THROUGH cognate B-cell–T-cell interactions and provision of cytokines, CD4⁺ T-cell antigen receptor (TCR) αβ⁺ T cells regulate immunoglobulin isotype synthesis¹. Murine IgGl 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 αβ 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⁺ αβ T cells. This phenotype is not evident in mice or humans that are congenitally deficient in specific αβ T-cell functions, but bears comparison with B-cell hyperactivity and autoimmunity in transplant rejection and in immunodeficiencies such as AIDS^{4, 5}.