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 cultures from various strains of mice were infected in vitro with murine cytomegalovirus (MCMV). Infectious centres were established in a small proportion (not greater than 1%) of the cells. Virus could be rescued from these cells by co-cultivation with syngeneic or allogeneic fibroblasts, but the frequency of rescue could not be altered by incubation with cyclic nucleotide analogues, iododeoxyuridine, cortisol, or allogeneic spleen cells. In addition a smaller fraction of the cell population, possibly a sub-population of the infectious centres, replicated virus spontaneously. The presence of mitogens did not affect these interactions qualitatively or quantitatively. A third response to infection was an inhibition in DNA synthesis, which was suffered by unstimulated cultures and by cells transformed by concanavalin A and bacterial lipopolysaccharides, although overall cell viability was maintained. This response was also mediated by u.v.-inactivated virus.
J Gen Virol 1978 Jan
PMID:Multiple interactions between murine cytomegalovirus and lymphoid cells in vitro. 20 68

Spleen cells from mice infected with the rough Brucella melitensis strain B115 were fused with NSO myeloma cells. Hybridoma supernatants were screened in ELISA with cell walls (CW), sonicated cell extracts (CE) and rough lipopolysaccharide (R-LPS) of B. melitensis strain B115 and whole B. melitensis B115 cells. Surprisingly, 22 monoclonal antibodies (mAbs) reacting in ELISA with both CW and CE but not with R-LPS and bacterial cells were shown by immunoblot analysis and ELISA to react with smooth lipopolysaccharide (S-LPS). These mAbs also reacted in ELISA with O polysaccharides (OPS) from the smooth Brucella abortus strain 99 and the smooth B. melitensis strain 16M and thus recognize epitopes present on the O-chain. Proteinase K LPS preparations from B. melitensis B115 analysed by immunoblotting with one mAb (12G12) recognizing S-LPS of both A and M specificity displayed the typical S-LPS high-molecular-mass ladder pattern but no S-LPS was detected in the phenol/water/chloroform/light petroleum LPS preparation of the same strain. mAb 12G12, specific for S-LPS, and a mAb (A68/03F03/D05) specific for R-LPS were used to localize the O-chain and R-LPS expressed in B. melitensis strain B115 by immunoelectron microscopy. Immunogold labelling was observed at the surface of B. melitensis B115 cells with the anti-R-LPS mAb but not with the anti-S-LPS mAb. In ultrathin sections, immunogold labelling with the S-LPS specific mAb was observed in the cytoplasm and in the periphery of the cytoplasm, probably at the cytoplasmic membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
J Gen Microbiol 1992 Jun
PMID:O-chain expression in the rough Brucella melitensis strain B115: induction of O-polysaccharide-specific monoclonal antibodies and intracellular localization demonstrated by immunoelectron microscopy. 138 11

Spleen cells from mice immunized with a Bordetella pertussis N-lauroyl sarcosine membrane extract (SME) were used to generate hybridoma cells lines producing monoclonal antibodies (mAbs). Seven mAbs were shown to be specific to B. pertussis lipo-oligosaccharide (LOS) by immunoblotting of SME or purified LOS following SDS-PAGE. All mAbs reacted with the B. pertussis Tohama I strain of the LOS AB phenotype, and did not react with the atypical variant strain 134 of the LOS B phenotype. The immune reactivity of the mAbs was retained after treatment of SME with proteinase K and was lost after sodium periodate treatment. No cross-reactivity was observed with the mAbs when tested against B. parapertussis and other Gram-negative bacteria. However, all mAbs reacted with B. bronchiseptica. Binding assays with live B. pertussis cells demonstrated that mAbs strongly reacted with cell surface exposed antigenic determinants. High bacterial cell lytic capability was observed for five of these mAbs. Concentrations between 0.22 and 2.2 micrograms mAb ml-1 (0.1 and 1 microgram per 450 microliter assay) purified by protein A were required to kill at least 50% of the bacteria. Competition immunoassays with biotinylated antibodies showed that the bacteriolytic and non-bacteriolytic mAbs were directed to different epitopes of the B. pertussis LOS A.
J Gen Microbiol 1991 Apr
PMID:Characterization and comparative bactericidal activity of monoclonal antibodies to Bordetella pertussis lipo-oligosaccharide A. 171 58

Spleen cells primed by Prospect Hill (PH) or Puumala (Pu) virus could cross-react with Hantaan virus (HV) 76-118 strain-infected target cells after in vitro stimulation with HV-infected cells, although anti-PH or anti-Pu immune serum showed no cross-reactive neutralizing (NT) activity to HV without complement. These results and our previous findings with cross-reactive cytotoxic T lymphocytes (CTLs) suggest that some epitopes recognized by CTLs might be common among the hantavirus genus, while the epitopes related to NT activity were mainly specific to each virus of this genus. Next, to evaluate the cross-reactive immunities demonstrated by in vitro study, we investigated the effect of transferring T lymphocytes and sera from BALB/c mice immunized with PH or Pu virus into nude mice before HV inoculation. Transferring T lymphocytes primed by PH or Pu virus reduced HV titres in lungs and spleens of nude mice, corresponding with the results of the in vitro CTL assays. Transferring anti-Pu immune serum also decreased HV titres in nude mice, which seemed to reflect complement-dependent NT activity. Moreover ICR mice previously immunized with PH or Pu virus showed resistance to challenge with a lethal dose of the HV KHF strain, indicating that cross-reactive immunity induced by PH or Pu virus could protect ICR mice against pathogenic HV infection.
J Gen Virol 1989 Apr
PMID:Cross-reactive immunity among different serotypes of virus causing haemorrhagic fever with renal syndrome. 256 43

Organs of naturally infected mink were examined for the presence of Aleutian disease virus (ADV) DNA by in situ hybridization. Spleen, lymph nodes, thymus, bone marrow, kidney, liver, lung and small intestine were found to be positive for ADV to differing extents. Infected lymphoid organs showed a focal distribution of positive cells. Southern blot analysis of DNA extracted from infected organs revealed replicative forms of viral DNA in spleen and bone marrow samples only. These findings are consistent with a lymphotropism of ADV in vivo. Compared to the situation after experimental infection of mink these results indicate additional sites of virus replication and/or persistence of the naturally occurring disease.
J Gen Virol 1988 Mar
PMID:Detection of Aleutian disease virus DNA in tissues of naturally infected mink. 283 33

Spleen cells from BALB/c (H-2d) mice vaccinated with vgB11, a recombinant vaccinia virus which expresses glycoprotein B (gB) of herpes simplex virus type 1 (HSV-1), lysed EMT6 (H-2d) target cells infected with vgB11 or with HSV-1 but did not lyse uninfected EMT6 cells or infected L-929 (H-2k) target cells. Unlabelled target cell competition of lysis showed that only syngeneic cells infected with vgB11 or HSV-1 inhibited lysis of radiolabelled HSV-1-infected targets. These results demonstrate that vgB11 induces H-2-restricted anti-HSV-1 cytotoxic T lymphocytes and that gB is the target antigen.
J Gen Virol 1988 Jul
PMID:A recombinant vaccinia virus expressing herpes simplex virus type 1 glycoprotein B induces cytotoxic T lymphocytes in mice. 283 6

Malignant rabbit fibroma virus (MV) is a lymphocytotropic leporipoxvirus which produces profound immunological dysfunction and lethal fibromyxosarcoma. We examined virus recovery from splenic lymphocytes as a function of time after inoculation in vivo, and correlated this with both immunological function and expression of virus-induced host suppressor activity. MV was most abundant in lymphocytes obtained 4 days following inoculation. At that time, immune function was relatively normal and host suppressor activity was not observed. By 7 days after infection, when active host immunosuppressor functions were observed, virus recovery was decreased. Eleven days post-inoculation host immune function began to recover despite increasing virus-induced tumours and developing opportunistic infection. Simultaneously, MV was no longer recoverable from spleen cells. Spleen cells from day 11 tumour-bearing rabbits did not support MV replication as efficiently as did normal or day 4 or 7 splenic lymphocytes, but they did not alter the ability of MV to grow in the latter cells. By fluorescence examination and cytofluorography, splenic lymphocytes bearing MV antigens were abundant 7 days after infection but disappeared by 11 days. This was temporally related to production of neutralizing antibody to MV, and development of virus-specific lymphocyte proliferative activity. The composition of splenic lymphocytes changed as well: the normal ratio of about 1:1 for B and T cells changed to 1:2 by day 7, and then inverted to almost 2:1 by day 11. Rabbits infected with MV thus appear to recover their immune function, concurrently eliminate virus-infected lymphocytes, and elaborate high titres of neutralizing serum antibodies despite progressive infections and tumour development.
J Gen Virol 1987 Feb
PMID:Virus-lymphocyte interactions during the course of immunosuppressive virus infection. 302 85

Mouse cytomegalovirus (MCMV) grew to higher titres in spleen, liver, kidney and salivary gland of mice, and caused more sickness and death in susceptible (CD1) mice following treatment with anti-interferon globulin (AIG). In the resistant (C3H) strain of mice, organ titres were higher following AIG treatment but there was no sickness or mortality. Spleen necrosis was more severe in AIG-treated mice, indicating that this necrosis was not caused by interferon-mediated activation of natural killer (NK) cells. CD1 mice developed a high level of NK activity during MCMV infection and this was greatly reduced by AIG treatment. AIG was equally effective in increasing virus titres in NK-deficient beige (bg/bg) C57 B1.6 mice which showed a low level of NK activity even after MCMV infection, suggesting that interferon protects against MCMV by its direct antiviral effect on cells rather than by activating NK cells.
J Gen Virol 1983 Feb
PMID:Interferon as a defence mechanism in mouse cytomegalovirus infection. 618 94

Interferon (IFN) production by spleen cells from normal mice, mice acutely infected with Semliki Forest virus (SFV) or mice immune to SFV was measured after stimulation in vitro with either infectious or inactivated SFV. All three classes of spleen cells made IFN-alpha beta in response to infectious SFV. Spleen cells taken from mice late, but not early, after infection, or from immune mice, made IFN-gamma in response to inactivated SFV. Amounts of INF-gamma and IFN-alpha beta were similar. Normal spleen cells made no IFN (of any type) in response to inactivated SFV. The cell type producing IFN-alpha beta appeared to be the macrophage, whilst both T-lymphocytes and macrophages were necessary for IFN-gamma production. During the acute infection, the ability of spleen cells to lyse both virus-infected and uninfected target cells arose earlier than the ability to produce IFN-gamma. However, cytotoxicity towards uninfected cells fell to near background levels by day 7, whilst cytotoxicity towards infected targets remained high at that time, when IFN-gamma production was at its peak. IFN-gamma production is therefore temporally associated with cytotoxicity specifically directed against virus-infected targets, and the ability to produce IFN-gamma is a late response to SFV infection.
J Gen Virol 1984 May
PMID:Gamma interferon production and cytotoxicity of spleen cells from mice infected with Semliki Forest virus. 632 89

Interactions involving the immune responses to equine herpesvirus types 1 and 4 (EHV-1 and EHV-4) were studied in a murine infection model. When mice were inoculated intranasally with EHV-1, virus replication occurred in the respiratory tract and clinical signs were produced. In contrast, mice that were similarly inoculated with EHV-4 produced no evidence of virus replication and showed no clinical signs. When mice that had been inoculated with live EHV-4 were challenged 1 month later with EHV-1 they were partially protected. Although clinical signs were apparent on reinfection, virus replication in the respiratory tract was reduced in these mice compared with control mice that had not been previously immunized. Mice primed with heat-inactivated EHV-4, however, were not so protected. Live EHV-4-primed mice developed very low levels of antibody to EHV-1 and the humoral response could not account for this protection. However, the infected mice did give a strong delayed-type hypersensitivity reaction in a skin test using either EHV-1 or EHV-4 antigen. Spleen cells from EHV-4-primed donors provided a source of immune cells, including T cells which were used for transfer to recipient mice which were then challenged with EHV-1. The cells were protective; there was a reduction of virus replication on challenge with EHV-1 which correlated with the number of cells transferred. Modulation of the protective effect of primed cell populations was tested after depletion in vivo by means of complement-mediated lysis. The depletion of CD4-bearing cells produced the least effect on the protection afforded by cell transfer. In contrast, depletion of CD8-bearing cells markedly reduced the protection in recipients. EHV-1 and EHV-4 are widespread in horses and cross-infections are common. These results gained from a murine model indicate that important interactions occur at the level of T cell immunity between the two virus types which warrant further investigation in the natural host.
J Gen Virol 1993 Nov
PMID:Interactions between equine herpesvirus type 1 and equine herpesvirus type 4: T cell responses in a murine infection model. 824 51


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