Abnormal phenotypic features of IgM+B cell subsets in patients with chronic hepatitis C virus infection

Abstract

Abstract. Hepatitis C virus (HCV) infection is associated with B cell abnormality; however the phenotypic profiles of immunoglobulin (Ig)M+B cell subsets in patients with HCV infection remain unclear. In the current study, the effect of HCV infection on IgM+B cell subsets was evaluated. The percentages, as well as the differentiation and activation features of peripheral IgM+B naive subsets [cluster of differentiation (CD)27-IgM+B cells] and IgM+B memory subsets (CD27+IgM+B cells) were assessed using flow cytometry in 27 patients with chronic hepatitis C (CHC) and 20 healthy controls (HCs). The frequency of CD27+IgM+B memory subsets detected in patients with CHC was significantly higher than that in HCs (P<0.05). Although the frequency of CD27-IgM+B naive subsets was similar in both groups, there was a significantly higher proportion of CD5+B cells detected in the CD27-IgM+B subsets of patients with CHC compared with HCs (P<0.05). Among CD27-IgM+B subsets, abnormal differentiation was associated with HCV infection, with significantly increased percentages of IgD+B cells and CD38+B cells in patients with CHC compared with HCs (P<0.05). In CD27+IgM+B memory subsets, the abnormality of cell differentiation was associated with a significantly increased percentage of CD38+B cells in patients with CHC compared with HCs (P<0.05). In addition, the percentage of activated CD27+IgM+B subsets in patients with CHC were significantly higher than those observed in HCs (P<0.05). The number of CD27-IgD+IgM+B, CD27-CD38+IgM+B and CD27+CD38+IgM+B cells were negatively correlated with HCV RNA in patients with CHC. These results suggest that HCV infection contributes to abnormalities in the percentage, differentiation and activation of IgM+B cell subsets and may disrupt the immune response mediated by IgM+B cells.

A Role for B Cells to Transmit Hepatitis C Virus Infection

“…Recently, a population of IgM + CD27 + memory B cells, were identified which can re-enter germinal center reactions and differentiate into antibody-secreting cells ( 61 – 63 ), however the generation and immune function of these cells is poorly understood. Kong et al ( 64 ) reported a higher frequency of this IgM + CD27 + memory B cell subset in chronic hepatitis C compared to healthy controls. Tucci et al ( 65 ) reported the presence of IgM + CD27 + B cell clones in chronic hepatitis C. Despite several attempts we were unable to isolate sufficient IgM + CD27 + B cells from our cohort of patients to demonstrate an enrichment of HCV RNA in this subpopulation.…”

Natural Killer Group 2D Receptor and B1a Cells Crosstalk in Post-Hepatitis C Virus Infection Hepatocellular Carcinoma and Cirrhosis

“… 8 B1a cells are immunoglobulin M-positive B (IgM+ B) cells and involved in viral infection pathogenesis. 9 …”

“…8 B1a cells are immunoglobulin M-positive B (IgM+ B) cells and involved in viral infection pathogenesis. 9 Even though the NKG2D receptor is not expressed in all B cell subsets, it has been observed that the absence of this receptor in hematological precursors affects peripheral B1a cell counts in cases of bacterial infections. 4 However, the association between host NKG2D receptor and B1a cell subsets in patients with HCV infection and its complications has not been elucidated.…”

“…13 According to Kong et al, patients with CHCV infection had a greater frequency of circulating IgM+B subsets in their peripheral blood. 9 The discrepancy can be explained as the former study compared patients with CHCV infection with healthy controls.…”