Relationship between composition of lymphoid cell infiltrates in the liver and replication status in chronic hepatitis B: an immunohistochemical study.
The purpose of this in situ immunophenotyping study was to assess the nature of lymphoid cells involved in chronic hepatitis B with various levels of replication. Replicative status was studied in 25 patients with chronic hepatitis B. Different subsets of T cells, B cells, natural killer cells, and follicular dendritic cells were counted with a computerized image analyzer. Twelve patients had chronic hepatitis B with a high level of replication, nine without replication, and four with a low level of replication. The number of CD3+ T cells was significantly higher in the liver of patients with replication. In all cases, CD8+ T cells were the most numerous cells in the lobules and CD4+ T cells were the most numerous cells in the portal tract. Intra-portal lymphoid follicles were observed in 33% of patients with a high level of replication. The CD57+ natural killer cells were more numerous in patients with a low level of replication. This study suggests that in immunocompetent patients, the intensity and type of hepatic immune response are directly determined by the HBV replication.
Mosnier
J F
JF
Service d'Anatomie et de Cytologie Pathologiques, Hôpital Beaujon, Clichy, France.
Pham
B N
BN
Walker
F
F
Dubois
S
S
Degos
F
F
Erlinger
S
S
Degott
C
C
D000328:Adult; D000368:Aged; D016175:B-Lymphocyte Subsets / Q000145:classification / Q000473:pathology*; D003713:Dendritic Cells / Q000473:pathology; D005260:Female; D006509:Hepatitis B / Q000473:pathology* / Q000821:virology; D006515:Hepatitis B virus / Q000302:isolation & purification* / Q000502:physiology; D006521:Hepatitis, Chronic / Q000473:pathology* / Q000821:virology; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007694:Killer Cells, Natural / Q000473:pathology; D008099:Liver / Q000473:pathology* / Q000821:virology; D008297:Male; D008875:Middle Aged; D016176:T-Lymphocyte Subsets / Q000145:classification / Q000473:pathology*; D014779:Virus Replication / Q000502:physiology