Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Individuals infected with the human immunodeficiency virus (HIV) have been reported to develop a number of malignant neoplasms. We recently treated an HIV patient who had acute monocytic leukaemia which was first evident in the skin. To our knowledge, this is the first report of a case of acute monocytic leukaemia occurring in a HIV-infected person.
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PMID:Acute monocytic leukaemia in a HIV-seropositive man. 145 3

NF kappa B is a potent mediator of specific gene expression in human monocytes and has been shown to play a role in transcription of the HIV-1 genome in promonocytic leukemias. There is little information available on the response of NF kappa B to cytokines in normal human monocytes. We have used a 32P-labeled oligonucleotide derived from human immunodeficiency virus (HIV-1) long terminal repeat, which contains a tandem repeat of the NF kappa B binding sequence, as a probe in a gel retardation assay to study this transcription factor. Using this assay, we have detected NF kappa B in extracts of nuclei from normal human monocytes. Treatment of normal monocytes with 12-0-tetradecanoyl phorbol-13-acetate (TPA) for 4-24 h caused the complete disappearance of NF kappa B from nuclear extracts of monocytes. A similar result was obtained with the mature monocytic leukemia cell line THP-1. The constitutive transcription factor SP1 was unaffected by addition of TPA. The disappearance of NF kappa B from the nucleus was concentration dependent between 10 and 50 ng/ml of phorbol ester. In THP-1 cells, TPA also induced a new, faster-migrating NF kappa B species not induced in monocytes. Protein kinase C inhibitor staurosporine, but not cyclic nucleotide-dependent protein kinase inhibitor HA-1004, also dramatically reduced constitutive levels of nuclear NF kappa B. Finally, TPA addition to monocytes infected with HIV-1 inhibited HIV-1 replication, as determined by reverse transcriptase assays, in a concentration-dependent manner. These results are in striking contrast to the increase in nuclear NF kappa B and HIV-1 replication induced by phorbol esters in promonocytic leukemia cells U937 and HL-60, and emphasize the importance of studying cytokine regulation of HIV-1 in normal monocytes.
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PMID:Phorbol ester reduces constitutive nuclear NF kappa B and inhibits HIV-1 production in mature human monocytic cells. 146 36

Zinc binding by integrase from Moloney murine leukaemia virus and a protein A fusion protein containing integrase from human immunodeficiency virus type 1 was demonstrated by a zinc blotting technique using 65ZnCl2. Autoradiography revealed a clear band that was absent from the appropriate controls. This band co-migrated with the major band in Coomassie-stained gels and in immunoblots. This binding activity was retained in the presence of competing divalent cations and was sensitive to oxidation. This is the first demonstration of zinc binding by intact retroviral integrase.
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PMID:Zinc binding by retroviral integrase. 147 53

Cavitating necrosis is rare in Pneumocystis carinii pneumonia. In this report, we describe an autopsy patient with adult T-cell leukemia associated with cavitating Pneumocystis carinii pneumonia. The patient, a 61-year-old woman, died of an acute crisis of adult T-cell leukemia associated with diffuse pulmonary infection of Pneumocystis carinii. Postmortem examination revealed necrotic foci in both lungs, one of which, in the left lower lobe, had a central cavitation. Microscopically, leukemic cell infiltration was abundant in the lung parenchyma but not in the necrotic lesions. Pneumocystis carinii organisms were distributed diffusely in the alveoli and also in the cavity wall. Intranuclear and intracytoplasmic inclusion bodies were scattered in the lung indicating cytomegalovirus infection. However, no bacterial or fungal infection was detected in the lungs, even in the necrotic lesions. Cavitating Pneumocystis carinii pneumonia occurs in other immunodeficiency diseases apart from AIDS. To our knowledge, this report is the first case of cavitating Pneumocystis carinii pneumonia in adult T-cell leukemia.
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PMID:Cavitating Pneumocystis pneumonia in an autopsied case of adult T-cell leukemia. 147 36

For the past several years immunologists have been fascinated by a series of experiments showing that transforming growth factor beta (TGF beta) suppresses T- and B-lymphocyte growth as well as IgM and IgG production by B cells. Moreover, while exerting chemotactic activity on monocytes and inducing expression of interleukin-1 and interleukin-6 by these cells, TGF beta interferes with bacterially induced tumor necrosis factor alpha production, oxygen radical formation and the adhesiveness of granulocytes to endothelial cells. These mechanisms may provide the basis for the effect of TGF beta to prevent the microvascular changes associated with brain edema formation in bacterial meningitis. Given the potential of lymphocytes as well as macrophages to produce TGF beta 1, this cytokine may exert negative feedback signals on the immune response, provided the cytokine is processed from its latent form to the bioactive homodimer. Potent effects of TGF beta have been observed in experimental animals including the inhibition of the generation of virus-specific cytotoxic T cells and antiviral antibodies as well as the diminution of cellular infiltrates with decreased major histocompatibility complex class-II expression and CD8+ T cells in the tissue of virally infected animals. TGF beta may also be of importance in tumor immunology. By the production of bioactive TGF beta as detected in glioblastoma and acute T-cell leukemia, tumor cells may induce an immunodeficiency state and escape immune surveillance. In inflammation, monitoring of TGF beta in the tissue will bring light on the immune regulation in acute and chronic inflammatory diseases.
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PMID:Modulation of the immune response by transforming growth factor beta. 148 57

Allogeneic fetal liver cell transplantation has been shown to be able to reconstitute lymphopoietic systems of mice when these systems are defective or destroyed. Lethally irradiated mice or mice with inherited severe combined immunodeficiency disease (SCID) were grafted with 14 days gestation allogeneic fetal liver cells, then subjected to a follow-up for the immune tolerance to the donor and the normal or subnormal immune reconstitution allowing prevention of diabetes in NOD mice or cure of leukemia in AKR mice and of immunodeficiency in SCID mice. Briefly, when normal CBA mice were lethally irradiated and then grafted with allogeneic fetal liver cells from Balb/c mice, a specific immune tolerance was induced to donor skin grafts. Unrelated skin grafts were rejected and a response to antigens was observed in these chimeras. However, despite the capacity to develop hyperacute rejection of skin allografts, following hyperimmunization, these chimeric mice did not produce anti-H2 cytotoxic antibodies. In SCID mice (CB17), the immune reconstitution occurred when mice were grafted with allogeneic (C57/B16) as well as with syngeneic fetal liver cells. Human cells were found in SCID mice following implantation of human fetal liver and thymus cells. When NOD mice were irradiated, then grafted with allogeneic fetal liver cells, a large part of donor cells were found in NOD recipients, correlating with a low incidence of diabetes. Leukemic AKR mice grafted with allogeneic fetal liver cells had virtually no leukemia relapse, suggesting a strong graft-versus-leukemia effect following such a transplant.
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PMID:Fetal liver cell transplantation in various murine models. 150 74

20 cats in a cat home were treated prophylactically and therapeutically with Baypamun HK. The animals were allocated into three groups as described. 7 freshly admitted clinically healthy cats were treated prophylactically on day 1, 2 and 9 with 1 ml Baypamun HK (group I). 7 cats, who already were allocated for one year in the home and were sick of the feline respiratory disease complex were treated as described for group I (group II). 6 further cats, who also showed symptoms of the feline respiratory disease complex and had stayed for one year in the home were treated with physiol.saline solution according to group I (group III). From all cats blood samples were taken at day 1, 3, 10 and 17. The blood samples were checked for antibodies against feline calicivirus (FCV), feline herpesvirus (FHV), panleukopenia virus (PLV), feline peritonitis virus (FIPV) and feline immunodeficiency virus (FIV). Also the occurrence of the feline leukemia virus (FeLV) was evaluated. The cellular immunity was evaluated by means of the lymphocyte transformations test (LTT), nitroblue-tetrazolium reduction test (NBT) and cytochrome C-reduction test (CRT). Mean value and standard deviation was calculated from the results. The significance was determined by the t-test. The animals were examined clinically daily for 20 days for the feline respiratory disease complex. When necessary, the animals were treated by homeopathic and antibiotic products. At the time of admission to the home all cats were or had been treated with an attenuated panleukopenia vaccine. The serologic parameters were not influenced in the cats of group I.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effectiveness of paramunization for the control of feline coryza]. 152 77

The pX region of the human T-cell leukemia/lymphotropic virus type I (HTLV-I) contains at least four open reading frames (orfI-orfIV). orf III and orf IV encode the regulatory HTLV-I proteins Rex and Tax, which together modulate viral expression, and the p21rex protein of unknown function. By using the reverse transcriptase and polymerase chain reaction techniques on the RNA of an HTLV-I-infected cell culture, we uncovered the existence of alternatively spliced mRNAs generated through the use of three splice acceptor sites. These mRNAs encoded protein isoforms derived from the HTLV-I orf I (p12I) and orf II (p13II and p30II). An additional acceptor splice site, used in the processing of the env and tax/rex mRNAs and a singly spliced mRNA for the p21rex protein, was also identified. All of these HTLV-I mRNAs were also detected in freshly isolated cells from HTLV-I-infected individuals. Thus HTLV-I, like the human immunodeficiency virus type 1, has developed fine posttranscriptional mechanisms to increase the complexity of its genome.
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PMID:Protein isoforms encoded by the pX region of human T-cell leukemia/lymphotropic virus type I. 152 97

The function of a putative NFAT-1 site in the human immunodeficiency virus type 1 enhancer has been analyzed. Activation by the T-cell antigen receptor is minimal in Jurkat cells and is mediated by the kappa B sites. The putative NFAT-1 region is not required for the response to anti-CD3 or to mitogens in T-cell, B-cell, or monocyte/macrophage leukemia lines, nor is it a cis-acting negative regulatory element.
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PMID:Activation of the human immunodeficiency virus type 1 enhancer is not dependent on NFAT-1. 153 84

High sequence variability in the envelope gene of human immunodeficiency virus has provoked interest in nonenvelope antigens as potential immunogens against retrovirus infection. However, the role of core protein antigens encoded by the gag gene in protective immunity against retroviruses is unclear. By using recombinant vaccinia viruses expressing the Friend murine leukemia helper virus (F-MuLV) gag gene, we could prime CD4+ T-helper cells and protectively immunize susceptible strains of mice against Friend retrovirus infection. Recovery from leukemic splenomegaly developed more slowly after immunization with vaccinia virus-F-MuLV gag than with vaccinia virus-F-MuLV env; however, genetic nonresponders to the envelope protein could be partially protected with Gag vaccines. Class switching of F-MuLV-neutralizing antibodies from immunoglobulin M to immunoglobulin G after challenge with Friend virus complex was facilitated in mice immunized with the Gag antigen. Sequential deletion of the gag gene revealed that the major protective epitope was located on the N-terminal hydrophobic protein p15.
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PMID:Protection against Friend retrovirus-induced leukemia by recombinant vaccinia viruses expressing the gag gene. 153 53


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