Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Astrocytes have been regarded as the matrix of the central nervous system and as nutritional, metabolic support to neurons. Recently, immunological roles of astrocytes have been reported, especially in multiple sclerosis and experimental allergic encephalitis. One observation shows that human glioma cells, which lack CD4 molecules, can be infected with human immunodeficiency virus in vitro. Another report described that human macrophages can be infected with human immunodeficiency virus through Fc gamma receptors expressed on their cell surfaces. These results prompted us to examine the functioning molecules, especially Fc gamma receptor for immunoglobulin G, expressed on the astroglial cell line. From erythrocyte-antibody rosette assays, redirected cytolysis and flow cytometric analysis, we have shown that human astrocytoma cell lines possess Fc gamma receptors on their cell surfaces. Furthermore, primary cultured murine astrocytes express Fc gamma II receptors, reacting with 2.4G2 monoclonal antibody. Surprisingly, murine astrocytes prepared from newborn BALB/c mice demonstrate killing activity against allogeneic T cell leukemia by antibody-dependent cellular cytotoxicity. After treatment with the macrophage activating factor, interferon-gamma, expression of Fc gamma receptors and killer activity of astrocytes were augmented. From these results, it is suspected that the astroglial cell lines play an important immunological role in the brain.
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PMID:Expression of Fc gamma receptors on astroglial cell lines and their role in the central nervous system. 138 16

Monocyte/macrophage infection by human immunodeficiency virus type 1 (HIV1) was studied for its effects on the production of tumour necrosis factor alpha (TNF alpha) and the expression of the manganese superoxide dismutase (MnSOD) gene. For this purpose, human peripheral blood monocytes were obtained from healthy HIV1-seronegative donors by centrifugal elutriation and infected with either the HIV1/LAV1 strain or with the primary HIV1/DAS isolate. The results showed that (1) HIV1/LAV1-infected macrophages did not produce any biologically detectable TNF alpha during the few hours following lentiviral infection, despite rises in the TNF alpha mRNA level; (2) MnSOD gene transcription in the macrophages increased, as measured 2 and 4 h after infection; (3) the level of the MnSOD gene expression declined during the late phases of lentiviral infection, but TNF alpha synthesis and gene expression rose; and (4) bispecific antibody comprised of anti-Fc gamma RI (anti-CD64) and anti-gp41 monoclonal antibodies inhibited the in vitro infection of monocyte-derived macrophages by HIV1/DAS.
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PMID:Functional consequences of monocyte/macrophage infection by HIV1. 153 48

We studied human megakaryocytes to determine if they both expressed and synthesized Fc gamma and CD4 membrane receptors. The strategy employed relied on demonstration of receptor protein and mRNA in megakaryocytes present in freshly made marrow smears, or in megakaryocytes isolated from aspirated normal bone marrow by counterflow centrifugal elutriation. Protein was detected immunochemically, whereas mRNA was detected either by in situ hybridization, or by reverse transcription, polymerase chain reaction (RT-PCR). Using these methods CD4 and Fc gamma RII protein and mRNA were detected in most megakaryocytes. Fc gamma RI and Fc gamma RIII protein was not detected in these cells. Megakaryocytes were also cultured with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) to determine the effect of this growth factor on Fc gamma RII expression. As has been noted in cells of the monocyte-macrophage lineage, exposure to rhGM-CSF resulted in a significant increase in the level of megakaryocyte Fc gamma RII mRNA and protein. These observations are significant because they provide a physiologic basis for known viral trophism displayed by megakaryocytes. They are also of interest because they suggest that alternative portals exist for entry of human immunodeficiency virus (HIV-1) into megakaryocytes and that such infection may play a role in acquired immunodeficiency syndrome (AIDS)-related thrombocytopenia.
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PMID:Expression of Fc gamma RII and CD4 receptors by normal human megakaryocytes. 153 89

Human monocyte-derived macrophages that express the CD4 molecule and the Fc receptor for IgG (Fc gamma R) play a major role in the pathogenesis of human immunodeficiency virus (HIV) infection. To explore this possibility further, human monoclonal antibody to glycoprotein 41 (gp41) was produced, and a heterobifunctional antibody composed of F(ab') x F(ab')2 fragments of monoclonal anti-gp41 and anti-Fc gamma RI 22.2 were constructed. Both antibodies were analyzed for neutralizing effects, and the role of the CD4 molecule in HIV infection was studied with human monocyte-derived macrophages. The bispecific antibody exhibited strong neutralizing properties, in contrast to the monoclonal anti-gp41 antibody. Moreover, in the presence of monoclonal anti-Leu-3a antibody, viral production was completely inhibited. These findings demonstrate the necessity of the CD4 molecule in HIV infection of human macrophages and emphasize the usefulness of such heterobifunctional antibody directed to virus and monocyte-derived macrophage Fc receptors in prevention of HIV infection.
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PMID:Bispecific antibody targeting of human immunodeficiency virus type 1 (HIV-1) glycoprotein 41 to human macrophages through the Fc IgG receptor I mediates neutralizing effects in HIV-1 infection. 153 93

Natural killer (NK) cells are a discrete subset of leukocytes, distinct from T and B lymphocytes. NK cells mediate spontaneous non-MHC-restricted killing of a wide variety of target cells without prior sensitization and appear to be involved in initial protection against certain viral infections. Depressed NK cell-mediated cytotoxicity, one of the many immunological defects observed in AIDS patients, may contribute to secondary virus infections. Here we report that clonal and purified polyclonal populations of NK cells, which expressed neither surface CD4 nor CD4 mRNA, were susceptible to infection with various isolates of human immunodeficiency virus type 1 (HIV-1). Viral replication was demonstrated by detection of p24 antigen intracellularly and in culture supernatants, by the presence of HIV DNA within infected cells, and by the ability of supernatants derived from HIV-infected NK cells to infect peripheral blood mononuclear cells or CD4+ cell lines. Infection of NK cells was not blocked by anti-CD4 or anti-Fc gamma RIII monoclonal antibodies. NK cells from HIV-infected and uninfected cultures were similar in their ability to lyse three different target cells. Considerable numbers of cells died in HIV-infected NK cell cultures. These results suggest that loss of NK cells in AIDS patients is a direct effect of HIV infection but that reduced NK cell function involves another mechanism. The possibility that NK cells serve as a potential reservoir for HIV-1 must be considered.
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PMID:In vitro infection of natural killer cells with different human immunodeficiency virus type 1 isolates. 167 64

Plasmacytoma-bearing mice (PC-mice) develop a polyclonal B cell immunodeficiency syndrome characterized by marked impairment of: a) primary antibody responses and b) proliferative responses to B cell mitogens. The present investigations used two-color flow cytometry to examine B lymphocytes from the spleens and lymph nodes of PC-mice and found decreased surface membrane expression of surface IgM (sIgM), transferrin receptors (TfR) and IgE FcR (CD23), increased expression of class II MHC, but normal expression of B220, Mel-14, Fc gamma RII, and Fc mu R. These changes were not related to the H chain class or the amount of Ig produced by the plasmacytoma. When cultured with IL-4, B lymphocytes from PC-mice increased their expression of sIgM and class II MHC, but not of CD23. Several findings implicate transforming growth factor-beta 1 (TGF-beta 1) in the mechanism that modulates receptor expression on B lymphocytes in PC-mice: a) ascites fluid from PC-mice contains large quantities of TGF-beta 1; b) supernatants of cultured spleen cells from PC mice contain up to eightfold more TGF-beta than is found with normal spleen cells; c) cloned plasmacytoma cells produce TGF-beta in vitro; and d) the abnormal phenotype of B cells from PC-mice, i.e., decreased CD23, sIgM, and TfR, and increased class II MHC, is induced on normal B cells cultured in the presence of TGF-beta 1. Because sIgM, TfR, class II MHC, and CD23 are molecules that play fundamental roles in the activation of normal B cells, their modulation by TGF-beta 1: a) identifies molecular mechanisms that could account for some of the known immunosuppressive properties of TGF-beta 1 and b) implicates TGF-beta in the pathogenesis of the polyclonal B cell immunodeficiency that is characteristic of plasma cell tumors.
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PMID:Immune dysfunction in mice with plasmacytomas. I. Evidence that transforming growth factor-beta contributes to the altered expression of activation receptors on host B lymphocytes. 182 99

Human immunodeficiency virus (HIV) complexed with human anti-HIV IgG can attach to Fc gamma receptors (Fch) of mononuclear phagocytes. To determine whether the FcR-mediated infection that results also requires interaction between HIV gp120 and cell membrane CD4, monocytic cells of the U937 line were transiently treated with phorbol 12,13-dibutyrate (PDB) so that they temporarily presented a CD4-FcR+ phenotype at the time of HIV infection. HIV production was not abolished, but only significantly delayed after infection of these cells with free virus. Leu3a monoclonal antibody or soluble recombinant CD4 completely blocked this delayed infection. This indicates that enough CD4 still remained at the membrane to allow infection of a reduced cell number. Infection of PDB-treated cells with virus preincubated with high anti-HIV IgG concentrations was inhibited, contrasting with what was observed with control cells infected under the same conditions. Inhibition of infection was also observed when HIV became attached to untreated U937 cells through the binding of CD4-IgG hybrid molecules to FcR. Thus, the binding of IgG-coated virus to FcR is not sufficient in itself to elicit productive infection of monocytic cells, which still requires the interaction of viral gp120 and membrane CD4.
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PMID:Infection of monocytic cells by HIV1: combined role of FcR and CD4. 183 82

Evidence of antibody-dependent enhancement of human immunodeficiency virus type 1 (HIV-1) infection via Fc receptor (FcR) was published previously (A. Takeda, C. U. Tuazon, and F. A. Ennis, Science 242:580-583, 1988). To define the entry mechanism of HIV-1 complexed with anti-HIV-1 antibody, we attempted to determine the receptor molecules responsible for mediating enhancement of HIV-1 infection of monocytic cells. Monoclonal antibodies to FcRI for immunoglobulin G substantially blocked antibody-dependent enhancement of HIV-1 infection. Furthermore, we demonstrate a requirement for the CD4 molecule in antibody-enhanced HIV-1 infection via FcR. Soluble CD4 prevented infection by HIV-1 antibody-treated virus, and enhancement of infection of virus-antibody complexes was abrogated by a monoclonal antibody to CD4 (anti-Leu3a antibody). Treatment of human macrophages with an anti-CD4 antibody also inhibited antibody-enhanced HIV-1 infection of macrophages, supporting our contention that antibody-dependent enhancement of HIV-1 infection via FcR requires CD4 interaction with the virus glycoprotein.
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PMID:Two receptors are required for antibody-dependent enhancement of human immunodeficiency virus type 1 infection: CD4 and Fc gamma R. 197 24

Fc gamma RIII on neutrophils is a phosphatidyl inositol glycan (PIG)-anchored protein that can be released from the cells by activation with chemotactic peptides. We have examined the expression of Fc gamma RIII (CD16), CD11b, and Fc gamma RII (CD32) on neutrophils from human immunodeficiency virus (HIV)-I-infected individuals by two-color FACS. In patients with AIDS and AIDS-related complex and in HIV-I positive intravenous drug abusers we observed a substantial population (25%) of neutrophils that were autofluorescent, and did not stain with the anti-Fc gamma RIII mAb 3G8. This population was largely absent (3%) in HIV-I negative control individuals. No changes in the expression of Fc gamma RII, CD11b, or another PIG-anchored protein, decay accelerating factor (CD55) on neutrophils, were found. The presence of the Fc gamma RIII negative neutrophil population may be related to altered functions leading to common bacterial infections in advanced AIDS.
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PMID:Change in expression of Fc gamma RIII (CD16) on neutrophils from human immunodeficiency virus-infected individuals. 213 22

Although CD4 is a major receptor for human immunodeficiency virus (HIV) infection of cells, studied by ourselves and others clearly show that the Fc receptor (FcR) also plays a role in infection, perhaps in conjunction with other surface receptors. IgG antibodies to HIV-1 will enhance infectivity in cells (such as monocyte-macrophages) that have surface Fc receptors; F(ab')2 fragments of antibodies did not enhance, and blocking of FcR inhibited enhancement. The high-affinity FcR for IgG (Fc gamma RI) appeared to be functional. Sera from HIV-1-infected patients had neutralizing activity at high concentrations, but enhanced infection at low concentrations (i.e., high dilutions). Our studies show that the CD4 receptor is required for antibody-mediated enhancement of infection, as enhancement can be blocked by recombinant soluble CD4 and by Leu3 antibody. Although enhancement can be demonstrated in vitro, the in vivo importance of enhancing antibodies remains to be defined in HIV-1 infection.
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PMID:FcR-mediated enhancement of HIV-1 infection by antibody. 222 46


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