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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 44 (1996), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In the present study the authors investigated the T-cell response to different enterobacteria or Helicobacter pylori and tested the hypothesis that the frequency of bacteria-specific T cells is increased in the intestine of patients with active inflammatory bowel disease (IBD), i.e. Crohn’s disease (CD) and ulcerative colitis (UC). The analysis of a large panel of T-cell clones (Tc) (n = 888) from peripheral blood, non-inflamed and inflamed intestine from IBD patients and control individuals shows that both peripheral blood and intestinal T-cell clones were selectively stimulated by either Salmonella typhimurium Yersinia enterocolitica 03, Escherichia coli or Helcobacter pylori sonicates, that only 〈 3% of all bacteria-reactive Tc were crossreactive and that proliferation to bacterial sonicates was inhibited by anti-MHC class II antibody. In addition, bacteria-specific Tc from IBD patients were more frequently isolated from inflamed intestine than from peripheral blood (P = 0.0039) or non-inflamed intestine. These data, from a large number of T-cell clones, are the first systematic analysis describing the response of individual T cells towards different bacterial species (ssp.). They show that T cells with specificity for distinct antigens or superantigens that are characteristic for a defined bacteria ssp. are present in normal, and increased in inflamed, IBD-intestine. These bacteria-specific Tc may play a role in IBD pathogenesis.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 8 (1978), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: IgA bound in vivo was shown by immunofluorescence on the plasma membrane of isolated hepatocytes from subjects with normal liver and patients with liver cirrhosis, chronic active hepatitis or fatty liver. IgA in sera with elevated IgA concentrations, especially from cases with alcoholic cirrhosis, was bound in vitro to isolated hepatocytes from rabbit and mouse. This was not due to the high IgA concentration per se. Moreover, polyclonal polymeric serum-type and secretory IgA, and three often polymeric monoclonal IgA preparations, showed similar binding properties. Conversely, purified polyclonal and monoclonal monomeric IgA did not show affinity for the hepatocytes. The binding of polymeric IgA did not seem to depend on the proportion of dimers and larger polymers, κ or λ-type light chains, heavy-chain subclasses, content of J chain or affinity for secretory component. The in vivo binding of IgA by hepatocytes is probably a physiological phenomenon which in part may explain the normal clearance of polymeric IgA from serum.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cytotoxic T lymphocytes (CTL) have previously been isolated from peripheral blood of patients with renal cell carcinoma (RCC). The CD8-positive CTL line MZ1257-CTL-5 (CTL-5) has been shown to lyse autologous cultured RCC cells in an HLA-A2 restricted fashion. Allogeneic, HLA-A2-matched RCC and melanoma cell lines were also lysed by CTL-5, suggesting that melanoma and renal cancer share antigenic determinants. The aim of the study was to determine whether RCC and melanoma share peptide epitopes that are recognized by CTL-5 in the context of HLA-A2 molecules. Peptides were acid-eluted from various cell lines, separated by reversed phase high performance liquid chromatography (RP-HPLC), and assessed for their ability to reconstitute the CTL-5-defined epitope by pulsing the peptides on HLA-A2 positive antigen-processing mutant cell line CEM × 721.174.T2 (T2). Peptides eluted from allogeneic HLA-A2-matched RCC and melanoma cell lines exhibited the CTL-5-defined epitope in the same HPLC fractions as peptides derived from the autologous RCC line. Renal cancer and melanoma cells preincubated with interferon-γ (IFN-γ) resulted in an additional peak of reconstitution activity in both cell types. This second lytic peak was also observed when high amounts of autologous RCC cells were used for peptide preparation without IFN-γ pretreatment, indicating that IFN-γ increases the amount of MHC class I/peptide complexes per cell, rather than inducing a neo-epitope.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Identification of the T-cell receptors (TCR) used by synovial cytotoxic T lymphocytes (CTL) of patients with reactive arthritis (ReA) may be crucial to better understanding the pathogenetic mechanism underlying the HLA-B27 association ofspondylarthropathies. The authors, therefore, sequenced 25 TCRB chains from HLA-B27-restricted CD8+ CTL clones and two clonal lines specific for self- or Yersinia enterocolitica antigen isolated from synovial fluids of 3HLA-B27+ patients with ReA and PBL of one healthy HLA-B27+ individual. Fourteen non-HLA-B27-restricted CTL served as controls. Both autoreactive and Y. enterocolitica specific HLA-B27-restricted CTL used a highlylimited set of VB genes with preferential rearrangement of three closely related VB families (VB 13,14,17), suggesting that these families contain a preferred site for contact with the HLA-B27 molecule. In addition, the presence of limited TCRBJ usage,limited heterogeneity in CDR3 sequences and dominant clones from individual donors among these CTL indicate that TCRB chain usage is further restricted by a limited set of peptides bound to the HLA-B27 molecule. Limited TCR usage by SF CTL of ReA patients may lay a basis for therapeutical manipulation of the T-cell response in the spondylarthropathies.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Der Chirurg 69 (1998), S. 522-529 
    ISSN: 1433-0385
    Keywords: Key words: Viral hepatitis ; Liver function ; Liver cirrhosis ; Immunprophylaxis ; Treatment of viral hepatitis. ; Schlüsselwörter: Virushepatitis ; Leberfunktion ; Lebercirrhose ; Immunprophylaxe ; Behandlung der Virushepatitis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung. Virushepatitiden gehören weltweit zu den wichtigsten Infektionskrankheiten. Allein über 300 Millionen chronische HBsAg-Träger und etwa die gleiche Anzahl chronischer Hepatitis-C-Virusträger werden geschätzt. Nach der Tuberkulose steht die Virushepatitis in der Statistik der infektiös bedingten Berufskrankheiten an zweiter Stelle. Insbesondere Teile Asiens, Afrikas, Lateinamerikas sowie der Mittelmeerraum und der Nahe Osten werden zu den Hochendemiegebieten der Virushepatitis gezählt. Aufgrund der immunologischen und molekularen Differenzierung sind heute die Virushepatitiden von A bis E einschließlich G weitgehend charakterisiert. Während die enteral übertragene Hepatitis A und E nur akute und in seltenen Fällen fulminante Verläufe induzieren, sind die Hepatitis B, ihre Koinfektion und Superinfektion mit Hepatitis Delta und die Hepatitis C insbesondere durch chronische Verläufe von großer medizinischer Bedeutung. Diese Erkrankungen können als Spätfolge in eine Lebercirrhose mit all ihren Komplikationen, einschließlich des primären Leberzellcarcinoms übergehen. Die für die Chirurgie besonderen Aspekte der Virushepatitis sollen diskutiert werden.
    Notes: Summary. Viral hepatitis belongs to the most important infectious diseases worldwide. More than 300 million chronic HBsAg carriers and chronic HCV carriers exist, respectively. High endemic areas of viral hepatitis are Asia, Africa, Latin America and the Near, Middle and Far East. Viral hepatitis is also very important in health care workers. Today viral hepatitis can be differentiated from type A to type E (G) based on immunological and molecular assays. While enterally transmitted hepatitis type A and type E only induce acute and rare fulminant disease, hepatitis type B, C and D often induce chronic progressive disease including liver cirrhosis with typical complications due to the portal hypertension and with a high rate of association with the development of primary liver cancer (HCC). This review focusses on viral hepatitis-related surgical problems, including liver transplantation.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-2307
    Keywords: Stomach neoplasms ; Pancreatic neoplasms ; Cell differentiation ; Histocompatibility antigens ; Interferon gamma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two new cell lines from stomach cancers and one from a pancreatic carcinoma are presented. MZ-GC-1 was established from a hepatic metastasis of a well differentiated gastric adenocarcinoma. MZ-GC-2 was derived from ascites induced by a poorly differentiated gastric adenocarcinoma. MZ-PC-1 originated from the pleural effusion of a moderately well differentiated pancreatic ductal adenocarcinoma. MZ-GC-1 cells were adherent and partially polarized, connected tightly via desmosomes. In contrast MZ-GC-2 cells consisted of slightly adherent or floating subpopulations and displayed no desmosomes. MZ-PC-1 cells were adherent and showed polarized growth, connected by apical junctional complexes. Cell doubling times were 7 days for MZ-GC-1 and 45 h for MZ-GC-2 and MZ-PC-1 cells. MZ-GC-2 and MZ-PC-1 gave rise to nude mouse tumours, resembling the original lesions. Chromosome analysis of the cell lines revealed a high range of numerical abnormalities. Each cell line had cytokeratin patterns fitting well to typical in vivo patterns. Furthermore the cell lines expressed a panel of antigens typical for gastrointestinal epithelia. Unique for MZ-PC-1 were high amounts of secreted Ca19-9. γ-Interferon enhanced HLA-class I antigens up to twofold and induced ICAM-1 expression on each cell line. HLA-class II antigens were differentially enhanced by γ-interferon. Due to their distinct characteristics the three tumour cell lines may be useful models in the investigation of the cell biology and immunogenicity of gastrointestinal tumours.
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  • 7
    ISSN: 1432-1440
    Keywords: Asymptomatic HBsAg-Carrier ; Characterization ; HBsAg-subtypes ; Immunserology and -histology ; Lebergesunder HBsAg-Träger ; Charakterisierung ; HBsAg-Subtypen ; Immunserologie und -histologie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Wir haben 129 Blutspender, bei denen bei Routineuntersuchungen HBsAg im Serum festgestellt wurde, zur diagnostischen Klärung einer möglichen Lebererkrankung untersucht. Zwölf hatten, als sie zur klinischen und leberbioptischen Untersuchung aufgenommen wurden, schon kein HBsAg mehr im Serum. Keiner von diesen hatte klinisch oder histologisch Anhalt für eine entzündliche Lebererkrankung. Zwei der 129 Patienten hatten eine milde, ikterische Hepatitis, verloren das Antigen während des Verlaufes und wurden anti-HBs-positiv. Die übrigen 115 Patienten, die klinisch gesund erschienen und keine frühere ikterische Leberkrankheit hatten, blieben HBsAg-positiv während des bisherigen Verlaufes von im Mittel 17,3±3,0 Beobachtungsmonaten. 40 dieser Patienten hatten histologisch eine normale Leber und 37 geringe bis deutliche Verfettungen des Parenchyms ohne Entzündungszeichen. 11 Patienten hatten eine leichte unspezifische Mesenchymaktivierung ohne fokale Nekrosen, 16 Patienten hatten neben Einzelzellnekrosen mit mesenchymaler Reaktion milde portale Infiltrationen, 6 hatten eine chronisch persistierende Hepatitis, 4 eine chronisch aggressive Hepatitis und 1 Patient eine posthepatitische Cirrhose. Eine Anzahl biochemischer und immunologischer Werte dieser Patientengruppen wurden mit denen einer Gruppe von 88 HBsAg-negativen Blutspendern verglichen. Signifikant höhere SGOT-Werte wurden nur in der Gruppe der Patienten mit Verfettungen, der Gruppe mit Nekrosen und Reaktionen und der Gruppe mit chronisch aggressiver Hepatitis gefunden. Die SGPT-Werte waren nur in den beiden letzteren Gruppen signifikant höher. Der Mittelwert der gamma-GT war nur in der Patientengruppe mit Verfettungen signifikant höher als in der HBsAg-Trägergruppe mit normaler Histologie, nicht aber verglichen mit dem HBsAg-negativen Kontrollkollektiv. Signifikant erhöht waren auch die Bilirubinwerte in allen Gruppen außer der Gruppe mit chronisch aggressiver Hepatitis, jedoch blieben die Mittelwerte immer im Normbereich. Die relativen Häufigkeiten der HBsAg-Subtypen verteilten sich gleichmäßig auf die verschiedenen Gruppen. Bei 7 Trägern fanden wir auch Anti-HBs im Serum. Autoimmunphänomene wurden nur selten beobachtet. Mit der direkten fluorescierenden Antikörpertechnik wurde in 77% der Leberbiopsien intrazytoplasmatisches HBsAg mit einer gleichmäßigen Häufigkeitsverteilung in den Gruppen festgestellt. Intranucleäres HBcAg konnte aber nur bei Patienten gefunden werden, die entweder eine chronisch entzündliche Lebererkrankung hatten oder entwickelten, während sie im Verlauf zur Kontrolle biopsiert wurden. Die Ergebnisse beweisen schlüssig, daß es vollkommen gesunde HBsAg-Träger mit normaler Leberhistologie gibt, die sich in bezug auf ihre Leberfunktion und Häufigkeit von positiven Autoimmunphänomenen nicht von normalen Kontrollpersonen unterscheiden. Diese Träger haben häufig intrazytoplasmatisches HBsAg aber nie HBcAg oder IgG in Kernen von Hepatocyten.
    Notes: Summary 129 blood donors found to be HBsAg-positive on routine testing were studied for evidence of hepatic disease. Twelve had already lost the antigen from the serum when histologically examined. None of these has had clinical or histological evidence of inflammatory liver disease. Two of the 129 patients showed mild icteric hepatitis, cleared the antigen during the follow up and became anti-HBs positive. The remaining 115 patients who appeared clinically healthy and who had no history of previous icteric liver disease remained HBsAg positive during a mean follow up period of 17.3±3.0 months. Forty patients from these had a normal liver histology and 37 mild to distinct steatosis but no signs of inflammatory liver disease. 11 patients a mild nonspecific mesenchymal activity but no focal necrosis, 16 patients had mild infiltration in portal tracts and a few necrotic parenchymal cells with mesenchymal reaction, 6 patients had chronic persistent hepatitis, 4 chronic aggressive hepatitis, and 1 definite posthepatitic cirrhosis. A number of biochemical and immunological variables of these patients were compared to those of a group of 88 HBsAg-negative blood donors. Significant higher SGOT values were found only in the groups of patients with steatosis, necrosis of parenchymal cells, and chronic aggressive hepatitis. SGPT values were significantly higher only in the two latter groups. The mean value for the gamma GT was significantly higher only in the group with steatosis, compared to the HBsAg carrier group with normal liver histology. A significant difference could not be established when compared to HBsAg-negative controls. Significantly higher, but still within normal range, were bilirubin values in all groups except for the 4 patients with chronic aggressive hepatitis. The relative frequencies of HBsAg subtypes were evenly distributed among the different groups. 7 carriers also had anti-HBs detectable in their serum. Autoimmune phenomena were rarely found. With the direct fluorescent antibody technique intracytoplasmic HBsAg was found in 77% of the liver biopsy specimens with an even distribution of the frequencies among the groups. Intranuclear HBcAg however could only be found in patients who either had or developed a chronic inflammatory liver disease when rebiopsied during the follow up. The results definitely establish that there are completely healthy HBsAg carriers with normal liver histology who do not differ from normal controls in their liver function and frequencies of positive autoimmune phenomena. They frequently have intracycloplasmic HBsAg but never HBcAg or IgG in the nuclei of their hepatocytes.
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  • 8
    ISSN: 1432-1440
    Keywords: Inflammatory liver diseases ; HBAg ; Lymphocytes ; Immunological reaction ; Fluorescent antibody technique ; Entzündliche Lebererkrankungen ; HBAg ; Lymphocyten ; Immunreaktionen ; Fluoreszierende Antikörper-Technik
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 127 Patienten mit verschiedenen entzündlichen Lebererkrankungen wurde die Fixation von HBAg an peripheren Lymphocyten untersucht. Bei 60 von diesen Patienten wurden im Parallelansatz die Fixation von HBAg an peripheren Lymphocyten und isolierten Leberzellen sowie die Fixation von IgG an isolierten Leberzellen geprüft. Membranfixiertes HBAg konnte an isolierten Hepatocyten auch bei Patienten mit positivem HBAg-Befund im Serum nicht nachgewiesen werden. HBAg an peripheren Lymphocyten fand sich hauptsächlich in der Phase des Verschwindens von HBAg im Serum (Zeitpunkt der Immunelimination). Membranfixiertes IgG fand sich vorwiegend bei HBAg-positiven protrahiert verlaufenden Hepatitiden und bei HBAg-positiver ACH und hoher entzündlicher Aktivität. Die Befunde sprechen bei persistierenden Antigenträgern für eine immunologische Toleranz gegenüber HBAg, für das Fortbestehen einer Virusinfektion der Leberzelle und für eine antikörpervermittelte Cyto- und Histotoxizität als pathogenetisches Prinzip bestimmter Verlaufsformen chronischer Lebererkrankungen. Die Definition der Antigendeterminante des Membran-fixierten Antikörpers steht noch aus.
    Notes: Summary The fixation of HBAg on lymphocytes was investigated in 127 patients with various inflammatory liver diseases. The fixation of HBAg on lymphocytes and isolated hepatocytes as well as the fixation of IgG on isolated hepatocytes were studied in 60 cases. Membrane-fixed HBAg could in no case be demonstrated on isolated hepatocytes whether these cells were derived from patients with or without HBAg in the serum. HBAg on lymphocytes was detectable in most cases of acute hepatitis during the phase when HBAg disappeared from the serum (time of immunoelimination). Membrane-fixed IgG could be mainly demonstrated in HBAg positive acute hepatitis with a protracted course or in HBAg-positive active chronic hepatitis and signs of inflammatory activity. The results obtained for HBAg-carriers indicate (a) an immunological tolerance against HBAg, (b) a persistance of the virus infection in liver cells, and (c) an antibody-mediated cyto- and histotoxicity as a pathogenetic principle for the course of certain chronic liver diseases. The antigenic determinant of the membrane-fixed antibody is not known until now.
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  • 9
    ISSN: 1432-1440
    Keywords: Asymptomatische HBsAg-Träger ; Lebererkrankungen ; Charakterisierung ; HBcAg ; Anti-HBc ; HBeAg (e-Antigen) ; DNApolymerase-Aktivität ; Immunhistologie ; Asymptomatic HBsAg-carriers ; Liver diseases ; Characterization ; HBcAg ; Anti-HBc ; HBeAg (e-antigen) ; DNApolymerase activity ; Immunohistology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary In this paper we report on anti-HBc-titers, HBeAg, DNApolymerase activity in the serum and intracellular HBsAg in healthy HBsAg-carriers and patients with HBsAg-positive inflammatory liver diseases. 32/44 patients with acure virus-B-hepatitis were negative for anti-HBc in the first week of the disease. Anti-HBc-titers in healthy HBsAg-carriers varied between 1:10 and 1:32,000 (medium titer 1:4,000). In HBsAg-positive CAH we found a medium titer between 1:32,000 and 1:64,000, in cases with CPH of about 1:16,000. All autoimmune type CAH showed anti-HBc-titers less than 1:10. By immunofluorescence we could demonstrate in a group of 71 asymptomatic HBsAg-carriers in none of the healthy HBsAg-carriers HBcAg in the liver cell nuclei. In contrast HBcAg could only be found in 4/5 HBsAg positive CAH- and 6/9 CPH patients. No elevated DNApolymerase activity could be demonstrated in healthy HBsAg-carriers. Out of 44 patients with virus-B-hepatitis only 3 showed elevated DNApolymerase activity. On the other hand DNApolymerase elevation was demonstrable in 17/37 cases with CAH and 9/15 with CPH. The investigations showed a strong correlation between the demonstration of HBeAg in the serum and the DNApolymerase activity. The characteristic findungs enabled us to differentiate between “healthy” HBsAg-carriers and HBsAg-carriers with inflammatory liver diseases.
    Notes: Zusammenfassung In der vorliegenden Arbeit wird über anti-HBc-Titer-Bestimmungen, HBeAg, DNApolymerase-Aktivität im Serum sowie über intrazellulär nachweisbares HBcAg bei gesunden HBsAg-Trägern und Patienten mit HBsAg-positiven entzündlichen Lebererkrankungen berichtet. 32/44 Patienten mit akuter Virus-B-Hepatitis hatten keine anti-HBc-Titer-Erhöhung in der ersten Krankheitswoche. Bei gesunden HBsAg-Trägern schwanken die anti-HBc-Titer zwischen 1:10 und 1:32000 (mittlerer Titer 1:4000). Bei HBsAg-positiven chronisch-aktiven Hepatitiden fand sich ein mittlerer Titer zwischen 1:32000 bis 1:64000, bei HBsAg-positiver CPH ein mittlerer Titer von 1:16000. Alle Patienten mit autoimmuner CAH (HBsAg-negativ) hatten anti-HBc-Titer unter 1:10. In einer Gruppe von 71 asymptomatischen HBsAg-Trägern konnten immunhistologisch bei keinem der gesunden HBsAG-Träger HBcAg im Leberzellkern nachgewiesen werden. Im Gegensatz dazu wurde HBcAg bei 4/5 HBsAg-positiven CAH- und 6/9 CPH-Patienten gefunden. Eine Erhöhung der DNApolymerase-Aktivität wurde bei keinem der gesunden HBsAg-Träger nachgewiesen. Von den 44 HBsAg-positiven akuten Virus-B-Hepatitiden hatten nur 3 Fälle eine Erhöhung der DNApolymerase-Aktivität. Andererseits fand sich eine DNApolymerase-Aktivität bei 17/37 Patienten mit HBsAg-positiver CAH und 9/15 Fällen mit CPH. Die Untersuchungen konnten eine enge Korrelation zwischen dem Nachweis des HBeAg im Serum und der DNApolymerase-Aktivität zeigen. Die Befundmuster ermöglichen eine klare Abgrenzung der “gesunden” HBsAg-Träger von den HBsAg-Trägern mit entzündlichen Lebererkrankungen.
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  • 10
    ISSN: 1432-1440
    Keywords: Hepatitis-B-core-Antigen ; Hepatitis-B-surface-Antigen ; akute Hepatitis ; chronisch aktive Hepatitis ; gesunde HB s Ag-Träger ; Leberbiopsie ; fluorescierende Antikörpertechnik ; Hepatitis-B-core-antigen ; hepatitis-B-surface-antigen ; acute hepatitis ; chronic active hepatitis ; healthy HB s Ag-carriers ; liver biopsy ; fluorescent antibody technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Liver biopsies of patients with inflammatory liver diseases and clinically healthy HB s Ag-carriers were examined for presence of intracellular HB s Ag, HB c Ag and IgG by direct immunofluorescence. The studies revealed the following results: 1. In most cases healthy HB s Ag-carriers had HB s Ag in the cytoplasm, but they did never show HB c Ag in the nuclei of hepatocytes. 2. In the early phase some patients with HB s Ag-positive acute hepatitis had HB c Ag and/or HB s Ag in their hepatocytes. In a normal course with complete recovery the immunoelimination may clear either phenomenon at variable stages of the disease. 3. Cases one year after complete recovery of acute virus B-hepatitis had no HB-components in their liver tissue. 2 cases without immunoelimination of HB s Ag developed chronic active hepatitis within one year and had HB c Ag in their liver cell nuclei. 4. Patients with HB s Ag-positive CAH and highly inflammatory activity had HB c Ag in the nuclei and a low percentage of cells with HB s Ag in the cytoplasm of hepatocytes. HB s Ag-negative cases with CAH never had HB-components in their tissue. 5. Patients with HB s Ag-positive and -negative CAH in complete remission never had HB c Ag and HB s Ag in their hepatocytes. 6. Most cases with HB s Ag-positive acute hepatitis and chronic active hepatitis positive for HB c Ag had also IgG in the same liver cell nuclei. The coincidence of this finding gives strong evidence for the presence of anti-HB c in these liver cell nuclei. The importance of this finding for the course of the disease is unknown.
    Notes: Zusammenfassung Wir untersuchten mit der direkten Immunfluorescenztechnik die Leberbiopsien von Patienten mit entzündlichen Lebererkrankungen auf intracelluläres HB s Ag, HB c Ag und IgG. Die Untersuchungen haben folgende Ergebnisse erbracht: 1. Klinisch gesunde HB s Ag-Träger hatten in den meisten Fällen HB s Ag im Cytoplasma, jedoch niemals HB c Ag in den Leberzellkernen. 2. Patienten mit HB s Ag-positiver akuter Hepatitis hatten in der Frühphase HB c Ag und/oder HB s Ag in den Hepatocyten. Unsere Befunde sprechen bei normalem Verlauf für eine komplette Immunelimination der HB-Komponenten zu verschiedenen Stadien der Erkrankung mit völliger Wiederherstellung. 3. Kontrollpunktate 1 Jahr nach Beginn einer HB s Ag-positiven Hepatitis zeigten bei völlig gesunden Patienten kein HB s Ag oder HB c Ag. Bei zwei Patienten ohne Immunelimination von HB s Ag entwickelte sich innerhalb eines Jahres eine chronisch aktive Hepatitis. Diese Patienten hatten HB c Ag in den Leberzellkernen. 4. Patienten mit HB s Ag-positiver CAH und Zeichen entzündlicher Aktivität hatten HB c Ag in den Zellkernen und in geringem Prozentsatz HB s Ag im Cytoplasma. HB s Ag-negative Fälle zeigten niemals HB-Komponenten im Gewebe. 5. In keinem Fall einer HB s Ag-positiven und -negativen CAH in Remission ließ sich HB s Ag und HB c Ag in Hepatocyten nachweisen. 6. In den meisten Fällen von HB s Ag-positiver AH und CAH, die HB c Ag-positiv waren, fand sich in den gleichen Zellkernen IgG. Die strenge Koinzidenz von HB c Ag und IgG läßt an das Vorliegen von anti-HB c in den Zellkernen denken. Die Bedeutung dieses Antikörpers in den Zellkernen für den weiteren Verlauf der Erkrankung ist unbekannt.
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