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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spleen cells from mice, 4 to 60 days after infection with mouse hepatitis virus type 4, produced interleukin-2, as well as interleukin-3, in the absence of exogenous stimulants in vitro. This unique lymphokine production by mouse hepatitis virus type 4 infection was controlled by host genes.
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PMID:Spontaneous production of interleukin-2 and interleukin-3 by spleen cells from mice infected with mouse hepatitis virus type 4. 284

Resistance to mouse hepatitis virus (MHV) in C3H mice is a genetic trait which appears 3-4 weeks after birth. However, when these animals were weaned on a low protein diet (8% casein), they remained susceptible to MHV-2 infection until they reached 8-9 weeks of age. During this period, the protein-restricted C3H mice were as susceptible to MHV-2 as the genetically susceptible congenic C3Hss strain. The delay in the emergence of resistance in the protein-restricted mice could be corrected by injecting these animals with spleen cells from 6-week-old C3H mice. Thymocytes from normal C3H mice, and splenocytes and thymocytes from protein-restricted C3H mice, were not protective. However, spleen cells from the protein-restricted mice were more responsive to phytohaemagglutinin, lipopolysaccharide and concanavalin A than spleen cells from normal C3H. The enhanced lymphoproliferative response in spleen cells from protein-restricted mice was abrogated by the addition of plastic-adherent cells obtained from normal C3H spleens. Spleen cells from protein-restricted and from genetically susceptible C3Hss mice also possessed more spontaneous cytotoxicity against MHV-infected 3T3 fibroblasts.
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PMID:Influences of nutrition on immunity and susceptibility to mouse hepatitis virus type 2. 299 Nov 26

Spleen cells from uninfected control mice selectively lysed BALB/c 3T3 fibroblasts infected with mouse hepatitis virus (MHV), a murine coronavirus. Lysis of infected cells occurred within 3 hr, and histocompatibility between effector and target cells was not required. This natural, cell-mediated, virus-associated cytotoxicity differed from NK cell- and T cell-mediated lysis. Spleen cells from animals infected with MHV were enriched in NK activity and were more cytotoxic to YAC-1 target cells, but did not show enhanced cytotoxicity for MHV-infected target cells. Spleen cells from beige mice, which are deficient in NK cell activity, were able to lyse MHV-infected target cells, as were spleen cells from nude mice, which are deficient in T cell activity. Lysis of MHV-infected target cells could be mediated by cells from the spleen and, to a lesser extent, by cells from the bone marrow, but not by resident peritoneal cells or thymocytes. We suggest the term "virus killer (VK) activity" for this phenomenon. VK activity of splenocytes from different mouse strains correlated with the ability of the splenocytes to bind purified radiolabeled MHV virions. MHV virions caused agglutination of spleen leukocytes from susceptible mouse strains, indicating that leukocyte agglutination or adsorption may provide a useful assay for coronaviruses such as MHV which lack hemagglutinating activity. SJL mouse splenocytes did not bind MHV and did not lyse infected targets. MHV bound relatively well to splenocytes of other mouse strains, but poorly to thymocytes and erythrocytes. Binding of MHV to leukocytes was not influenced by 6 mM EDTA or EGTA, indicating a lack of requirement for Mg++ or Ca++. VK activity was also resistant to EDTA and EGTA, in contrast to NK activity, which was sensitive to those chelating agents. VK activity was also unaffected by actinomycin D, cycloheximide, or puromycin, indicating that new protein synthesis was not required for lysis. Antibody to interferon-alpha/beta did not block lysis, nor was there substantially enhanced lysis mediated by leukocytes from mice infected with virus and thus exposed to high levels of interferon. VK activity was blocked by antibody directed against the peplomeric glycoprotein E2 of MHV. VK activity required infected target cells, because cells with adsorbed MHV virions were not lysed by splenocytes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural cytotoxicity against mouse hepatitis virus-infected target cells. I. Correlation of cytotoxicity with virus binding to leukocytes. 300 98

Interaction of two potential immunosuppressive factors, sublethal pesticide exposure and viral inhibition of lymphocyte mitogenesis, was examined in mixed lymphocyte reaction (MLR). Inbred (C57Bl/6 x A/J)F mice, semisusceptible to mouse hepatitis virus 3 (MHV3) infection were exposed to selected pesticides and subsequently infected with the MHV3 virus. The mortality of animals was examined as a function of pesticide exposure. Two pesticides were selected for further studies: the organochlorine pesticide dieldrin, which increased the cumulative mortality of animals, and the carbamate pesticide aminocarb, which did not affect the virus-induced cumulative mortality of animals. Spleen lymphocytes from dieldrin- and aminocarb-exposed C57Bl/6 mice (susceptible to MHV3 infection) were used as responder cells in one-way MLR. A marked immunosuppression of the MLR proliferative response was observed in the dieldrin group, whereas sublethal exposure to aminocarb did not affect the in vitro MLR response. The MLR cultures were subsequently infected in vitro with the MHV3 virus, which resulted in a time-dependent and virus dose-dependent inhibition of lymphocyte proliferation. However, no synergism was observed with the addition of either the MHV3 virus-induced inhibition of in vitro MLR lymphoproliferative response or dieldrin-related immunosuppression, since in vitro MHV3 infection of cells from dieldrin-exposed mice did not aggravate the dieldrin-related immunosuppression. In addition, no "hidden" aminocarb-related damage of the lymphoproliferative response was noted, as the kinetics of the virus-induced inhibition in the aminocarb group were analogous to the control. In conclusion, dieldrin-induced immunosuppression of the cellular immune response, rather than MHV3 virus-induced inhibition of lymphoproliferative activity itself, was the primary factor potentially responsible for the impaired cellular response. Furthermore, the data support the observation that cell-mediated immunity can be a potential target for the adverse effects of pesticide exposure.
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PMID:Virus-pesticide interactions with murine cellular immunity after sublethal exposure to dieldrin and aminocarb. 341 41

A total of 26 children aged 2 to 14 with the initial (6), formed (14) and terminal (6) stages of liver cirrhosis were examined by a method of radionuclide scintigraphy with 99mTc-colloid. 34 children aged 7 to 14 examined in the catamnesis of virus hepatitis, were controls. A set of indices characterizing function of the reticuloendothelial system (RES), the effective hepatic blood flow, metric parameters of the liver and spleen were obtained from an analysis of the curves of the heart, liver and spleen area, and digital imaging of the liver with the marked costal arch. It was shown that at the initial stage of disease indices of the time course of the radioactive colloid were of compensated nature. Spleen function was elevated, liver and spleen sizes were increased. The formed stage was characterized by the signs of subcompensation of liver function: changes of indices of RP retention in the blood, a decrease in the indices of the total and hepatic radioactive colloid. The terminal stage was characterized by marked disorder of liver RES function which was not compensated for by a high splenic uptake, image deformation and focal RP distribution. Irrespective of a stage of disease the syndrome of portal hypertension was shown to manifest itself in splenomegaly and an increase in the radioactive colloid uptake by the liver over 15%. The accuracy of the set of signs was 90%.
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PMID:[Hepatic scintigraphy using 99mTc-colloid in liver cirrhosis in children]. 349 80

This study was based on our model of experimental autoimmune hepatitis produced by immunizing C57BL/6 (B6) mice with syngeneic liver proteins and Freund's complete adjuvant. Spleen cells obtained from these hepatitis mice were transferred to syngeneic normal recipient mice, and histological changes occurring in the liver and the role of cellular immunity in producing liver damages in recipient mice were investigated. Sensitized spleen cells from these immunized (donor) mice were fractionated by a nylon wool column and injected intravenously into normal B6 mice. Histology of the liver of the recipient mice showed mild infiltration of mononuclear cells around the periportal area 7 days after the transfer of sensitized spleen cells, and changes were most prominent in the mice injected with the fraction of nylon wool column adherent spleen cells. Induction of these liver lesions in the recipient mice was blocked by treatment of sensitized donor spleen cells with anti-Thy 1,2 monoclonal antibody and guinea pig complement before injection. Lymphocyte reactivity to liver-specific lipoprotein (LSP) in recipient mice was studied by a lymphocyte transformation system, and a high immune response was demonstrated with the fraction of nylon wool column non-adherent (T-enriched) spleen cells. These data seem to indicate T-cell interactions between donor and recipient mice in the transfer study using our experimental autoimmune hepatitis model.
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PMID:Study of cellular immunity in experimental autoimmune hepatitis in mice: transfer of spleen cells sensitized with liver proteins. 387 43

Spleen cells obtained from C57BL/6 (B6) mice with an experimental autoimmune hepatitis were transferred to normal C57BL/6 recipient mice. Most prominent liver damages occurred in the recipient mice injected with sensitized nylon wool column-adherent spleen cells from the donor mice. Production of such liver damage was blocked by treatment of the sensitized adherent spleen cells with anti-Thy 1,2 monoclonal antibody and complement before injection. Based on these in vivo results, a microcytotoxicity assay was performed using isolated C57BL/6 hepatocytes as target cells and sensitized spleen cells obtained from hepatitis donor mice as effector cells. The fraction of sensitized nylon wool-adherent spleen cells demonstrated a high cytotoxic activity against isolated syngeneic hepatocytes, although the other fractions and spleen cells of control animals showed no such effect. The cytotoxic activity of sensitized-adherent spleen cells against target hepatocytes was significantly reduced after treatment with anti-Thy 1,2 antibody and complement, but it increased after depletion of B cells and Fc receptor-bearing T-cells. Although these sensitized nylon wool-adherent spleen cells showed high cytotoxic activities against syngeneic hepatocytes, their cytotoxicity against allogeneic hepatocytes was lower. They exerted no cytotoxic activity against syngeneic renal glomerular cells and EL-4 thymoma cells. These results suggest that sensitized T-cells in the nylon wool column-adherent fraction play the role of cytotoxic killer cells against target liver cells in vitro.
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PMID:Cell-mediated cytotoxicity of sensitized spleen cells against target liver cells--in vivo and in vitro study with a mouse model of experimental autoimmune hepatitis. 402 89

Resistance of SJL/J mice to intracranial inoculation with the JHM strain of mouse hepatitis, a coronavirus, is dependent upon the age of the animals at inoculation. Animals 12 weeks of age or older are resistant, whereas those 6 weeks or younger are uniformly susceptible to viral infection. Spleen cells or thioglycolate elicited peritoneal exudate cells can transfer resistance from 12-week-old to 6-week-old recipients. Removal of the adherent cells from either spleen or peritoneal cells ablated protection. Adherent cells from 12-week-old mice were protective even after depletion of Ia- and Thy-1-bearing cells. Antiviral antibody, thioglycolate injection into 6-week-old animals, and nylon wool-purified T cells were ineffective in mediating resistance. Adherent cells transferred 4 days before virus challenge, but not after challenge, were protective. Thus, there is an age-related change in SJL mice that protects from acute central nervous system disease, which may be due to maturation of a specialized adherent cell population.
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PMID:Resistance to fatal central nervous system disease by mouse hepatitis virus, strain JHM. II. Adherent cell-mediated protection. 624 28

Genetically athymic nu/nu (nude) rats, deficient in T cells, die from infection with various Toxoplasma gondii strains, including RH and Prugniaud strains. In contrast, these strains cause chronic infections without apparent symptoms in immunocompetent non-nude rats. We show here that nude rats die in two to three weeks after RH infection and three to four weeks after Prugniaud infection. Histological examination of brains from nude rats at different time points after infection, revealed an absence of lesions after RH strain infection and cysts with usually no inflammation after Prugniaud infection. Lungs from nude rats developed a fibrin alveolitis using either strain, whereas myocarditis with focal areas of necrosis were observed only after Prugniaud infection. Cysts and, in some cases, tachyzoites in the necrotic lesions were easily identifiable. The two strains of T. gondii elicited in nude rats a granulomatous hepatitis that only differed in intensity. Spleen and mesenteric lymph nodes appeared totally non reactive in both cases. This model allows immunological and parasitological studies by comparison with immunocompetent rat infection. Published data concerning toxoplasma pathology in AIDS, therefore, suggest that acute toxoplasma infection in nude rats may be a useful model for studying disseminated forms of toxoplasma infection found in AIDS patients.
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PMID:Pathology of Toxoplasma gondii infection in the nude rat. An experimental model of toxoplasmosis in the immunocompromised host? 783 Nov 53

Spleen cells cultured from Balb/c mice immunized with the JHM strain of mouse hepatitis virus (JHMV) have CD8+ cytotoxic T cells (CTL) specific for both the S and N proteins, but not the M or HE proteins. T cell lines were established from the brains of Balb/c mice infected with JHMV. The majority of the lines (20 of 22) were specific for JHMV. Analysis of the viral structural proteins which served as target structures indicate that most (15 of 20) were specific for the N protein. One line was specific for the S protein and four lines were specific for JHMV but the protein recognized could not be determined. These data suggest that early during infection there is a preferential recruitment of N protein specific CTL into the CNS of infected mice.
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PMID:JHM virus-specific cytotoxic T cells derived from the central nervous system. 820 62


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