the authors of today's open access paper picked two areas of aging in order to examine their bidirectional relationship. Firstly the accumulation of senescent cells, and secondly immunosenescence, the age-related decline of immune system function. Cells become senescent constantly in the body, largely as a result of somatic cells reaching the Hayflick limit on replication. Wound healing, potentially cancerous molecular damage, and the signaling of other senescent cells are also relevant causes of cellular senescence. Some senescent cells self-destruct, while others are destroyed by the immune system. That immune surveillance of senescent cells becomes slower and less effective as the immune system falls into immunosenescence in later life, allowing for senescent cell accumulation. Equally, senescent cells secrete inflammatory, disruptive signaling that causes chronic inflammation as well as harmful changes in cell behavior in the hematopoietic system responsible for generating new immune cells. Inflammation also contributes to the involution of the thymus, where T cells mature, accelerating the decline of adaptive immune function by r...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs