644 Roles of T and B Cells in Murine Thyroiditis

That a central immunological unresponsive state exists to our own body constituents is widely accepted. The precise role played by the various cell types of the lymphoid system in the maintenance or abrogation of this unresponsiveness to self remains unclear. A large number of nonself-antigens require the collaboration of thymus-derived (T) and bone marrow-derived (B) lymphocytes (1, 2). Although both T and B cells may be made unresponsive, only one cell type need be in order that the intact animal remain unresponsive (3). In a rabbit model, the cellular events in the termination of unresponsiveness to bovine serum albumin (BSA), 1 by the injection of cross-reacting albumins, were best explained by assuming that the T cells, but not the B cells, were unresponsive to BSA and to cross-reacting determinants on other albumins (4). Such a situation may explain the apparent ease with which unresponsiveness to self components may be abrogated in autoimmune disorders such as thyroiditis (5-7) and rheumatic fever (8). The present investigations were undertaken to directly assess by adoptive transfer, antigen-binding and antigen-suicide techniques, the interactions of T and B cells during the induction of autoantibody to syngeneic thyroglobulin (Tg) and during the production of thyroid lesions.