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Progress in medical virology. Fortschritte der medizinischen Virusforschung. Progrès en virologie médicale 02/1981; 27:66-76.
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ABSTRACT: The tissue distribution of hepatitis B virus antigens was correlated with the distribution of immunoglobulins and complement and with histopathological changes. Although no circulating antibody was detected, the participation of humoral immune mechanisms in the elimination of HBsAg from the circulation was suggested by presence of HBsAg, immunoglobulins, and C'3 in germinal centers of mesenteric lymph nodes and HBsAg mixed with immunoglobulins in the mesangium of kidney glomeruli. The results support the hypothesis that the immune status of HBV chimpanzee carriers is associated with hyporesponsiveness rather than tolerance.
Journal of Medical Primatology 02/1979; 8(4):222-32. · 1.30 Impact Factor
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Gastroenterology 03/1978; 74(2 Pt 1):182-7. · 11.68 Impact Factor
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New England Journal of Medicine 11/1977; 297(14):787-8. · 53.30 Impact Factor
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ABSTRACT: Lung tissue, lymph nodes, and spleen from infants 4-15 weeks old who died of Pneumocystis carinii pneumonia were studied by immunofluorescence and immunoelectron microscopy. The results strongly suggest that antibodies to P. carinii synthetized in lungs by inflammatory infiltrates and in regional lymph nodes are essential in the elimination of P. carinii from infected lungs through their opsonization of the P. carinii organisms. Disintegration of P. carinii conglomerates subsequent to the binding of complement preceded their phagocytosis by lung alveolar macrophages. The immunomorphologic findings strongly supported the hypothesis that the replication of P. carinii at the rate leading to clinical symptoms is due to impaired and delayed synthesis both of antibodies to P. carinii and of complement.
National Cancer Institute monograph 11/1976; 43:163-9.
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ABSTRACT: Sera of the influenza patients and healthy controls were tested for some types of autoantibody (SMA, ANA, ABBA, AMA). They were detected in 83.8% of the patients' sera and in 16.6% of controls. SMA were present in 77.4%, ANA in 54.8%, and ABBA in 16.1% of the patient's sera. AMA were not detected. A majority of the sera contained more than one autoantibody type. The possible mechanisms of induction of the autoantibodies in virus infection and their possible role in disease are briefly discussed.
Acta virologica 07/1976; 20(3):202-7. · 0.68 Impact Factor
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Pediatria polska 02/1976; 51(1):1-7.
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Acta virologica 05/1975; 19(2):169. · 0.68 Impact Factor
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The Lancet 09/1974; 2(7879):477-82. · 38.28 Impact Factor
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The Journal of Infectious Diseases 05/1973; 127(4):424-8. · 6.41 Impact Factor
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The Journal of Infectious Diseases 11/1972; 126(4):372-7. · 6.41 Impact Factor
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ABSTRACT: In a significant percentage of examined cases of fulminant hepatitis, subacute hepatitis, chronic aggressive hepatitis, liver cirrhosis and chronic persistent hepatitis, Australia (hepatitis-associated) antigen (Au HAA) was identified in the liver and in extrahepatic locations. The several immunofluorescent patterns of Au HAA localization in hepatocytes strongly suggested various stages of Au HAA accumulation and release. Deposits of a mixture of immunoglobulins G and M and occasionally beta1C-globulin were found in the cytoplasm of Au HAA containing hepatocytes, on their plasma membranes, on or in the nuclei, in the cytoplasm of Kupffer cells and, rarely, in the sinusoids. The accompanying tissue changes were hepatocellular degeneration and necrosis. These intra- and extracellular complexes of Au HAA and immunoglobulins displayed strong affinity for guinea pig complement in the immunohistochemical complement fixation reaction. When tested by immunodiffusion in agar, IgG dissociated from these complexes by potassium thiocyanate (KSCN) treatment showed anti-Au HAA specificity. In fulminant hepatitis neither Au HAA nor immunoglobulins and complement were found in the liver. In chronic aggressive hepatitis and subacute hepatitis the amount of the Au HAA immune complexes identified in the liver was approximately inversely proportional to the extent and severity of the parenchymal lesions. In liver cirrhosis and chronic persistent hepatitis there was a positive correlation between the amount of the Au HAA immune complexes found in the liver and the degree of hepatocellular damage. The deposits of Au HAA, identified in extrahepatic locations including germinal centers of lymph nodes and spleen, kidney glomeruli and blood vessel walls, were as a rule accompanied by deposits of IgG, IgM, beta1C-globulin and fibrin. All these deposits showed strong affinity for guinea pig complement in the immunohistochemical reaction of complement fixation. Germinal center activation, chronic membraneous glomerulonephritis, panarteritis and simple arteriolar hyalinosis were found at sites of localization of these deposits.
American Journal Of Pathology 08/1972; 68(1):31-56. · 4.89 Impact Factor
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Polish medical journal 02/1972; 11(6):1459-66.
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Polish medical journal 02/1972; 11(6):1750-60.
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Gruźlica i choroby płuc; tuberculosis et pneumonologia 10/1971; 39(9):867-73.
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Annals of the New York Academy of Sciences 06/1971; 177:156-70. · 3.15 Impact Factor
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The Journal of Infectious Diseases 04/1971; 123(3):251-6. · 6.41 Impact Factor
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The Lancet 04/1971; 1(7699):598. · 38.28 Impact Factor
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Nature: New biology 02/1971; 229(3):92-4.
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Medycyna doświadczalna i mikrobiologia 02/1971; 23(2):85-9.
