Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of lymphocytes in chronic granulomatous inflammations is frequently thought to indicate that thymus-dependent cellular immune mechanisms are involved in the pathogenesis of such processes. Therefore, in the present studies, a model of a granulomatous heaptitis (induced by heat-inactivated group A streptococci) was used to determine whether liver granulomata, consisting of macrophages and lymphocytes, could also be evoked in neonatally thymectomized or in congenitally thymus-deficient nude mice. The morphological (light and electron microscopical, immunohistological) investigations were supplemented with selective determination of T- and B-lymphocyte function. The thymus-deficient mice, after injection of streptococci, developed liver granulomata that did differ neither quanlitatively nor quantitatively from those of control animals with thymus. Lymphocytes were found within the granulomata in both animal groups. There was no evidence for functional disorder of the RES in thymus-deficient mice; on the contrary, RES-activity seemed to be increased. Phagocytosis of streptococci, their intracellular breakdown and streptococcal antigen-degradation occurred as fast or faster in such animals. PHA- and LPS-stimulation of spleen lymphocytes indicated a considerable depletion of T-cells in neonatally thymectomized mice and a complete absence of T-cells in congenitally thymus-deficient nude mice. However, radioimmunological determination of antibodies to group A streptococcal carbohydrate revealed that both groups of experimental animals possessed functionally active B-cells. Therefore, the granulomatous hepatitis described here can be defined as a focal reaction of the liver RES with "B-lymphocyte trapping". Cellular immune mechanisms are not involved in the pathogenesis of these lesions.
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PMID:Animal experimental studies on chronic granulomatous inflammation and T-lymphocyte-system. 108 34

With the onset of a remission phase of chronic aggressive hepatitis in a young female patient, two different auto-antibodies were found which had not previously been in evidence. These antibodies were identified as Donath-Landsteiner antibodies, the cause of a secondary auto-immune hemolytic anemia observed during this period, and anti-nuclear antibodies. Both antibodies were of the IgG class, both could be adsorbed onto the patient's own erythrocytes as well as P1-positive test erythrocytes, and both antibodies were present in the subsequent erythrocyte eluate. Separation of the two antibodies present in the serum as well as in the antibody-containing erythrocyte eluate was possible by absorption of the antinuclear factors using preparations of liver and thymus cell nuclei, but the anti-erythrocyte activity was not diminished by this procedure. Rapid remission of the auto-immune hemolytic anemia was achieved by a therapeutic application of corticosteroids. Long-term therapy has resulted in no recurrence of the auto-immune hemolytic anemia until now.
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PMID:[Autoimmune hemolytic anemia with Donath-Landsteiner antibodies and antinuclear factors during the course of chronic-aggressive hepatitis]. 108 45

A group of 83 two-to-eighteen-week-old chickens with acute infectious hepato-myelopoietic disease (a German form of inclusion-body-hepatitis) were observed to have the following histologic lesions: panmyelophthisis, small foci of liver necrosis, often with intranuclear inclusion bodies in hepatocytes (15 to 20% of chickens), involution-like atrophy of the bursa of Fabricius and thymus, loss of lymphatic tissue in spleen and cecal tonsils, and nonpurulent myocarditis. In 18 survivors 6 to 8 weeks after clinical signs of disease, nonpurulent myocarditis but normal lymphatic organs and bone marrow were present. A group of 75 chickens were infected after hatching with the field isolant "1942." Between the 3rd and 9th weeks postinoculation the same histologic changes-though mostly milder-were demonstrated. This syndrome differs somewhat from the syndrome described as inclusion body hepatitis in America and Europe.
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PMID:Lesions in chickens with spontaneous or experimental infectious hepato-myelopoietic disease (inclusion body hepatitis) in Germany. 115 54

Using a sensitive infant mouse bioassay to detect infectious virus, the pattern of mouse hepatitis virus (MHV) JHM dissemination in blood and other tissues was examined during the first 5 days following intranasal inoculation. MHV replicated in nasal turbinates of both susceptible BALB and resistant SJL mice from days 1 through 5, but BALB mice had higher titers on days 1 and 2. Viremia was detectable on days 1 through 5 in BALB mice, but only on days 3 and 5 in SJL mice. Transient virus replication occurred in the lungs of both mouse genotypes at 1 and 2 days, then ceased. This correlated with more consistently demonstrable virus in blood collected from the left atrium of the heart, compared to jugular vein, portal vein and right atrial blood. Virus was associated equally with the plasma and cellular fractions of blood on day 3, but was primarily in the buffy coat of the cellular fraction on day 5. Interferon-alpha/beta was detected in serum and spleen, but not liver or brain of BALB mice or in any tissue of SJL mice. BALB serum and spleen interferon was first detected at 36 h, peaked between 48 and 72 h, and was undetectable by 108 h. The distribution of virus in nose, cervical, axillary and mesenteric lymph nodes, spleen, Peyer's patch, thymus, bone marrow and liver was examined at 1, 2, and 3 days. The resulting pattern suggested lymphatic spread of virus to cervical lymph node and mesenteric lymph node as pathways of dissemination in addition to viremia.
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PMID:Viremic dissemination of mouse hepatitis virus-JHM following intranasal inoculation of mice. 130 44

A virulent strain of serotype 8 fowl adenovirus (FAV) was isolated from an outbreak of inclusion body hepatitis (IBH) in broiler flocks. Post-mortem changes included characteristic liver lesions with intranuclear inclusion bodies in the hepatocytes and severe lymphocytic depletion in the bursa, thymus and spleen. The packed cell volume was reduced by 50 per cent or more and varying amounts of cell depletion were observed in the bone marrow. Typical IBH was reproduced in specific pathogen-free chickens inoculated orally with the FAV isolated from the natural infection. There was severe depletion of lymphocytes in the bursa, thymus and spleen of the experimentally infected birds and FAV antigens were detected by ELISA and immunocytochemical staining in various lymphoid tissues. Humoral antibody responses against sheep red blood cells, detected by the haemagglutination test, were decreased in the chickens infected with FAV. These findings suggest that the damage caused by replication of this virulent strain of FAV in lymphoid tissues compromises the immunological capabilities of infected chickens.
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PMID:Effects of fowl adenovirus infection on the immune system of chickens. 133 81

Cortisone acetate was administered to a group of guinea pigs (Cavia porcellus) at 0 (control), 20 (low) or 200 (high) mg/kg. Steroid was given daily for two individual 7 day periods, separated by 7 days of no treatment. The effects of this steroid on body weight gain, thymic weight, total and differential leukocyte counts, serum antibody titer against a bacterin, dermal hypersensitivity response to a sensitizing agent and histological evaluation of lymphoid and other tissues were evaluated. Significant differences in body weight gain (p less than 0.05) and thymic weight (p less than .01) were noted. For total leukocyte count, no significant difference among treatment groups at individual time points was noted (p greater than .10), while significant differences were seen in lymphocyte and neutrophil counts (p less than .01). A significant difference in antibody titer among the treatment groups was observed (p less than .01). For the dermal hypersensitivity response, there was no consistent pattern among the treatment groups in gross (macroscopic) skin reactions. Microscopically, differences were seen in the inflammatory response among the treatment groups. Histologically, steroid related changes were seen in thymus, spleen, lymph node and liver. At necropsy, 24 of 40 animals had lesions of focal necrotizing hepatitis. Three affected animals died and remaining animals showed no clinical illness. The cause of the necrotizing hepatitis could not be determined by culture, special stains, electron microscopy, serology or by attempts at transmission with affected liver samples.
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PMID:Immune modulation in the guinea pig using cortisone acetate. 184 84

Epstein-Barr virus (EBV) is often associated with lethal lymphoproliferative diseases in immunologically compromised individuals. Recently, we have studied a 20-month-old boy with X-linked lymphoproliferative disease (XLP) who had succumbed to infectious mononucleosis (IM) complicated by fulminant hepatitis and virus-associated hemophagocytic syndrome following EBV infection. EBV genomes were detected in peripheral blood lymphocytes (PBL), cervical and mesenteric lymph nodes, liver, spleen, thymus, and bone marrow. According to restriction endonuclease analyses, the EBV-DNA pattern was similar in all samples except for the EBV-DNA from the bone marrow. Additionally, circular EBV-DNA (suggesting a latent infection) predominated in spontaneously established lymphoblastoid cell lines (LCLs) derived from both the lymph node and cord lymphocytes co-cultured with PBL. In contrast, both circular and linear EBV-DNA (suggesting a lytic infection) were noted in spontaneously established LCLs derived from his PBL. Furthermore, LCLs derived from both the lymph node and cord lymphocytes co-cultured with PBL expressed fewer reactive cells for early antigen (EA) and viral capsid antigen (VCA) than spontaneous LCLs from his PBL, thus providing evidence for different B cellular susceptibility to EBV infection in this patient with XLP. Finally, defective EBV-specific cytotoxic T cell activity was observed in this patient. Latent EBV infected cells may easily escape immunosurveillance by the host. These findings may explain the fatal course of EBV infection in this patient.
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PMID:Differential cellular susceptibility to Epstein-Barr virus infection in a patient with X-linked lymphoproliferative disease. 217 37

Antibodies against thymus epithelial cells (anti-TEC) and the basal cell layer (BCLA) of squamous epithelia have been described in association with HDV-related chronic liver disease (CLD). Data are lacking on their presence during nAnB virus infection. Sera from 51 patients with nAnB post-transfusion hepatitis, including acute and chronic cases diagnosed during a prospective study on candidates for cardiac surgery, and 167 with various forms of CLD were tested for the presence of anti-TEC and BCLA using indirect immunofluorescence on human thymus and rat forestomach sections. Both antibodies mainly occurred in nAnB, HDV and cryptogenic CLD (anti-TEC: 51%, 47% and 42%; BCLA: 29%, 38% and 31%, respectively). The prevalence of anti-TEC in nAnB CLD turned out to be higher than that recorded in alcoholic, HBV-related, autoimmune, liver and kidney microsomal antibody positive CLD and primary biliary cirrhosis (p ranging from less than 0.03 to less than 0.0004). Two monoclonal antibodies (Mabs) to cytokeratins gave a pattern superimposable on that of spontaneous anti-TEC (both Mabs) and BCLA (only one). Antibodies against epithelial constituents, presumably targeting cytokeratin-associated antigens, occur not only in HDV CLD, as previously reported, but also in nAnB CLD, where they might represent a diagnostic aid, due to the unavailability of reliable serological markers of nAnB infection. The close similarity of anti-TEC and BCLA status between nAnB and cryptogenic CLD suggests a nAnB etiology of at least a proportion of chronic liver patients at present scored as cryptogenic.
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PMID:Serum antibodies to thymus epithelial cells in non-A, non-B and cryptogenic chronic liver disease. 247 4

In previous studies it has been suggested that activation of cellular immunity may have a role in controlling the activity of chronic non-A, non-B liver disease. We conducted a pilot study of therapy with a bovine thymus extract for 6 weeks in 15 consecutive patients with chronic non-A, non-B hepatitis, most of them sporadic cases. Treatment induced immunomodulation, and in five patients a significant but transient diminution in aminotransferase levels was observed associated with increments in several parameters of cellular immunity. This suggests that a longer administration of this or other related compounds, or treatment with a more potent immunomodulating agent, might be effective in these patients.
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PMID:A pilot study of thymus extract in chronic non-A, non-B hepatitis. 251 54

Viral pathogenicity may be regulated by host defense mechanisms at the virus-immune cell interaction level. The immune system plays an important role in the outcome of acute disease induced by the mouse hepatitis virus type 3 (MHV3) virus. The lymphoid cells act as effectors in the virus elimination as well as targets for viral replication. In order to demonstrate a correlation between MHV3 pathogenicity and viral replication in lymphocytes, genetically-determined resistant A/J and susceptible C57BL/6 mice were infected with pathogenic (L2-MHV3) or nonpathogenic (YAC-MHV3) viral strains. Pathogenicity and histopathologic studies have revealed that lymphoid organs such as thymus and spleen, showed injuries or atrophy in susceptible mice infected with L2-MHV3. No histopathologic lesions in the lymphoid organs occurred in C57BL/6 mice infected with YAC-MHV3 or A/J mice infected with both viruses. The mechanisms involved in the lymphoid injuries were studied regarding viral replication in the lymphoid organs and cells in infected mice. Results indicate that cell depletion in lymphoid organs is caused by a complete viral replication in lymphoid cells. Thy1.2+ and surface IgM+ lymphoid cells from susceptible C57BL/6 mice infected with L2-MHV3 were permissive to viral replication and to subsequent cell lysis. No cell lysis, however, occurred in lymphoid cells from C57BL/6 mice infected with YAC-MHV3 and A/J mice infected with both virus strains. In vitro studies, with purified T and B cell populations were performed to determine the mechanism effecting susceptibility or resistance to viral-induced cell lysis occurring in such cells. A blockade, probably occurring at the viral RNA polymerase activity level, prevents viral replication in resistant cells between the stages of fixation of the virus at the cell-surface receptor and the viral protein translation. These experiments indicate that an intrinsic virus-specific resistant mechanism occurs in lymphoid cells that plays a major role in the viral pathogenicity.
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PMID:Mouse hepatitis virus 3 replication in T and B lymphocytes correlate with viral pathogenicity. 254 12


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