In summary, we demonstrate that IFNγ is critical for the in vitro formation of a T-bethiIRF4int pre-ASC population that is remarkably similar to the T-bethi DN2 cells that accumulate in SLE patients who present with high autoAb titers, elevated disease activity and increased systemic levels of IFNγ. Here, IFNG is linked to systemic lupus erythematosus.