Published online May 28, 2020. doi: 10.3748/wjg.v26.i20.2645
Peer-review started: February 03, 2020
First decision: February 29, 2020
Revised: March 27, 2020
Accepted: May 13, 2020
Article in press: May 13, 2020
Published online: May 28, 2020
Recently, B cell-activating factor (BAFF) receptors and B cell subsets play diverse but crucial roles in modulating B cell function. Therefore, analysis of their expression and subpopulation frequencies could provide more insights into the immunological characteristics of B cell selection in patients with hepatocellular carcinoma (HCC).
To evaluate the association of BAFF receptors on B cell subsets according to clinical outcome of patients with chronic HBV infection.
This study aimed to compare the expression of BAFF receptors and the distribution of B cell subsets in the peripheral blood of patients with HBV-related HCC compared to individuals without HCC and healthy controls.
Peripheral blood samples collected from chronic HBV infected patients with or without HCC and healthy controls were assessed for BAFF receptors [BAFF-R(B cell-activating factor receptor), transmembrane activator and cyclophilin ligand interactor, B-cell maturation antigen] and B cell subpopulations by multicolor flow cytometry.
The frequency of BAFF-R expression on B cells was significantly decreased in HBV-related HCC compared with HBV patients without HCC and healthy controls. In addition, the frequency of CD27+IgD+ memory B cells, CD27+IgD- class switched memory B cells and plasmablasts were significantly lower in patients with HCC compared to the non-HCC group. However, the frequency of naïve and transitional B cell did not differ significantly among groups. Moreover, decreased BAFF-R expression on B cells was significantly correlated with tumor size and more advanced Barcelona Clinic Liver Cancer stages.
The expression of BAFF-R on B cells was significantly decreased that involved in the different frequencies of B cells maturation in patients with HCC.
Larger samples and the mechanistic roles of B cell-mediated immune response in hepa-tocarcinogenesis are needed to further validate.