Bcl6 is a transcription factor selectively expressed in T follicular helper (Tfh) cells and plays a critical role in their development. Bcl6 expression is regulated by interleukin-6 (IL-6) and interleukin-21 (IL-21), and its overexpression promotes Tfh-related gene expression while inhibiting differentiation of other T helper (Th) lineages, including Th1, Th2, and Th17. Bcl6 deficiency leads to impaired Tfh cell development and germinal center reactions, as well as altered production of other effector T cell subsets. Bcl6 functions by binding to DNA and inhibiting the expression of genes associated with Th17 and other Th lineages. It also inhibits RORγt function but not its expression, similar to Foxp3. In vivo studies show that Bcl6 deficiency results in reduced Tfh cell development and germinal center reactions, with increased production of Th1, Th2, and Th17 cytokines. Bcl6 is required for the proper development of Tfh cells and germinal center reactions. Bcl6 acts as a master transcriptional factor in Tfh cell differentiation, similar to RORγt and RORα, which are induced by IL-6 or IL-21 in the presence of TGFβ. Bcl6 is regulated by IL-6 and IL-21 but does not regulate IL-21 expression. Bcl6 deficiency does not inhibit IL-21 expression, likely due to Th17 cells. Bcl6 is necessary for Tfh cell generation and germinal center reactions, and its expression in both T and B cells is required for these processes. Bcl6 is selectively induced by IL-21 or IL-6 in the absence of TGFβ signaling, and its function depends on DNA binding. Bcl6 deficiency results in increased production of IL-4, IL-17, and IL-22, but not IL-21. Bcl6 is essential for the development of Tfh cells and germinal center reactions, and its absence leads to impaired Tfh cell development and altered immune responses.Bcl6 is a transcription factor selectively expressed in T follicular helper (Tfh) cells and plays a critical role in their development. Bcl6 expression is regulated by interleukin-6 (IL-6) and interleukin-21 (IL-21), and its overexpression promotes Tfh-related gene expression while inhibiting differentiation of other T helper (Th) lineages, including Th1, Th2, and Th17. Bcl6 deficiency leads to impaired Tfh cell development and germinal center reactions, as well as altered production of other effector T cell subsets. Bcl6 functions by binding to DNA and inhibiting the expression of genes associated with Th17 and other Th lineages. It also inhibits RORγt function but not its expression, similar to Foxp3. In vivo studies show that Bcl6 deficiency results in reduced Tfh cell development and germinal center reactions, with increased production of Th1, Th2, and Th17 cytokines. Bcl6 is required for the proper development of Tfh cells and germinal center reactions. Bcl6 acts as a master transcriptional factor in Tfh cell differentiation, similar to RORγt and RORα, which are induced by IL-6 or IL-21 in the presence of TGFβ. Bcl6 is regulated by IL-6 and IL-21 but does not regulate IL-21 expression. Bcl6 deficiency does not inhibit IL-21 expression, likely due to Th17 cells. Bcl6 is necessary for Tfh cell generation and germinal center reactions, and its expression in both T and B cells is required for these processes. Bcl6 is selectively induced by IL-21 or IL-6 in the absence of TGFβ signaling, and its function depends on DNA binding. Bcl6 deficiency results in increased production of IL-4, IL-17, and IL-22, but not IL-21. Bcl6 is essential for the development of Tfh cells and germinal center reactions, and its absence leads to impaired Tfh cell development and altered immune responses.