Endocrine Abstracts

Background: Graves’ disease (GD) is characterized by lymphocytic infiltration and autoimmune activation. The gut microbiota plays a pivotal role in immune regulation. The underlying mechanism of the gut microbiota in GD autoimmunity remains elusive. The present study aimed to investigate the role of the gut microbiota in the humoral immunity of GD.

Methods: A total of 45 healthy controls (HCs) and 68 GD patients [52 without treatment (U_GD) and 16 with treatment (T_GD)] were enrolled in the study. B-cell subset distribution and CD32b expression on B cells were analyzed by flow cytometry. Cytokines were measured by enzyme-linked immunosorbent assays. The gut microbial composition was analyzed by 16S rRNA gene sequencing.

Results: In the discovery cohort, we observed aberrant B-cell subset distribution, decreased CD32b expression and elevated proinflammatory cytokines in U_GD patents compared with HCs. The diversity and structure of the microbial community in U_GD patients were different from those of HCs, and some alterations in gut microbiota were significantly correlated with changes in humoral immunity. Moreover, we identified a fecal microbiome index that could be used to distinguish U_GD patients from HCs in the validation cohort, whereas the structure of the microbial community and B-cell activation-related cytokines in T_GD patients were similar to those of HCs.

Conclusions: The interaction between the microbiota and humoral immunity is involved in the development of GD, and antithyroid drug therapy could relieve the disease by rebuilding homeostasis of gut microbiota.