Abstract
We can conclude from the properties of the Id-16/6 system that a relatively restricted group of B cell clones is activated in systemic lupus erythematosus. Whether this is a property of the immunogeneic stimulus that causes the diseases (if indeed there is one), or whether the observations are due to an idiotypic network that favors the selection of Id-16/6-cxpressing B cells is not known. These alternatives are under investigation. Apart from these theoretical considerations, the high frequency of Id-16/6(+) autoantibodies, including pathogenic autoantibodies, in systemic lupus erythematosus may point to targets amenable to the specific therapy of the disease.