CD32b expression is down-regulated on double-negative memory B cells in patients with Hashimoto's thyroiditis

- The percentage of double-negative memory B cells was increased in HT patients.
- The expression level of CD32b was decreased in HT patients.
- B cell subset distribution was regulated by B cell receptor stimulation.
- CD32b down-regulation was mediated by the CD40-CD40L pathway.

Inhibitory CD32b receptors on B cells are critical for humoral immunity. The humoral response plays a role in the pathogenesis of Hashimoto's thyroiditis (HT). This study aimed to investigate B cell subset distribution and CD32b expression within these subsets in HT patients. B cell subset distribution and CD32b expression were analyzed in 60 HT patients and 21 healthy donors. Subset distribution and CD32b expression following stimulation with α-Ig and α-CD40 were also assessed. The percentage of double-negative (DN) memory cells was increased in the HT patients, while the expression level of CD32b on DN memory cells was decreased. Redistribution of B cell subsets was detected in response to stimulation with α-Ig. In addition, the expression level of CD32b was reduced following α-CD40 stimulation. These results suggest that abnormal B cell subset distribution and decreased CD32b expression on DN memory cells might be involved in the pathogenesis of HT.