Liver transplant recipients develop premature immune senescence, the normal process by which the immune system ages and becomes less effective, researchers at the University of Cambridge have found.
Full details appear in the May issue of
Liver Transplantation, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases (AASLD).
The University of Cambridge research team investigated whether the chronic immune stress of liver disease and organ transplantation accelerates aging of the immune system, which in turn contributes to excess morbidity and mortality in established liver graft recipients. Study leader Dr. Graeme Alexander explains, "There is a marked increase in the prevalence of cardiac disease, malignancy, cerebrovascular disease and infections in patients with established liver grafts, affecting a majority of cases eventually and which in the past have been attributed to agents used to suppress immune responses. However, an alternative (and not exclusive) hypothesis is that liver transplant recipients develop premature immune senescence which is also associated with these same pathologies, perhaps consequent to chronic alloantigenic stimulation."
The study participants included 97 liver transplant recipients with established grafts (at least 3 years) and 41 age and sex-matched controls. When cases were compared with controls for each marker of immune senescence, the researchers discovered that liver graft recipients had shorter T-cell telomeres and more cells of a mature phenotype than healthy age-matched controls. Telomeres are chromosomal structures that shorten each time a cell divides. Scientists theorize that telomeres eventually become so short that they stop functioning, which causes the cell to stop proliferating. T-cells are lymphocytes, major players of the immune system. With age, these cells become less active, making the body more vulnerable. These cells are the focus of much research on the aging immune system.