CCL19/MIP-3β as a key mediator in the production of anti-GPIIb/IIIa antibody-producing B cells in patients with chronic hepatitis C.

The roles of specific cytokines and chemokines in modulating the production of anti-GPIIb/IIIa antibody-producing B cells remain poorly understood. We aimed to assess key mediators that influence the number of anti-glycoprotein (GP) IIb/IIIa antibody-producing B cells in patients with hepatitis C virus (HCV). This study used a subset of a previously reported cohort in Japan. We first evaluated the number of anti-GPIIb/IIIa antibody-producing B cells using an enzyme-linked immunospot assay in samples from 22 patients who received direct-acting antivirals (DAA)-based therapy and achieved a sustained virological response (SVR). To identify the key mediators, we then analyzed levels of cytokines, chemokines, and inflammation markers in serum samples obtained from the same cohort using Bio-Plex Multiplex Immunoassays. The analysis revealed a significant correlation between the frequency of anti-GPIIb/IIIa antibody-producing B cells and CCL19/macrophage inflammatory protein-3 beta (MIP-3β) (r = 0.590, p = 0.006). After DAA treatment for HCV, both the frequency of these B cells and the levels of CCL19/MIP-3β significantly decreased. Furthermore, the frequency of anti-GPIIb/IIIa antibody-producing B cells and levels of CCL19/MIP-3β were significantly higher in the thrombocytopenia group compared to the non-thrombocytopenia group (p = 0.001 and p = 0.029, respectively). These results suggest that CCL19/MIP-3β may be a key mediator in the production of anti-GPIIb/IIIa antibody-producing B cells in patients with HCV.