z-logo
Premium
Increased PD‐1 and decreased CD28 expression in chronic hepatitis B patients with advanced hepatocellular carcinoma
Author(s) -
Hsu PingNing,
Yang TsueyChing,
Kao JungTa,
Cheng KenSheng,
Lee YiJu,
Wang YuanMin,
Hsieh ChinTung,
Lin ChengWen,
Wu YiYing
Publication year - 2010
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2010.02323.x
Subject(s) - hepatocellular carcinoma , medicine , portal vein thrombosis , hepatitis b virus , thrombosis , gastroenterology , immune system , cd28 , hepatitis b , hbsag , immunology , pathology , t cell , virus
Background/aims: Hepatitis B infection is a well‐known cause of hepatocellular carcinoma (HCC). This study aims to investigate the role that the co‐stimulatory molecule CD28 and co‐inhibitory molecule programmed death‐1 (PD‐1) play in compromising the function of tumour‐infiltrating lymphocytes (TIL) in hepatitis B virus (HBV)‐related HCC. Methods: A total of 45 patients with HBV‐related HCC were enrolled during the period February 2008 to March 2010. The immune phenotype and the expression of PD‐1, CD28 and CD127 in TIL in biopsy specimens and in peripheral blood lymphocytes (PBL) from the same patients were analysed by flow cytometry. Results: Among the 45 patients, there was a male predominance (80%) and the mean age was 50 ± 13.68 years (range: 29–71). The majority of TIL were CD45RO + CD69 + . PD‐1 expression was higher and CD28 and CD127 expression levels were lower in TIL than in PBL. The prevalence of portal vein thrombosis was 40%. Furthermore, tumour thrombosis invasion into the portal vein correlated with the expression level of the PD‐1 co‐inhibitory molecule. Conclusion: PD‐1 + tumour‐infiltrating lymphocytes correlate with portal vein thrombosis and might serve as a potential prognostic marker of and a novel therapeutic target for HBV‐related HCC.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here