In-situ immunophenotyping study of hepatic-infiltrating cytotoxic cells in chronic active hepatitis C

Fiore, Giorgio; Angarano, Immacolata; Caccetta, Luigi; Serrone, M; Jirillo, Emilio; Schiraldi, O; Antonaci, Salvatore

doi:10.1097/00042737-199705000-00015

Cited by 39 publications

(33 citation statements)

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“…Senaldi et al studied isolated hepatocytes from the livers of children with suspected hepatitis and found HLA classⅠexpression on the surface of 85%-100% hepatocytes [26] . Later, Fiore et al showed HLA classⅠexpression on the hepatocytes of all chronic hepatitis C (CHC) cases studied, but found no association between the intensity of expression of these molecules and inflammatory activity [27] . Van den Oord et al proved that the pattern of expression of HLA classⅠmolecules was independent of inflammatory activity, but in areas of spotty necrosis the expression had a focal membranous pattern [28] .…”

Section: Discussionmentioning

confidence: 99%

Composition of inflammatory infiltrate and its correlation with HBV/HCV antigen expression

Walewska-Zielecka¹,

Madaliński²,

Jabłońska³

et al. 2008

WJG

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of HBsAg expression in hepatocytes. Inflammatory infiltrates accompanied the focal expression of HCV antigens. A direct correlation between antigen expression and inflammatory reaction in situ was noted more often in hepatitis C than B. CONCLUSION: Irrespective of the etiology and activity of hepatitis, components of the inflammatory infiltrate in liver were similar. Overall inflammatory activity did not correlate with the expression of HBsAg and HCVAg; HBcAg expression, however, accompanied chronic hepatitis B of moderate and severe activity. INTRODUCTIONA cytopathic effect is absent in hepatocytes during viral replication, which is a characteristic feature of infection with hepatotropic viruses. Necrosis of hepatocytes is considered to be a result of cellular immunity reactions directed against viral antigens on the surface of these cells [1,2] . It is assumed that immunological mechanisms, insufficient for the full eradication of viruses, are responsible for liver damage and extrahepatic manifestations of infection [3] . Extrahepatic manifestations of hepatitis B virus (HBV) and hepatitis C virus (HCV) Bozena Walewska-Zielecka, Kazimierz Madalinski, Paulina Godzik, Joanna Cielecka-Kuszyk, Bogumila Litwinska, Department of Virology, National Institute of Public Health, National Institute of Hygiene, Warsaw 00-791, Poland Joanna Jablonska, Department of Hepatology and AIDS, Warsaw Medical University, Warsaw 01-201, Poland Author contributions: Walewska-Zielecka B designed and performed research; Madalinski K and Godzik P equally contributed to write the paper; Jablonska J collected the patient data; Cielecka-Kuszyk J contributed to data interpretation and wrote parts of the paper; Litwinska B contributed to data interpretation and collection of funds. Abstract AIM: To study the composition of liver inflammatory infiltrate in biopsy material from patients chronically infected with hepatotropic viruses and to evaluate the correlation of inflammatory infiltrate with hepatitis B virus (HBV) and hepatitis C virus (HCV) viral antigen expression in chronic B and C hepatitis. METHODS: The phenotype of inflammatory cells was evaluated by the EnVision system, using a panel of monoclonal antibodies. HBV and HCV antigens were detected with the use of monoclonal anti-HBs, polyclonal anti-HBc and anti-HCV antibodies, respectively. RESULTS: The cellular composition of liver inflammatory infiltrate was similar in the patients with B and C hepatitis: ~50%-60% of cells were T helper lymphocytes. Approximately 25% were T cytotoxic lymphocytes; B lymphocytes comprised 15% of inflammatory infiltrate; other cells, including NK, totalled 10%. Expression of HLA antigens paralleled inflammatory activity. Portal lymphadenoplasia was found more often in hepatitis C (54.5%) than in hepatitis B (30.6%). Expression of HBcAg was found more often in chronic B hepatitis of moderate or severe activity. Overall inflammatory activity in HBV-infected cases did not correlate with the intensity

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Section: Discussionmentioning

confidence: 99%

Composition of inflammatory infiltrate and its correlation with HBV/HCV antigen expression

Walewska-Zielecka¹,

Madaliński²,

Jabłońska³

et al. 2008

WJG

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“…[98][99][100] However, strong, multispecific interferon gamma-producing, HCV-specific CD8 ϩ T cells are one of the characteristic features of patients who recover from an acute HCV infection. 66,68,69,72,[101][102][103][104][105][106][107][108][109][110][111][112][113][114] In a chronic HCV infection, although the frequencies of HCV-specific CD8 ϩ T cells may be normal, the cells exhibit a dysfunctional or stunned phenotype. 66,100,115,116 Recent data indicate that most HCV-specific CD8 ϩ T cells express the inhibitory receptor programmed death 1 (PD-1) at the time of acute infection.…”

Section: Role Of Cd8 T Cellsmentioning

confidence: 99%

Acute hepatitis C virus infection: A chronic problem

et al. 2008

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S ince the discovery of the hepatitis C virus (HCV) in the late 1980s, there has been an explosion of information regarding its natural history, treatment, and replication cycle. Nonetheless, there are still relatively few data regarding acute HCV infection. By convention, the term acute hepatitis refers to the presence of clinical signs or symptoms of hepatitis for a period of 6 months or fewer after the presumed time of HCV exposure. Early studies of posttransfusion patients who developed non-A, non-B hepatitis provide a clinical picture of early infection. 1 Following the availability of specific serologic and virologic tests, most such patients were shown to have acute HCV infection. After acute infection, HCV RNA may become detectable in the serum/plasma in as little as 2 weeks ( Fig. 1). Several weeks later, a high percentage of patients experience an increase in serum aminotransferase levels consistent with the development of acute hepatocellular injury. In the majority of cases, patients develop mild constitutional symptoms, including abdominal pain, nausea, vomiting, anorexia, and fatigue. During this acute infection, serum aminotransferases often peak below 1000 IU/mL and may return to normal levels. A minority develops sufficient elevations in bilirubin to lead to overt jaundice or the development of dark urine. Unless the clinical suspicion is high, few patients will be tested for HCV RNA or HCV antibody seroconversion. However, in the majority-but not all-of infected patients, HCV RNA persists, and a chronic disease state develops.The reasons for the general lack of data regarding acute HCV infection are multifactorial and include (1) the relatively high percentage of asymptomatic or unrecognized early infections, (2) the lack of large-scale identification of chronic carriers in the general population who serve as a reservoir for infection, and (3) the decreased number of acute infections that occur in controlled clinical settings such as that of blood transfusions. These factors and the lack of nonprimate animal models necessitate reliance on retrospective studies in chronic carriers, the use of limited historical collections of banked sera, and the extrapolation of outcomes based on small disease outbreaks in unique settings (for example, transmission from a physician to a patient in the operating room setting or following parenteral exposure in healthcare workers). Moreover, there exist only a limited number of population cohorts that continue to experience high rates of HCV transmission (for example, Egypt); nonetheless, there is a growing body of information regarding the clinical presentation, natural history, and treatment outcomes of acute HCV infection.In this article, we review the current information regarding our understanding of the epidemiology, virology, and immunology of HCV with a particular emphasis on acute HCV infection. In addition, we review recent data related to interferon-based treatment intervention and propose an algorithm for the diagnosis and management of acute HCV inf...

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“…Two T-cell clones from patient 1 were identified twice (clones 1-17 and 5-11) in the cells sorted with anti-BV2. The nomenclature used to refer to each clone (for example, [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] indicates that clones 1 and 17, arbitrarily assigned these numbers when cultured in microtiter plates, turned out to be identical or sibs of each other on sequence analysis. One T-cell clone from patient 3 was also isolated twice (clone 3-7).…”

Section: T-cell Cloningmentioning

confidence: 99%

“…1,2 Previous studies using molecular approaches have shown that clonal expansions are present within the T-cell infiltrates. 3 These are referred to as clonotypes to reflect that they were identified by molecular approaches rather than by culture and characterization of intact cells.…”

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confidence: 99%

T-cell clones derived by CD3 stimulation from hepatitis C virus explanted liver tissue are not representative of dominant clones present in vivo

Davey

Rosen

Woody³

et al. 2001

Liver Transplantation

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In-situ immunophenotyping study of hepatic-infiltrating cytotoxic cells in chronic active hepatitis C

Cited by 39 publications

References 0 publications

Composition of inflammatory infiltrate and its correlation with HBV/HCV antigen expression

Composition of inflammatory infiltrate and its correlation with HBV/HCV antigen expression

Acute hepatitis C virus infection: A chronic problem

T-cell clones derived by CD3 stimulation from hepatitis C virus explanted liver tissue are not representative of dominant clones present in vivo

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