Follicular B helper T cells
However, the biomechanisms by which TFH cells mediate germinal center tolerance are yet to be fully understood.
[13][14] There is also a minor sub-class within this population of GC Tfh cells that express the gene Foxp3, encoding for a transcription factor.
[15] Therefore, TFR cells are a uniquely inhibitory influence during a germinal center reaction.
Specifically, germinal center-dependent memory B cells are the drivers of recall antibody production during a secondary immune response.
[19] Unchecked or overactive TFH cell immune responses have the potential to mount unwarranted germinal centers, composed of aberrantly mutated B cells that can drive antibody-mediated autoimmune diseases.
Elevated levels of TFH-like cells can be detected in the blood of a subset of human patients with systemic lupus erythematosus (SLE) and Sjögren syndrome.
[20] However, scientific evidence suggesting TFH cells can definitively cause autoimmunity in humans remains incomplete.
A subset of naive T cells in the T cell zone are activated by antigen and migrate to the follicles where they differentiate into T FH cells that interact with and instruct Follicular B (Fo B) cells to undergo isotype switching, somatic hypermutation, and rapid cellular division to seed germinal centers (GC). Within these germinal centers, T FH cells continue to provide help to GC B cells to facilitate their production of high affinity antibody producing plasma cells (PC) and long-lived memory (Mem) B cells.