Autoantibodies in aging: an attempt to correct a weakening debridement mechanism.
Autoantibodies are present in small quantities throughout most of the host life but increase with aging. It is unlikely they are the etiologic cause of aging. They probably do contribute to some of the pathologic changes seen in aging such as amyloid deposits. Autoantibodies, when they are part of a functioning microdebridement system, like other antibodies, are one method of increasing tissue debridement. Autoantibodies are a broad biologic phenomenon capable of doing far more good than harm. Inflammation weakens with aging and thus microdebridement is weakened. The immune system weakens with aging but is stimulated by the increasing accumulation of antigen derived from tissue debris. Autoantibodies are an attempt to enhance debridement in a weakening system. The autoantibody should not be condemned because of the failure of other aspects of the debridement system. Improving tissue debridement would not stop eventual senescence but it might decrease some of the pathologic and physiologic changes of aging and improve the quality of life. Improving tissue debridement is currently more attainable than altering the etiology of senescence. Factors promoting immunologic stimulation by tissue fractions are reviewed. The possible value of increasing tissue debridement in damage preceding arteriosclerotic vascular change is discussed. The role of the aging extracellular matrix in the weakening of ground substance and decreasing early cellular inflammation is reviewed.
O J
OJ
Stone
D000375:Aging / Q000276:immunology*; D000686:Amyloidosis / Q000276:immunology; D001323:Autoantibodies / Q000502:physiology*; D003646:Debridement; D006801:Humans; D007249:Inflammation / Q000276:immunology; D008055:Lipids / Q000276:immunology; D008954:Models, Biological; D014947:Wounds and Injuries / Q000276:immunology
D001323:Autoantibodies; D008055:Lipids