Roles of Endogenous IL-10 and IL-10-Competent and CD5+ B Cells in Autoimmune Thyroiditis in NOD.H-2h4 Mice

Interleukin (IL)-10 is a highly important anti-inflammatory cytokine in the immune system. CD1d(hi) and CD5(+) B cells are both traditionally defined IL-10-secreting B cells. In recent years, a B cell group with combined markers of CD1d(hi) and CD5(+) has been widely studied as it has been reported to suppress autoimmunity in mouse models of autoimmune diseases through IL-10 mechanisms. From the perspective of origination, CD1d(hi) and CD5(+) B cells are developed from different B cell lineages. Whether the regulatory capacity of these 2 B cell groups is consistent with their ability to secrete IL-10 has not been determined. In this study, we generated IL-10 knockout NOD.H-2(h4) mice to investigate the function of endogenous IL-10 in autoimmune thyroiditis and conducted adoptive transfer experiments to explore the respective roles of CD5(+) and CD1d(hi) B cells. In our results, the IL-10(-/-) NOD.H-2(h4) mice developed thyroiditis, similar to wild-type NOD.H-2(h4) mice. The CD5(+) B cells were more capable of secreting IL-10 than CD1d(hi) B cells in flow cytometric analysis, but the CD1d(hi) B cells showed more suppressive effects on thyroiditis development and autoantibody production, as well as Th17 cell response. In conclusion, endogenous IL-10 does not play an important role in autoimmune thyroiditis. CD1d(hi) B cells may play regulatory roles through mechanisms other than secreting IL-10.