Immunology and the liver

Peters, Marion G.; Vierling, John M.; Gershwin, M. Eric; Milich, David R.; Chisari, Francis V.; Hoofnagle, Jay H.

doi:10.1002/hep.1840130529

Cited by 142 publications

(62 citation statements)

References 97 publications

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“…However, other mechanisms may also contribute to impaired neutralizing antibody production in LCMV-infected mice, such as the CD8 + T cell-mediated destruction of antigen presenting cells or polyclonal B cell activation observed after infection with viscerotropic strains such as LCMV-WE [31,32]. Similar mechanisms may also operate during HIV and hepatitis B virus infections in humans, where, as in LCMV infection of mice, only non-neutralizing antibodies are induced early and there is a delayed and frequently low titered neutralizing antibody response [33,34].…”

Section: Discussionmentioning

confidence: 99%

Virus infection‐associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF‐α/LTα

et al. 2005

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We previously showed that influenza virus infection of mice induces a depletion of bone marrow B lineage cells due to apoptosis of early B cells mediated by a mechanism involving TNF-a/LTa. Here we demonstrate that this effect is also observed with acute lymphocytic choriomeningitis virus (LCMV) infection and resulted in a deficiency of both splenic transitional B cells and mature follicular B cells. To determine whether there was an associated impairment of humoral immunity, we infected mice with LCMV and 10 days later at the peak of the B cell depletion, inoculated them with influenza virus. We found that influenza virus-specific antibody titers were dramatically reduced in mice recovering from LCMV infection compared to those in mice infected with influenza virus alone. Further, we showed that there was no reduction of the influenza virus-specific antibody response in LCMV-infected TNF-a/LTa-deficient mice, suggesting that TNF-a/LTa-mediated effects on bone marrow and/or peripheral lymphocytes were responsible for the observed impairment in humoral immunity. These results show that the TNF-a/LTa production induced following infection with diverse viruses has detrimental effects on early B cells in the bone marrow, and may be among the factors that lead to the severely compromised humoral immunity observed to subsequent heterologous infections.

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Section: Discussionmentioning

confidence: 99%

Virus infection‐associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF‐α/LTα

et al. 2005

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“…The mechanisms responsible for the variable clinical course and outcome of HBV infection are not known. There is considerable evidence suggesting that HBV is not directly cytopathic (3), and that the hepatitis is caused by immune responses against virus-infected hepatocytes (4). In vitro studies have shown that hepatitis B surface antigen (HBsAg)-and hepatitis B core antigen (HBcAg)-expressing transfectants can serve as targets for MHC class I-restricted cytotoxic T lymphocytes (CTLs) that are generated from both acute and chronic hepatitis B patients (5)(6)(7)(8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Purification and characterization of a naturally processed hepatitis B virus peptide recognized by CD8+ cytotoxic T lymphocytes.

Tsai

Chen²,

Yeh³

et al. 1996

J. Clin. Invest.

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“…Few or no class I and class II human leucocyte antigens (HLA) appear to be expressed by normal hepatocytes [1], It is postulated that the variable findings that have appeared in the literature in recent years may represent unrecognized immunological agents promoting the expression of HLA products at the hepatocyte membrane [2], HLA antigen expression in many liver diseases has been well documented. These include hepatitis B virus infection [3][4][5] and hepatoceilular carcinoma {HCC) [2,[5][6][7].…”

Section: Introductionmentioning

confidence: 99%

HLA expression in hepatocellular carcinoma cell lines

Wadee

Paterson

Coplan

et al. 1994

Clinical and Experimental Immunology

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SUMMARYThe present study undertook to investigate the biological significance of human leucocyte antigen expression in hepatoceilular carcinoma and to elucidate lhc role of potential modulating agents on human leucocyte antigen expression. These studies used several hepatic tumour-derived cell lines as in vitro model systems. The cell lines included PLC/PRF/5 (Alexander cell line), Hep3B. HepG2, TONG PHC, HA22T/VGH, HA59T/VGH and Mahlavu, The cell lines K562 and Raji were used as negative and positive controls, respectively. K562, a B tymphoid-derived cell line, was shown to express negligible amounts of human leucocyte anligens, while Raji, an erythromyeloid-derived cell line, expressed both class I and class II human leucocyte anligens as well as their respective invariant chains, ^2-niicroglobulin and Ii. Using an ELISA, experiments performed on these cell lines confirmed the natural expression of class I and class II antigens by the HA22T/VGH and HA59T/VGH cell lines, whereas PLC/PRF/5 displayed class II surface antigens only. The effects of modulating agents such as interferon-gamma sodium bulyrate and clofazimine on human leucocyte antigen expression were investigated using the HA22T/VGH, HA59T/VGH and TONG PHC cell lines. These agents increased class 1 and class II human leucocyte antigen expression on HA22T/VGH and TONG PHC cells, but had no effect on the HA59T/VGH cell line. The results suggest a potential use for these agents as modulators of human leucocyte antigen expression by human heptocellular cell lines.

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Immunology and the liver

Cited by 142 publications

References 97 publications

Virus infection‐associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF‐α/LTα

Virus infection‐associated bone marrow B cell depletion and impairment of humoral immunity to heterologous infection mediated by TNF‐α/LTα

Purification and characterization of a naturally processed hepatitis B virus peptide recognized by CD8+ cytotoxic T lymphocytes.

HLA expression in hepatocellular carcinoma cell lines

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