The conventional paradigm to explain systemic lupus erythematosus (SLE) is that disease results from tissue deposition of pathogenic autoantibodies and immune complexes, secondary to activation of autoreactive B cells in the context of help from αΒ T cells. Recent work in murine lupus has confirmed this notion and demonstrated that autoantigen-specific αΒ T cells are absolutely required for full penetrance of disease, with such autoreactive αΒ T cells, even in Fasintact mice, likely arising from defects in peripheral tolerance. These studies have also revealed a network of regulation that also involves nonclassical pathogenic and downregulatory αΒ and γδ T cells, suggesting that the lupus immune system involves more complex interactions than the conventional paradigm suggests.