Interleukin-10 influences susceptibility to experimental autoimmune thyroiditis independently of the H-2 gene.

Both BALB/c and C57BL/6 mice are relatively resistant to experimental autoimmune thyroiditis (EAT) due to their histocompatibility (H-2) genetic background; however, susceptibility to EAT is also influenced by other genetic factors. Given the curative effect of interleukin-10 (IL-10) on thyroiditis, in the present study, we investigated whether IL-10 functions as a non-H-2 genetic factor that influences the development of EAT in mice with an EAT-resistant genetic background. In this study, we observed that the development of EAT could be induced in both C57BL/6 IL-10‑deficient (IL-10-/-) and BALB/c IL-10-/- female mice following immunization with mTg, which indicated that IL-10 may be a non-H-2 factor that affects susceptibility to EAT. However, the role of the H-2 factor remained dominant, as the incidence of EAT was low and its severity was mild. We further investigated the underlying pathogenic mechanisms of EAT in IL-10-/- female mice. We found that Th1 cells, Th17 cells, CD4+CD25+Foxp3+ regulatory T cells, and their associated cytokines were all involved in the development of EAT. The absence of IL-10 promoted the polarization of pathogenic cells and the production of associated cytokines, and suppressed the proliferation of protective T cell clones. Together, these factors may contribute to the development of EAT in IL-10-/- mice. In conclusion, our data demonstrate that IL-10 plays a critical role in the susceptibility to EAT, and a better understanding of the role of IL-10 in autoimmune thyroiditis may facilitate the development of novel strategies for the treatment of autoimmune thyroid diseases.