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)

Spleen cells and peripheral blood lymphocytes from chickens infected with reticuloendotheliosis virus (REV) were depressed in their responsiveness to phytohemagglutinin (PHA). When spleen cells from uninfected chickens were co-cultured with spleen cells from chickens infected with REV at 2 weeks of age, the PHA response by the normal cells was completely suppressed. Although spleen cells from chickens infected with REV at 6 or 9 weeks of age were also suppressed in their ability to respond to PHA, they did not suppress the mitogenic response of normal cells in mixed cultures.
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PMID:Depression of mitogen response in spleen cells from reticuloendotheliosis virus-infected chickens and their suppressive effect on normal lymphocyte response. 64 50

Several parameters of the cellular and humoral immune responses of chickens infected with reticuloendotheliosis virus (REV-T), an avian defective acute leukemia virus, or with its helper virus, reticuloendotheliosis-associated virus (REV-A), were evaluated. Spleen cells from chickens infected with REV-T (REV-A) or REV-A exhibited depressed mixed lymphocyte and mitogen responses in vitro. Allograft rejection was delayed by 6 to 14 days in birds infected with REV-A. The specific antitumor cell immune response was also studied by a 51Cr-release cytotoxicity assay. Lymphocytes from chickens infected with low numbers of the REV-T-transformed cells exhibited significant levels of cytolytic reactivity against the 51Cr-labeled REV-T tumor cells in vitro. The mitogen response of lymphocytes from these injected birds was similar to that of uninjected chickens. In contrast, lymphocytes from chickens injected with higher numbers of REV-T-transformed cells exhibited suppressed mitogen reactivity and failed to develop detectable levels of cytotoxic activity directed against the REV-T tumor cells. These results suggest that the general depression of cellular immune competence which occurs during REV-T (REV-A) infection could contribute to the development of this acute leukemia by inhibiting the proliferation of cytotoxic cells directed against the tumor cell antigens. The cytotoxic effect observed after the injection of chickens with non-immunosuppressive levels of REV-T-transformed cells appears to be specific for the REV-T tumor cell antigens since cells transformed by Marek's disease virus or avian erythroblastosis virus were not lysed. In marked contrast, birds whose cellular immune responses were suppressed by infection with REV-A were capable of producing a humoral immune response to viral antigens. Detectable levels of viral antibody, however, did not appear until 12 to 15 days after REV-A infection. Since REV-T (REV-A) induced an acute leukemia resulting in death within 7 to 14 days, it appears unlikely that the ability of chickens to make antiviral antibody influences the development of lethal reticuloendotheliosis.
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PMID:Specificity in the immunosuppression induced by avian reticuloendotheliosis virus. 618 91

Previously, we demonstrated that cytotoxic T lymphocytes (CTLs) from MHC: B19B19 and MHC: B21B21 chickens inoculated with a non-oncogenic Marek's disease virus (MDV) vaccine strain, SB-1/12 can lyse syngeneic reticuloendotheliosis virus (REV)-transformed cell lines expressing MDV pp38 or gB genes. In this study, we report the characterization of MDV gB-specific CTLs in chickens immunized with recombinant fowlpox virus expressing MDV gB gene (rFPV-gB). Spleen cells from rFPV-gB inoculated chickens (MHC: B19B19), depleted for CD4+, CD8+, TCR gamma delta+, TCR alpha beta 1+ or TCR alpha beta 2+ cells were used as effector cells in chromium release assays. Effector cells depleted of CD8+ or TCR alpha beta 1+, but not CD4+, TCR gamma delta+ or TCR alpha beta 2+ markedly reduced the percentage of specific release (%SR). Compared to the %SR caused by the SB-1/12-sensitized CTLs, the %SR caused by rFPV-gB-sensitized CTLs was low, but statistically significant. This is a first report on the induction of MDV gB-specific CD8+ CTLs in chickens immunized with rFPV-gB vaccine.
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PMID:Cytotoxic T lymphocyte response in chickens immunized with a recombinant fowlpox virus expressing Marek's disease herpesvirus glycoprotein B. 961 70

Spleen necrosis virus (SNV) and Reticuloendotheliosis virus strain A (REV-A) belong to the family of reticuloendotheliosis viruses and are 90% sequence related. SNV-derived retroviral vectors produced by the REV-A-based D17.2G packaging cell line were shown to infect human cells (H.-M. Koo, A. M. C. Brown, Y. Ron, and J. P. Dougherty, J. Virol. 65:4769-4776, 1991), while similar vectors produced by another SNV-based packaging cell line, DSH134G, are not infectious in human cells (reviewed by R. Dornburg, Gene Ther. 2:301-310, 1995). Here we describe a careful reevaluation of the infectivity of vectors produced from the most commonly used REV-A- or SNV-based packaging cells obtained from various sources with, among them, one batch of D17.2G packaging cells obtained from the American Type Culture Collection. None of these packaging cells produced vectors able to infect human cells. Thus, contrary to previously published data, we conclude that REV-based vectors are not infectious in human cells.
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PMID:Avian reticuloendotheliosis virus strain A and spleen necrosis virus do not infect human cells. 1059 Jan 42

An antigen for gel precipitation was prepared from chick embryo fibroblast cultures inoculated with the Reticuloendotheliosis virus. The specificity of the reaction was confirmed with reference Reticuloendotheliosis and Spleen necrosis sera. No precipitation reactions occurred between this antigen and Marek's disease, Newcastle disease, Infectious bronchitis, Pasteurella Multocida and Haemorrhagic enteritis antisera.
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PMID:Reticuloendotheliosis antigen for the agar gel precipitation test. 1877 Mar 34

In avian species, the Reticuloendotheliosis virus (REV) causes severe immunosuppression and other symptoms, including avian dwarfing syndrome, and chronic tumors in lymphoid and other tissues. The pathogenesis of REV and its interaction with the host have yet to be fully elucidated with transcriptional studies on the changes in host gene expression after REV infection at the body level. In this study, the Spleen Necrosis Virus (SNV) was used to inoculate the one-day-old specific pathogen free (SPF) chicken to simulate congenital infection. We identified 1507 differentially expressed genes (DEGs) at 7, 14 and 21 dpi using Next Generation Sequencing (NGS) technology. Through the Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of these DEGs, it was found that DEGs were mainly involved in the categories of signal transduction, immune system and signaling molecules and interaction. Among them, Pattern recognition receptors (PRRs), chemokine, T cell receptor, JAK-STAT, TNF, and NF-kappa B signaling pathway, and the Hematopoietic cell lineage play an important role in the tumorigenic and immunosuppressive regulation of REV. In addition, a series of DEGs associated with inflammatory factors (CCL4, TNFRSF18, CDKN2), apoptosis (IRF1, PDCD1, WNT5A), innate immunity (TLR, MAD5, TRIM25), and adaptive immunity (LY6E, CD36, LAG3) were also discovered. We further verified 33 selected immune- relevant DEGs using quantitative RT-PCR (qRT-PCR). These findings provide new insights and research directions for revealing the pathogenesis of REV infection and the interaction between REV and the chicken immune system.
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PMID:Transcriptional analysis of host responses related to immunity in chicken spleen tissues infected with reticuloendotheliosis virus strain SNV. 3122 42