Enhanced peripheral γδT cells cytotoxicity potential in patients with HBV-associated acute-on-chronic liver failure might contribute to the disease progression.
Chen M, Hu P, Peng H, Zeng W, Shi X, Lei Y, Hu H, Zhang D, Ren H. J Clin Immunol. 2012 Aug;32(4):877-85. doi: 10.1007/s10875-012-9678-z. Epub 2012 Mar 14.
Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Institute for Viral Hepatitis, Department of Infectious Diseases, Second Affiliated Hospital, Chongqing Medical University, No.74 Lin Jiang Rd., Yu Zhong District, 400010, Chongqing, People's Republic of China. email@example.com
The current study explored the characteristics of γδ T cells in the blood of HBV-associated acute-on-chronic liver failure (HBV-ACLF) patients and examined the relationship between γδ T cells and the clinical parameters.
Blood samples were obtained from 26 patients with HBV-ACLF, 40 patients with chronic hepatitis B virus (HBV) infection (CHBV), and 25 healthy controls (HC). The frequencies of γδ T cells, subtype Vδ1T or Vδ2T, and CD45RO(+)γδ T cells were determined using flow cytometry. Intracellular cytokine staining analysis was used to evaluate the proportion of the IFN-γ-, TNF-α-, or IL-17-producing γδ T cells, and CD107a- or granzyme B-positive γδ T cells.
We found that the proportion of γδ T cells in blood samples from HBV-ACLF patients was much lower than in samples from CHBV patients or healthy controls. After stimulation with PMA and ionomycin, γδ T cells from HBV-ACLF patients produced the greatest amount of TNF-α or IL-17 among the three groups. Granzyme B- or CD107a-positive γδ T cells were significantly more frequent than in CHBV or control samples. There was a negative correlation between the percent of TNF-α(+)γδ T cells and ALT or AST levels, and between the percent of CD107a(+)γδ T cells and TBiL or DBiL levels.
These results suggest that γδ T cells might participate in liver injury in HBV-ACLF patients by producing increased amounts of inflammatory cytokines and/or cytotoxicity ability. These findings provide novel information regarding the pathogenesis of HBV-ACLF.