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Chronic hepatitis B (CHB) virus infection, which can be divided into immune‐tolerant (IT), immune‐active (IA), inactive carrier (IC) phases, and HBeAg‐negative hepatitis (ENEG), can induce liver cirrhosis and eventually hepatocellular carcinoma (HCC). CD3+CD56+ NKT‐like cells play an important role in antiviral immune response. However, the mechanism of NKT‐like cells to mediate immune tolerance remains largely elusive. In this study, we observed circulating NKT‐like cells from IC and IT CHB patients were phenotypically and functionally impaired, manifested by increased expression of inhibitory receptor TIGIT and decreased capacity of secreting antiviral cytokines. Besides, TIGIT+ NKT‐like cells of IC and IT CHB patients expressed lower levels of cytotoxic cytokines than the TIGIT− subset. Furthermore, increased expression of CD155, the ligand of TIGIT, on plasmacytoid dendritic cells (pDCs) was detected in IC and IT CHB patients. Importantly, the co‐culture of NKT‐like cells and pDCs showed that NKT‐like cells restored their antiviral ability after TIGIT blockade upon HBV peptide stimulation in IC and IT CHB patients. In conclusion, our findings suggest that the TIGIT pathway may mediate immune tolerance in IT CHB patients and lead to functional impairment in IC patients, indicating that TIGIT may be a potential therapeutic checkpoint for immunotherapy of CHB patients. [ABSTRACT FROM AUTHOR]

A study published in the journal MedComm explores the effects of short-term fasting on acute liver failure (ALF) induced by lipopolysaccharide (LPS) and D-galactosamine (D-GalN) in mice. The researchers found that 24-hour fasting significantly reduced liver injury and improved survival rates in mice. The fasting also suppressed hepatocyte apoptosis, or cell death, which is a major factor in liver failure. The study suggests that short-term fasting may be a potential therapeutic intervention for liver diseases and highlights the importance of the Sirt1-autophagy signaling pathway in this process. [Extracted from the article]

Natural killer (NK) cells are regarded as the host's first line of defense against viral infection. Moreover, the involvement of NK cells in chronic obstructive pulmonary disease (COPD) has been documented. However, the specific mechanism and biological changes of NK cells in COPD development have not been determined. In this study, we extracted NK cells from the peripheral blood of 18 COPD patients who were recovering from an acute exacerbation and 45 healthy donors (HDs), then we labeled NK cells with different antibodies and analyzed with flow cytometry. The data showed that the frequencies of total NK cells in the peripheral blood of COPD patients were lower compared with HDs. Moreover, the inhibitory receptors on NK cells expressed higher levels and the expression of activating receptors were generally low. Importantly, both the expression levels of CD96 in NK cells and the frequencies of CD96+ NK cells were significantly upregulated in COPD patients. These findings suggest that surface receptor CD96 from NK cells may be a risk factor in the evolution of COPD. [ABSTRACT FROM AUTHOR]