The increased frequency of organ transplant operations over the decades has given rise to some startling statistics; five-year survival of transplanted tissue is only 50% for lung transplants, 67% for liver transplants and not much better for other organs.1 These bleak statistics are attributable to the destruction of transplanted tissue by the host's (tissue recipient's) immune system, which ultimately leads to the rejection of the transplanted organ.
Despite the widespread use of immunosuppressive drugs and advancements in medical technology, the immune system remains a formidable factor in successful organ transplantation.2
Certain aspects of the immune system are responsible for suppressing inflammation and inhibiting transplant rejection. Important inhibitory components of the immune system are Treg, (or T regulatory cells). The inflammatory cytokines IL-1β, IL-2, IL-6, IL-15, IL-21 and tumor necrosis factor-alpha (TNF-α), by inhibiting the function of Treg cells and promoting the activation of cytotoxic T cells, are responsible for the intensity of the attack against the transplanted tissue by the host's immune system.3
New findings demonstrate that calcineurin inhibitors (CNIs), immunosuppressive drugs widely prescribed to transplant patients, fail to address an important underlying cause of transplant rejection—insufficient levels of protective Treg cells.
Several nutrients have been shown in peer-reviewed studies to target the specific inflammatory cytokines that are dually responsible for the stimulation of aggressive T cells and the suppression of protective Treg cells.