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Chronic hepatitis B: The interplay between intrahepatic lymphocyte population and viral antigens in relation to liver damage
Author(s) -
Giadans Cecilia G.,
Ríos Daniela A.,
Ameigeiras Beatriz,
Pietrantonio Adriana M.,
Lucatelli Néstor L.,
Haddad Leila,
Mullen Eduardo,
Heinrich Fabiana,
De Matteo Elena,
Flichman Diego,
Valva Pamela,
Preciado María V.
Publication year - 2019
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/jvh.13078
Subject(s) - immunology , liver damage , antigen , population , chronic hepatitis , lymphocyte , hepatitis b , viral hepatitis , virology , medicine , biology , virus , environmental health
Summary In Chronic hepatitis B ( CHB ) infection, virus and immune response interplay is thought to be responsible for pathogenesis. Yet, the impact of each immune cell population and viral protein expression in liver damage is still unknown. Our aim was to study the interplay between intrahepatic immune response and viral activity in relation to CHB liver damage. Immunostaining was performed in 29 liver biopsies from untreated CHB patients to characterize liver infiltrate [Th ( CD 4+), CTL ( CD 8+), Treg (FoxP3+), Th17 ( IL ‐17A+) and Th1 (T‐bet+)] and viral antigen expression ( HB sAg and HB cAg). Inflammatory activity and fibrosis were assessed using the HAI and METAVIR scoring system. All studied populations were identified in the portal‐periportal (P‐P) areas with a CD 4+ lymphocyte predominance, while only CD 8+ and FoxP3+ cells were observed in the intralobular area. Both P‐P CD 4+ and intralobular CD 8+ cell frequencies were increased among severe hepatitis cases. Concerning HB sAg and HB cAg expression, a mutually exclusive pattern was observed. HB cAg was mainly detected among HB eAg‐positive patients and was associated with hepatitis severity and higher frequency of P‐P FoxP3+, intralobular CD 8+ and FoxP3+ cells. HB sAg was identified among HB eAg‐negative cases with less severe hepatitis grade and lower frequency of P‐P CD 4+ and intralobular FoxP3+ lymphocytes. In conclusion, the HBV antigen profile expression seen during CHB infection may be reflecting different stages of viral replication which impacts the host immune response and liver damage process. While HB cAg might be an inducer of a regulatory microenvironment, the intralobular CTL population seemed to have a key role in hepatitis severity.