Inflamm-aging: autoimmunity, and the immune-risk phenotype.
Aging of the immune system, or immunosenescence, is a complex subject best defined as a decline in cell-mediated immunity, particularly with respect to T cell function. Paradoxically with the decline in immune function is an increase in autoantibody frequency. It has been postulated that the accumulation of anamnestic cells over time and/or environmental/infectious mimics leads to the production of autoantibodies, sometimes accompanied by autoimmune disease. This specific phenotype has given rise to the concept of a specific cluster of cytokine profiles, coined an immune-risk phenotype (IRP). The IRP is likely dictated by not only cytokine production, but also defects in activation-induced cell death and also a shift in T cell subsets. These concepts are an important bridge between basic immune function and clinical immunology in the hopes for generation of effective reconstitution to improve immune function in the elderly.
Department of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, TB 192, One Shields Avenue, Davis, CA 95616-8660, USA.
Eric
E
Boren
M Eric
ME
Gershwin
D000368:Aged; D000375:Aging / Q000276:immunology*; D000818:Animals; D001323:Autoantibodies / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D010641:Phenotype
D001323:Autoantibodies