title: Possible recruitment of peripheral blood CXCR3+ CD27+ CD19+ B cells to the liver of chronic hepatitis C patients.
abstract: It has been suggested that hepatitis C virus (HCV) infects not only hepatocytes but also immune cells, including B cells. HCV infection of B cells is the likely cause of B-cell dysregulation disorders such as mixed cryoglobulinemia, rheumatoid factor production, and B-cell lymphoproliferative disorders that may evolve into non-Hodgkin's lymphoma. To clarify the effects of chronic HCV infection on B-cell dynamics, peripheral B cells from chronic hepatitis C patients (CHC) were characterized. We found that the frequency of CD27(+) B cells, that is memory phenotype, was significantly reduced in the peripheral blood of CHC. At the same time, the amount of IFN-gamma-inducible protein-10 (IP-10), a CXCR3 ligand, was markedly elevated in the plasma of CHC. Furthermore, the CD27(+) B-cell population was found to highly express CXCR3 in CHC, thus suggesting that the CD27(+) B-cell population was recruited from peripheral blood to the inflammatory site of the liver of CHC, where IP-10 is produced. Immunohistochemical analyses of intrahepatic lymphocytes indicated that CXCR3(+) B cells were infiltrated in the liver of CHC. Our results thus offer new insight into the role of memory B cells in the HCV pathogenesis.
authors.affiliation: Department of Research on Blood and Biological Products, National Institute of Infectious Diseases, Tokyo, Japan. miz@nih.go.jp
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Mizuochi
authors.forename: Masahiko
authors.initials: M
authors.lastname: Ito
authors.forename: Koji
authors.initials: K
authors.lastname: Saito
authors.forename: Michiyuki
authors.initials: M
authors.lastname: Kasai
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Kunimura
authors.forename: Toshio
authors.initials: T
authors.lastname: Morohoshi
authors.forename: Haruka
authors.initials: H
authors.lastname: Momose
authors.forename: Isao
authors.initials: I
authors.lastname: Hamaguchi
authors.forename: Kenji
authors.initials: K
authors.lastname: Takai
authors.forename: Shiro
authors.initials: S
authors.lastname: Iino
authors.forename: Miho
authors.initials: M
authors.lastname: Suzuki
authors.forename: Satoshi
authors.initials: S
authors.lastname: Mochida
authors.forename: Kenji
authors.initials: K
authors.lastname: Ikebuchi
authors.forename: Kazunari
authors.initials: K
authors.lastname: Yamaguchi
mesh_terms: D000328:Adult; D000368:Aged; D018941:Antigens, CD19 / Q000097:blood*; D001402:B-Lymphocytes / Q000276:immunology*; D016022:Case-Control Studies; D002465:Cell Movement; D005260:Female; D005434:Flow Cytometry; D019698:Hepatitis C, Chronic / Q000097:blood / Q000276:immunology* / Q000473:pathology; D006801:Humans; D008024:Ligands; D008099:Liver / Q000276:immunology / Q000473:pathology / Q000821:virology*; D008297:Male; D008875:Middle Aged; D054367:Receptors, CXCR3 / Q000097:blood*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7 / Q000097:blood*
chemical_list: D018941:Antigens, CD19; C515187:CXCR3 protein, human; D008024:Ligands; D054367:Receptors, CXCR3; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7