IGHE and Autoimmunity: Together, DGKαζ deficiency in Tregs led to enhanced Tfh and GC-B cell as well as non-GC B cell responses with prominent polarization to the Tfh2/13 lineage and IgG1/IgE responses, which provided mechanistic explanation of development of autoantibodies and lupus-like diseases and the IgG1-predominant autoimmunity in Treg-αζDKO mice.