Through cognate B-cell-T-cell interactions and provision of cytokines, CD4(+) T-cell antigen receptor (TCR) alpha beta(+) T cells regulate immunoglobulin isotype synthesis(1), Murine IgG1 and IgE secretion is therefore substantially T-cell-dependent, whereas IgM and IgG3 secretion is not(2,3). Here we report that in the absence of alpha beta T cells, B cells expand, differentiate and secrete copious amounts of antibodies of ’T-dependent’ isotypes. Moreover, the antibodies are reactive towards self-antigens, as in patients with systemic lupus erythematosus, so autoantibodies of ’T-dependent’ type can develop without the help of CD4(+) alpha beta T cells. This phenotype is not evident in mice or humans that ape congenitally deficient in specific alpha beta T-cell functions, but bears comparison with B-cell hyperactivity and autoimmunity in transplant rejection and in immunodeficiencies such as AIDS(4,5).