Gene/Protein Disease Symptom Drug Enzyme Compound
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 453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of 67 liver biopsies (20 kidney transplant recipients and 47 outpatients with hepatitis) was investigated for the presence of hepatitis B antigen core (HBc) and surface (HBs) components by immunofluorescence and electron microscopy. The variable appearance of the core in liver cell nuclei and of the surface in the cytoplasm allowed the recognition of expression patterns which, together with histologic parameters, could be integrated into four reaction types of diagnostic and prognostic implications: Type I (Elimination Type). No components or only occasional expression of HBc; histologically, classic lobular hepatitis; clinically, acute, self-limited viral hepatitis. Type II (HBc Predominance, or Immunosuppression Type). Abundant core expression in each liver cell nucleus and moderate appearance of HBs; histologically, nonaggressive inflammation (nonspecific reactive or portal hepatitis); clinically, mild, chronic, persistent hepatitis in transplant patients. Type III (HBs Predominance, or Nonaggressive Type). Prominent HBs expression largely in the absence of HBc; histologically, nonaggressive inflammation (nonspecific reactive and portal hepatitis) or normal liver tissue, together with ground-glass hepatocytes in light microscopy, as a correlate of HBs-containing hepatocytes; clinically, hepatitis B antigen carrier, or chronic persistent hepatitis. Type IV (HBc+s Equivalence, or Aggressive Type). Spotty expression of both components, especially of core; histologically, periportal hepatitis; clinically, mainly corresponds to chronic aggressive hepatitis and to acute hepatitis with possible transition to chronicity. As a unifying concept for these types, it is suggested that immune responsiveness determines the reaction pattern, the key mechanism being immune elimination of affected cells. Between efficient elimination (type I) and effective immunosuppression (type II), a graded elimination insufficiency is found in chronic forms (types III and IV), explaining the persistence and probably also the aggressiveness of hepatitis B virus infection.
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PMID:Pattern of core and surface expression in liver tissue reflects state of specific immune response in hepatitis B. 108 35

To comprehensively study autoantibodies in patients with chronic hepatitis (CH), especially those with hepatitis C virus (HCV) infection, proteins extracted from HepG2 cells were separated by two-dimensional electrophoresis. Spots reacting with sera from 15 patients with CH-C were detected by Western blotting. Proteins extracted from the spots were subjected to mass spectroscopy for identification by mass fingerprinting. Antigenicity of the proteins identified was confirmed by Western blotting and enzyme-linked immunoabsorbent assay. The localization of the autoantigens so detected was investigated by immunohistochemistry. Among 20 protein spots detected, four were identified as actin, heat shock protein (HSP) 70, HSP60, and a novel protein (hepalaminin). Hepalaminin consists of two domains of laminin beta-2 and a specific domain. Autoantibodies against the specific domain were detected in 60.8% of patients with CH-C, 37.7% of those with CH-B, 42.3% of those with autoimmune CH, 28.6% of nonalcoholic steatohepatitis, 10.0% of asymptomatic HCV carriers, but in no healthy volunteers. Antihepalaminin positivity in CH-C and CH-B was related to histologic grading. Immunohistochemical staining demonstrated that hepalaminin is present in the cytoplasm of hepatocytes and cholangiocytes but not of fibroblasts or the vascular epithelium. Hepalaminin is a novel protein expressed in hepatocytes and cholangiocytes. Autoimmunity to this protein may exacerbate inflammation in chronic viral hepatitis.
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PMID:Identification of a new autoantibody in patients with chronic hepatitis. 1560 81