These results suggest that the ability of Bcl6 to inhibit the initiation of secondary Teff differentiation programs in developing Tfh cells is dose-dependent and can be partially overcome in highly reactive environments, such as in autoimmune diseases, thereby leading to the acquisition of hybrid Tfh/Teff phenotypes, such as IL-17+ Tfh cells, with enhanced pathogenic functions. This evidence concerns the gene BCL6 and autoimmune disease.