The role of Tregs cells in regulating immunity in IgG4-related diseases

Research has demonstrated abundant Treg infiltration within the lesional tissues of patients with IgG4-RD, often accompanied by increased Treg counts in peripheral blood, suggesting a compensatory host response aimed at suppressing aberrant immune activation. However, these Tregs appear to be subject to functional dysregulation or plasticity.

On one hand, through the secretion of inhibitory cytokines such as IL-10 and TGF-, Tregs directly facilitate the production of IgG4 antibodies by plasma cells and contribute to tissue fibrosis. On the other hand, their immunosuppressive capacity may be relatively insufficient to effectively curb the hyperactivation of follicular helper T cells (Tfh) and B cells, resulting in the generation of pathogenic autoantibodies and the perpetuation of chronic inflammation.