Loss of immune competence with age may be due to auto-anti-idiotypic antibody regulation

Abstract

The decline in immune function with ageing involves both a loss of B-cell function^1,2 and a decline in T-cell function^3–5. This picture has been complicated by the recent observation that normal old mice produce more B-cell mitogen-induced autoantibodies to syngeneic erythrocytes than do young animals⁶. They also produce elevated levels of IgM and IgA anti-IgG au toa n-tibodies7 and increased suppressor-cell activites^8–10. It is therefore difficult to explain the relationships between autoantibody production, increased suppressor-cell activities and the loss of immune competence in old animals. Recently, auto-anti-idiotypic antibody regulation has been proposed to explain a rapid decline in the antibody-forming cell response to antigen during a normal immune response in young adult mice¹¹. Schrater et al.¹² have suggested that this antibody, produced during the immune response, combines with B-cell-surface antigen receptors and thus inhibits antibody secretion. If the number of B cells is normal in old animals¹³, but their function is impaired, it may be that the decline in immune competence with age is due to auto-anti-idiotypic antibody regulation, perhaps affecting the B-cell-surface antigen receptors and preventing the cell from responding normally to exogenous antigens. We have therefore investigated whether auto-anti-idiotypic antibody could be detected in immune splenic B cells from old and young mice of the same strain. We report here that auto-anti-idiotypic antibody regulation seems to have a role in the loss of B-cell function with age.