Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vesicular stomatitis virus (VSV) is a mitogen for mouse spleen cells, and infectious virus is not required for mitogenesis. At concentrations between 10 and 100 microgram per culture, VSV stimulated DNA synthesis and blast transformation. Maximal activation by VSV occurred 48 h after culture initiation. Spleen cells depleted of T-lymphocytes by treatment with anti-Thy 1.2 and complement and those obtained from congenitally athymic BALB/c nu/nu mice were activated by VSV, suggesting that VSV is a B-cell mitogen. Activation of spleen cells was independent of the host in which the virus was grown, since VSV grown in BHK-21, HKCC, or MDBK cells was mitogenic. The mitogenesis was specific for VSV, since MDBK cell-grown WSN influenza virus was not a mitogen in this in vitro activation system, VSV-specific antibody prevented VSV mitogenesis, and VSV was mitogenic for spleen cells from C3H/HeJ mice which were resistant to mitogenesis by endotoxin.
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PMID:Activation of mouse lymphocytes by vesicular stomatitis virus. 625 36

The effect on respiratory burst of splenic cells from mice pretreated with oil-in-water emulsions of muramyl dipeptide (MDP), trehalose dimycolate (TDM), or the combination of MDP with TDM was studied by luminol-dependent chemiluminescence in response to stimulation by zymosan. Spleen cells from mice pretreated with TDM, but not those of mice treated with MDP, generated increased chemiluminescence. Spleen cells from animals pretreated with the combination of MDP and TDM exhibited markedly enhanced chemiluminescence activity. The effect of enhanced activity of preparations containing MDP combined with TDM was further examined in vivo by an aerosol infection of pretreated mice with a mouse-pathogenic influenza virus. Pretreatment with 6-O-acyl analogs and one ubiquinone derivative of MDP alone did not induce any resistance against influenza virus. Significant protection was conferred only when MDP and certain analogs were combined with TDM. The enhancement of nonspecific resistance to influenza virus infection was related to the chemical structure of the synthetic immunostimulant. A greater degree of protection was induced by the combination of TDM with the lipophilic derivatives like B 30-MDP and L-18 MDP.
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PMID:Stimulation of chemiluminescence and resistance against aerogenic influenza virus infection by synthetic muramyl dipeptide combined with trehalose dimycolate. 631 68

Spleen cells from C57BL/10(H-2b) mice, when stimulated in vitro to Kk alloantigens, lysed syngeneic influenza A virus-infected tumour cell targets but not uninfected or vaccinia- or Sendai virus-infected targets. Peritoneal macrophage targets infected with influenza virus were not lysed. Lysis of H-2k targets and EL4-A influenza virus-infected targets was abrogated by treatment of effectors with anti-Thy 1.2 plus C and anti-Lyt 2 plus C but not by anti-Lyt 1 plus C or anti-GM-1, a natural killer cell-specific, monoclonal antibody plus C. Cold target inhibition experiments indicated that one and the same population of Tc cells see H-2Kk and H-2b plus influenza virus. Sensitization of C57BL/10 mice to Kk in vivo did not potentiate virus clearance from lungs. The data are discussed in relation to observed Ir gene effects and variation and modulation of H-2 antigens on tumour cells.
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PMID:Alloreactive cytotoxic T lymphocytes lyse syngeneic influenza-infected tumour cell targets. 642 19

A total of 267 passerine birds distributed among 37 species were netted during spring 1980 and summer 1981 in the Laurentian and Montreal areas. All the cloacal swabs collected at that time wer free of influenza viruses. Three and five days after oral administration of avian or human influenza A virus strains, 108 isolates were obtained from 42 of 134 passerine birds. Positive samples were recovered mainly from the respiratory and the digestive tract and also from liver. Spleen and kidneys. Viral replication is cells from trachea, lungs, gizzard and caecum was detected by indirect immunofluorescence using a monoclonal antibody to influenza A virus nucleoprotein. Viral transmission from inoculated to non inoculated birds placed in the same cages was not observed. On the other hand a similar experimental inoculation of young mallard ducks showed that extensive viral transmission occurred from inoculated to non inoculated ducklings and that infection was found exclusively in the digestive tract. Furthermore viruses were detected in samples of drinking water from all cages containing infected ducks. Passerine birds do not represent an important reservoir of influenza viruses but might contribute to the formation and spreading of recombinants potentially pathogenic for man and animals.
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PMID:[Role of passerine birds in the ecology of influenza viruses]. 668 60

Spleen cytotoxic T cells killing influenza virus-infected target cells are cross-reactive for the different type A influenza viruses, in contrast to the circulating antibodies, which show fine specificity for each A virus subtype variant. This finding has raised the question of whether a single T cell can recognize cells infected with all type A viruses. T-killer cell lines with specificity for alloantigens and the male Y antigen can be selected by means of growth factors present in the supernatant of T cells stimulated with concanavalin A (refs 3-7). We report here that we have been able to establish clones of mouse T cells killing target cells infected with influenza virus. Our cell line maintains the same specificity as the heterogeneous spleen cell population from infected mice, in as far as the T-killer cells are specific for A influenza virus, but do not discriminate between the different type A viruses. The cell line maintains H-2 restriction and does not kill cells infected with B influenza virus. The cells grow in the presence of T-cell growth factor and do not require antigen for growth although they maintain their receptors for type A virus. They can also be stimulated by irradiated T-helper cells from mice primed by type A influenza infection in the presence of type A virus-infected cells.
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PMID:Cross-reactivity for different type A influenza viruses of a cloned T-killer cell line. 696 71

Mice injected with inactivated (UV light-irradiated) influenza virus produce specific antibody, become sensitized for a delayed-type hypersensitivity reaction, but do not generate specific cytotoxic T (Tc) cells. If injected 4-5 days later with infectious virus, the formation of Tc cells is suppressed by > 90%. If A strain viruses are used, the suppression observed is cross-reactive within A strain viruses but does not extend to B/LEE or to Sendai virus. Serum from mice injected with UV-irradiated virus contains antibodies which on adoptive transfer can inhibit Tc cell formation when infectious homologous virus is used to challenge the recipients. Spleen cells from the same mice, upon adoptive transfer, also inhibit (50-70%) Tc cell formation if transferred within 24 h of injection of infectious virus, and the specificity pattern observed is cross-reactive within A strains. The activity of the cells mediating suppression is destroyed by monospecific anti-Thy-1.2 antibody and complement. The immune cells require I region sharing between donor and recipient mice for their suppressor activity to be effective. (There is also a partial requirement for K, D region sharing, but the possible rejection of transferred cells is not excluded.) Dilution assays in which clonal expansion of Tc precursors is used to estimate their frequency and the presence of T helper (Th) cells indicate that suppressed mice possess Tc precursors and primed cells which, upon restimulation, act as Th cells. Furthermore, injection of irradiated Th cells with inactivated virus does not significantly reduce the ensuing suppression.
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PMID:Selective suppression of the cytotoxic T cell response to influenza virus in mice. 697 Jan 26

Spleen cells from mice immunized with vaccinia or influenza viruses were mixed with spleen cells from mice immunized by dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH) and transferred into irradiated syngeneic recipient mice which were subsequently restimulated with trinitrophyenylates (TNP) or unmodified viruses. One week later, spleens were removed and assayed for indirect anti-DNP plaque-forming cells (PFC). When spleen cells from both influenza and vaccinia primed mice were restimulated with the haptenated form of the virus used for the initial immunization there was an enhanced PFC response compared to that seen with spleen cells from unprimed mice.
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PMID:An assay for virus-specific help for B cells. 697 Jul 84

In mice infected with influenza A2/Port Chalmers and B/Hong Kong viruses the formation of antibody-producing cells (APC) to the thymus-dependent antigen, sheep red blood cells (SRBC) was found to be inhibited much stronger than that to the thymus-independent antigen (polyvinylpyrrolidone K-90). Influenza A/PR-8/34 virus was approximately similarly active in both systems. Spleen cells of mouse donors infected with influenza virus were characterized by a markedly reduced capacity to form APC to ARBC when inoculated into irradiated recipients. This capacity was recovered if the donor spleen cells of infected animals were inoculated into recipients in mixture with T-lymphocytes of intact animals. Possible mechanisms of lymphocyte damage in influenza infection are discussed.
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PMID:[Changes in the functional activity of T- and B-lymphocytes in experimental infection due to different strains of the influenza virus]. 697 71

The influence of different antigen delivery systems on antibody isotype and lymphokine profile has been investigated using influenza nucleoprotein as a model antigen system. Mice exposed to live or inactivated influenza virus produced antibody against whole virus or recombinant nucleoprotein (rNP), which was predominantly of the IgG2a isotype. Spleen or lymph node cells from these mice rapidly produced large amounts of interferon-gamma (IFN-gamma), but no detectable interleukin-5 (IL-5) when stimulated in vitro with specific antigen. In contrast, after primary immunization with rNP or p206-229 in different adjuvants (CFA, quil A or alhydrogel), specific antibody was predominantly of the IgG1 isotype and relatively lower amounts of IFN-gamma but no IL-5 were detected following in vitro antigenic stimulation. Secondary immunization, however, resulted in detection of IgG2a antibodies and increased levels of IFN-gamma. IL-5 was only detected after secondary immunization with peptide in adjuvant. Mice infected with aro A- Salmonella typhimurium expressing NP produced antibody of both IgG1 and IgG2a isotypes and large amounts of IFN-gamma and no IL-5, following in vitro antigenic stimulation, and therefore parallelled the pattern seen with whole virus more closely than that seen following primary immunization with protein or peptide in conventional adjuvants. The results suggest that the antigen delivery vehicle influences both quantitative and qualitative differences in the type of immune response elicited, which may be important in determining the potency of protective immunity induced.
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PMID:Influence of the antigen delivery system on immunoglobulin isotype selection and cytokine production in response to influenza A nucleoprotein. 826 59

In attempt to increase the induction of peptide-specific cytolytic T cells (CTL) we investigated the effect of the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) gene product on the activation of peptide-specific CTL. Spleen cells of CH3 mice immunized against the influenza nucleoprotein peptide 50-63 (NP 50-63) were restimulated in vitro (i) with peptide-pulsed syngeneic fibroblast cells (Ltk-) as antigen-presenting cells, which were in addition (ii) infected with NDV or (iii) stably transfected with the HN cDNA of NDV. A greater than sixfold increase in peptide-specific CTL responses was observed in cultures restimulated with peptide-pulsed Ltk- cells which co-expressed viral hemagglutinin due to either infection or transfection. A similar augmentation was seen in CTL responses against other types of antigen (major histocompatibility complex alloantigens, minor histocompatibility antigens or tumor antigens) when suboptimal cultures were stimulated with the respective antigen-presenting cells modified by NDV infection. These findings suggest that NDV or viral HN expressed on antigen-presenting cells or tumor cells can exert a T cell co-stimulatory function.
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PMID:Viral hemagglutinin augments peptide-specific cytotoxic T cell responses. 840 59


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