1972
DOI: 10.1016/s0140-6736(72)91153-1
|View full text |Cite
|
Sign up to set email alerts
|

Cytoplasmic Localisation of Australia Antigen in the Liver

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

1
15
0
15

Year Published

1973
1973
2007
2007

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 75 publications
(31 citation statements)
references
References 12 publications
1
15
0
15
Order By: Relevance
“…A similar distribution was noted previously using immunofluorescent techniques in two other studies (Hadziyannis et al, 1972;Shikata, 1973). This may be due to release of the surface antigen from damaged cells as intimated above, and Shikata (1973) noted in several such biopsies that neighbouring Kupffer cells were positive, suggesting recent phagocytosis of material containing HBsAg.…”
Section: Discussionsupporting
confidence: 89%
See 1 more Smart Citation
“…A similar distribution was noted previously using immunofluorescent techniques in two other studies (Hadziyannis et al, 1972;Shikata, 1973). This may be due to release of the surface antigen from damaged cells as intimated above, and Shikata (1973) noted in several such biopsies that neighbouring Kupffer cells were positive, suggesting recent phagocytosis of material containing HBsAg.…”
Section: Discussionsupporting
confidence: 89%
“…In early studies, HBsAgwasapparently found mainly in the nuclei (Coyne et al, 1970;Nielsen and Elling, 1971), whereas, more recently, it has been observed only in the cytoplasm (Hadziyannis et al, 1972;Shikata, 1973). It now seems likely that the antisera employed in the earlier immunofluorescent studies also contained antibodies directed at the hepatitis B core-antigen (HBcAg) or against nuclear proteins (Gerber and Paronetto, 1974).…”
Section: Discussionmentioning
confidence: 99%
“…If there is, as these results suggest, an appropriate cellular immune response to HBsAg in the patients who develop chronic liver disease, why does the virus infection persist? Little is known about the role of humoral antibody in the recovery from hepatitis B infection but we have argued elsewhere ) that a defect in the production of antibody to HBsAg would allow virus particles to penetrate uninfected hepatocytes and establish a cycle of infection, in spite of the destruction by sensitized lymphocytes of those hepatocytes in which the virus had previously replicated-This continuous destruction of infected cells would explain the relatively small number of hepatocytes which can be shown to contain HBsAg when liver biopsies from patients with antigen-positive active chronic hepatitis have been examined by immunofluorescent techniques (Hadziyannis et al, 1972). In contrast, in healthy carriers, ie, those without histological evidence of liver disease, where both cellular and humoral responses to the antigen are absent there are large numbers of cells with HBsAg in the cytoplasm.…”
Section: Discussionmentioning
confidence: 99%
“…Although the majority of these individuals in a recent series (Woolf, Boyes, Jones, Whittaker, Tapp, MacSween, Renton, Stratton, and Dymock, 1974) showed some evidence of liver damage, there are some carriers with entirely normal liver histology. In these, HBsAg can be shown to be present in many hepatocytes (Hadziyannis, Vissoulis, Moussouros, and Afroudakis, 1972), which has led to the suggestion that the virus may not be cytopathic and that the destruction of infected cells in patients with acute virus B hepatitis and in those with chronic forms of liver damage is due to the development of an immune response to the infectious 'Present address: Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA Received for publication 21 April 1975. agent. Dudley, Fox, and Sherlock (1972) suggested that the persistence of HBsAg-whether or not liver disease was present-is related to a defect in cellular immunity and they found an impairment in lymphocyte response to phytohaemagglutinin (PHA), a T-cell mitogen, in patients with chronic liver disease and persistent antigenaemia as compared with normal controls (Giustino, Dudley, and Sherlock, 1972).…”
mentioning
confidence: 99%
“…lF, in which the cytoplaslm of the hepatocyte is partially filled with diffuse, intensely staining antigen 38 days after exposure to acute-phase serum. Cytoplasmic hepatitis B antigen in hepatocytes of patients with HB antigenemia, dem-onstrated by inimunofluorescence methods, has been observed by a number of workers (17,22,23).…”
Section: Exposure Of Cultures To Acute-phase Seramentioning
confidence: 96%