Differentiation of B Cells and the Clonal Abortion Theory

Abstract

During the early years of research on immunological tolerance (1), it was generally believed that induction of the phenomenon could only be achieved in embryonic or very young animals, implying a special susceptibility of immature lymphoid cells. A plausible mechanism for tolerance emerged in 1957, when Burnet (2) postulated his clonal selection theory, and ascribed tolerance to a deletion of clones through contact between immature lymphocytes with their corresponding antigen. This straightforward view of the problem received a number of challenges during the 1960’s. A watershed was the discovery by Dresser (3) that small amounts of de-aggregated proteins could induce tolerance in adult mice. A further complication was the discovery of the helper function of T lymphocytes and the demonstration that, in some tolerance models, tolerance was confined to the T lymphocyte compartment (4). Then, when the important role of suppressor T cells in antibody formation and immunological tolerance became clear (5,6), the idea of clonal deletion as a general explanation of tolerance lost favour in many quarters.