Do age-associated changes in 'physiologic' autoantibodies contribute to infection, atherosclerosis, and Alzheimer's disease?

More than 25 years ago, Pierre Grabar proposed that the age-associated increase in serum autoantibodies reflected a homeostatic function of the immune system that defended the internal milieu by targeting senescent molecules and cells for elimination. This mini-review examines recent evidence that autoantibodies may influence the risk of the elderly developing infectious, atherosclerotic, or Alzheimer's disease. Auto-anti-idiotypic antibodies suppress the antibody response to the nominal antigen and, thus, may contribute to the increased risk of infection and poor response to vaccines in the elderly. In contrast, low levels of autoantibodies to oxidised low-density lipoproteins or to the amyloid beta peptide may contribute to the increased risk of developing atherosclerosis of Alzheimer's disease, respectively.