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)

T cell immune responses in syngeneic WKA/H rats were analyzed by using lymphoid cell lines, TARS-1, TART-1, and TARL-2, infected with human T-lymphotropic virus type 1 (HTLV-1). Spleen cells of rats in which these cell lines had been rejected were sensitized in vitro with the same cell lines, and cells cytotoxic to these HTLV-1+ cell lines, and cells cytotoxic to these HTLV-1+ cell lines were generated. The effector cells were CTL of the CD5+ CD8+ phenotype and showed restriction of MHC class I Ag. Direct tests as well as cold target cell inhibition tests with an array of cell populations showed that these CTL reacted only with syngeneic HTLV-1+ cell lines. When xenogeneic HTLV-1+ cell lines were similarly utilized for in vitro sensitization, rat CTL specific for syngeneic HTLV-1+ cells were generated. They were not, however, reactive with xenogeneic HTLV-1+ cells used for sensitization. Syngeneic rat cells selectively expressing gag, env, or pX gene coded Ag were prepared by infection of recombinant vaccinia viruses. In cold target cell inhibition tests of anti-HTLV-1 CTL with thus prepared cells, cytotoxicity against the syngeneic HTLV-1+ cells line, TARS-1, was inhibited by syngeneic cells expressing gag gene or env gene coded Ag. Inhibition was, however, more consistent and more dominant by cells with gag gene than those with env gene. Syngeneic cells with pX gene and MHC class I incompatible cells with gag, env, or pX gene did not inhibit cytotoxicity.
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PMID:Rat cytotoxic T lymphocytes against human T-lymphotropic virus type 1-infected cells recognize gag gene and env gene encoded antigens. 247 89

Modified env gene or gp55 gene in Spleen Focus Forming Virus, polycythemic strain, K-1 was molecularly cloned and its structure was characterized gp55 is a fusion glycoprotein consisting of N terminal 2/3 of xenotropic virus-related gp70 and C terminal half of F-MuLV p15E. A unique structure at the 3' and of the gp55 gene with 6 base pairs + 1 base pairs insert was identified. Gp55 may be hooked by the lipid bilayer of the cell membrane of the SFFV-intected cells, and additional glycosylation on the cell surface may modify the growth regulation of the cells. Possible origin of SFFV-specific gp55 gene was discussed.
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PMID:[Modified env gene in Friend spleen focus forming virus--structure, origin, and its role in leukemogenesis]. 385 23

Spleen cells from Rfv-3r/s mice with Friend virus-induced erythroleukemia were analyzed for expression of virus-induced proteins with monoclonal antiviral antibodies and conventional antisera. Leukemic spleen cells, 30-60 d after virus inoculation, expressed decreased amounts of ecotropic Friend murine leukemia helper virus gag- and env-encoded cell surface and intracellular proteins compared with leukemic cells tested 8-10 d after virus inoculation. In contrast, the spleen focus-forming virus-induced protein, gp55, was present on both leukemia cell populations. This difference appeared to be mediated by the humoral antibody response in Rfv-3r/s mice, which could recognize only ecotropic gag and env proteins, and not gp55. A new gp70 molecule cross-reactive with a recombinant Friend mink cell focus-inducing virus was found in large quantities on late leukemic cells. This protein appeared to be derived from a recombinant virus produced during the course of Friend virus infection. The appearance of this new gp70 suggests that recombinant viruses other than spleen focus-forming virus may play a role in Friend virus-induced erythroleukemia.
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PMID:New cell surface gp70 related to Friend mink cell focus-inducing virus is expressed on Friend virus-induced erythroleukemic spleen cells after elimination of ecotropic Friend virus gp70 in Rfv-3r/s mice. 697 19

We investigated the ability of human recombinant interleukin-7 (IL-7) to enhance the immune responses of mice vaccinated with either the alum-associated or liposome-formulated recombinant human immunodeficiency virus (HIV)-envelope protein, env-2-3SF2 (a nonglycosylated denatured gp 120 of HIV-1SF2 produced in genetically engineered yeast). Pathogen-free (C3H) mice were vaccinated on days 0, 14, and 28 with 10 micrograms of either the alum-associated env-2-3SF2 or liposome-formulated env-2-3SF2, both containing a lipophylic muramyl tripeptide, MTP-PE. Liposome-formulated IL-7 (5 micrograms/mouse) or empty liposomes were given on days 7, 14, 21, and 28. Antibody response against the immunized antigen, evaluated on day 21 and day 35 or 42, showed that liposome-formulated antigen induced higher antibody titer than did alum-associated antigen, and these antibody responses can be enhanced by concurrent administration of IL-7 liposomes. Spleen cells were harvested on day 21 and day 35 or 42 to evaluate cytotoxic T lymphocyte responses directed against autologous cells infected with vaccinia virus-expressing HIV-envelope protein. Mice treated with liposome-formulated antigen expressed the highest cytotoxic t-lymphocyte (CTL) activity, regardless of whether IL-7 liposome was given as an immune potentiator. In contrast, spleen cells from mice vaccinated with alum-associated antigen exhibited minimal CTL response, which was enhanced by concurrent IL-7 liposome treatment. Collectively, IL-7 liposome treatment enhanced the antibody production of the alum-associated or liposome-formulated env-2-3SF2, whereas its enhancement of CTL activity was detected only in mice vaccinated with alum-associated antigen.
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PMID:Effect of MTP-PE liposomes and interleukin-7 on induction of antibody and cell-mediated immune responses to a recombinant HIV-envelope protein. 802 14

Human endogenous retrovirus type W (HERV-W) envelope glycoprotein (Env) has recently been reported to induce fusion in cells expressing the RD-114 and type D retrovirus receptor (RDR) and to serve as a functional retroviral envelope protein. In this report, another biological function for HERV-W was demonstrated by testing its ability to protect cells against retroviral infection. Spleen necrosis virus (SNV), a gammaretrovirus was chosen for testing resistance because it uses RDR to enter cells. An HERV-W Env expression plasmid was transfected into canine osteosarcoma cells (D-17), which are permissive for SNV infection. Cell fusion assays were performed to demonstrate biological function of HERV-W Env in D-17 cells. The presence of HERV-W env sequences was confirmed in stably transfected cell clones by using polymerase chain reaction. Viral infectivity assays were performed with SNV and amphotropic Murine leukemia virus (MLV-A) pseudotyped vector viruses to measure titers in D-17 cells expressing HERV-W Env and in negative control cells. The HERV-W Env caused fusion of D-17 cells in culture and greatly reduced infection by SNV vector virus. A 1000- to 10,000-fold decrease in SNV infectivity was observed for D-17 cells expressing HERV-W Env as compared to D-17 cells that were not expressing HERV-W Env. In contrast, infection by MLV-A pseudotyped vector virus was not significantly reduced. Thus, HERV-W Env confers host cell resistance to infection by SNV. This is the first report of a human endogenous retrovirus gene product blocking infection by any exogenous retrovirus.
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PMID:The envelope glycoprotein of human endogenous retrovirus HERV-W induces cellular resistance to spleen necrosis virus. 1266 92

Mycobacterial infection has been implicated as a possible factor in AIDS progression in populations where HIV-1 and Mycobacterium tuberculosis are coendemic. In support of this concept, we have previously shown that HIV-1-transgenic (Tg) mice infected with mycobacteria display enhanced viral gene and protein expression. In this study, we demonstrate that the induction of HIV-1 observed in this model is dependent on Toll-like receptor 2 (TLR2), a pattern recognition receptor known to be involved in mycobacteria-host interaction. Spleen cells from HIV-1-Tg mice deficient in TLR2 (Tg/TLR2(-/-)) were found to be completely defective in p24 production induced in response to live M. tuberculosis or Mycobacterium avium as well as certain mycobacterial products. Importantly, following in vivo mycobacterial infection, Tg/TLR2(-/-) mice failed to display the enhanced HIV-1 gag/env mRNA and p24 protein synthesis exhibited by wild-type Tg animals. Together, these results argue that TLR2 plays a crucial role in the activation of HIV-1 expression by mycobacterial coinfections.
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PMID:Cutting edge: in vivo induction of integrated HIV-1 expression by mycobacteria is critically dependent on Toll-like receptor 2. 1287 96

Increase in systemic levels of lipopolysaccharide (LPS) contributes to the pathogenesis of distant organ injury after burn. Stress signals elicited from burn influence transcriptional activities of mouse endogenous retroviruses (MuERVs) in various distant organs. The involvement of LPS pathways in the burn-mediated regulation of MuERVs in the spleen was investigated in this study. Spleen harbors substantial numbers of tissue macrophages, a key responder to LPS stimulation. Spleen tissues collected from CD14 (LPS receptor) knockout (KO) and wild type (WT) mice after burn were subjected to RT-PCR analysis of MuERV expression. There was a substantial induction of 2 bands and a marked downregulation of a band in CD14 KO mice compared to WT mice after burn. Sequence analysis of these CD14- and burn-dependent bands identified 3 new alternatively spliced and 2 defective env transcripts of MuERVs as well as novel splicing signals. Chromosomal loci of putative MuERVs sharing the unique U3 sequences of these transcripts were mapped by surveying the entire genome of C57BL/6J mice. In addition, coding potentials, transcriptional regulatory elements, and adjacent cellular genes of these putative MuERVs were analyzed. The results from these studies suggest that injury-triggered LPS/CD14 signaling events play roles in the transcriptional regulation of certain MuERVs carrying unique U3 promoter sequences.
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PMID:CD14-mediated alterations in transcription and splicing of endogenous retroviruses after injury. 1550 8

Combined antiretroviral therapy (cART) does not eradicate HIV, which persists for years and can re-establish replication if treatment is stopped. The current challenge is identifying those tissues harboring virus through cART. Here, we used HIV env-nef single genome sequencing and HIV gag droplet digital PCR (ddPCR) to survey 50 tissues from five subjects on cART with no detectable plasma viral load at death. The spleen most consistently contained multiple proviral and expressed sequences (4/5 participants). Spleen-derived HIV demonstrated two distinct phylogenetic patterns: multiple identical sequences, often from different tissues, as well as diverse viral sequences on long terminal branches. Our results suggested that ddPCR may overestimate the size of the tissue-based viral reservoir. The spleen, a lymphatic organ at the intersection of the immune and circulatory systems, may play a key role in viral persistence.
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PMID:The Spleen Is an HIV-1 Sanctuary During Combined Antiretroviral Therapy. 2908 41