We previously performed analysis of the B cell response in HCV-infected patients with and without mixed cryoglobulinemia (MC), and the impact of rituximab treatment on B cell function in these patients. Despite activation and clonal expansion of B-cells in chronic HCV infection we had observed a reduction in the total number of B cells and in the size of the naive B cell subset in patients with MC compared to HCV-infected patients without MC and healthy controls. The reduced frequency of naive B cells in HCV-infected patients with MC was associated with decreased ex vivo expression of the antiapoptotic protein Bcl-2 compared to HCV-infected patients without MC and healthy controls, and with an increased in vitro sensitivity of naive B-cells to apoptosis. These results suggested that the increased size of the immature B-cell subset was due to a secondary egress from the bone marrow to compensate for the B-cell loss in the periphery. Based on this previous work and the published literature we published a letter to the editor, Hepatology.
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