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)

Here we report the serological and immunochemical characterization of neutrophil-bound Ig (NBIg) and neutrophil-binding Ig in the serum of 15 individuals infected by the human immunodeficiency virus (HIV). We found no correlation between the presence or amount of NBIg or neutrophil-binding Ig in serum and either the serum concentration of IgG or the level of immune complexes (IC), as determined by the C1q-binding test. Twelve of the 15 eluates prepared from the neutrophils of the HIV-infected individuals reacted with donor neutrophils. These results indicate that NBIg in these men was not adhered IC nor passively absorbed Ig. This was supported by analysis of the sera of 13 of the 15 men by sucrose density-gradient centrifugation: neutrophil-binding Ig consisted predominantly of monomeric IgG. However, also low levels of IC capable of binding to neutrophils were detected in nine sera. Immunofluorescence studies revealed that neutrophil-binding Ig in the sera reacted with neutrophil-specific, non-polymorphic antigens that are not attached to the cell membrane via phosphatidyl-inositol linkage and, more specifically, not located on neutrophil FcRIII. None of the sera and eluates showed reactivity in the immunoprecipitation technique. Moreover, none of the eluates reacted with blotted neutrophil glycoproteins, whereas three sera reacted reproducibly and five sera reacted occasionally with a number of glycoproteins of different molecular weights in this technique. The latter results probably represent reactivity against cryptic and/or cytoplasmic antigens. Thus, NBIg in HIV infection has an autoantibody nature, but the full identity of the target antigens could not be clarified. These characteristics are not essentially different from those of the autoantibodies in classical autoimmune granulocytopenia.
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PMID:Neutrophil-bound immunoglobulin in HIV infection is of autoantibody nature. 201 67

The modulation of soluble CD16 titers in human immunodeficiency virus (HIV)-infected patients' serum, with an initial increase in Centers for Disease Control (CDC) clinical stage II and III patients followed by a dramatic drop in patients with AIDS (CDC clinical stage IV), is reported. These changes are statistically correlated with the CDC staging system, the number of CD4+ cells, the amount of p24 antigen in serum, and the anti-p24 antibody titers, indicating the potential value of soluble CD16 titer as an easily available serum marker of disease progression. To evaluate a possible link between this observation and the expression of membrane-associated CD16/FcRIII, flow cytometry immunofluorescence analysis was performed on peripheral blood lymphocytes from patients in three CDC stages; no specific changes in the number of natural killer cells expressing CD16+ antigens or in the total number of Leu19+ cells were found. However, there was a statistical correlation between the absolute number of T cells expressing CD16 antigens (CD3+/CD16+) and the modulated titers of soluble CD16 in HIV-infected serum.
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PMID:Changes of soluble CD16 levels in serum of HIV-infected patients: correlation with clinical and biologic prognostic factors. 213 3

Antibodies that enhance human immunodeficiency virus (HIV) infectivity have been found in the blood of infected individuals and in infected or immunized animals. These findings raise serious concern for the development of a safe vaccine against acquired immunodeficiency syndrome. To address the in vivo relevance and mechanism of this phenomenon, antibody-dependent enhancement of HIV infectivity in peripheral blood macrophages, lymphocytes, and human fibroblastoid cells was studied. Neither Leu3a, a monoclonal antibody directed against the CD4 receptor, nor soluble recombinant CD4 even at high concentrations prevented this enhancement. The addition of monoclonal antibody to the Fc receptor III (anti-FcRIII), but not of antibodies that react with FcRI or FcRII, inhibited HIV type 1 and HIV type 2 enhancement in peripheral blood macrophages. Although enhancement of HIV infection in CD4+ lymphocytes could not be blocked by anti-FcRIII, it was inhibited by the addition of human immunoglobulin G aggregates. The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein.
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PMID:The Fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells. 278 47

Fc-receptor (FcR)-mediated phagocytosis and FcR (FcRI, FcRII and FcRIII) membrane expression was studied on freshly separated and cultured monocytes (Mo) from 20 AIDS patients and 20 healthy controls. Both Mo and Mo-derived macrophages from AIDS patients presented a significant defect in their capacity to ingest IgG-coated erythrocytes (EA) compared to control cells. This functional defect did not depend on a decline in the number of FcR+ cells or on a decrease in the expression of FcR on their surface. In fact, the percentages of phagocytes reacting with anti-FcRI MoAb (32.2) or anti-FcRII MoAb (IV.3) were similar for controls and AIDS patients, while the percentage of FcRIII-positive Mo (MoAb 3G8) was higher in the AIDS population than in controls, though this difference was not seen on cultured Mo. The level of FcRI expression, evaluated as mean fluorescence intensity (MFI), was higher on freshly separated Mo from AIDS patients than from controls but this difference disappeared also with differentiation of Mo to Mo-derived macrophages in vitro. Parallel analysis of FcRII and FcRIII on phagocytes revealed no differences in the MFI between the AIDS and control groups. Some observations suggested that this functional defect might be secondary to phagocyte priming by circulating IFN-gamma: (1) in vitro stimulation of Mo with hrIFN-gamma, which increased FcRI expression, actually reduced phagocytosis of IgG-coated particles; and (2) IFN-gamma concentrations were increased in AIDS patients' plasma. In spite of these findings, no significant correlation was found between plasma IFN-gamma concentrations and FcR-mediated ingestion in AIDS patients, making the hypothesis uncertain. Even if the basis for the impaired FcR-mediated phagocytosis in AIDS patients remains unclear, this functional defect may have a role in the immunopathogenesis of AIDS, constituting a component cause of the immunodeficiency.
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PMID:Fc receptors expression and function in mononuclear phagocytes from AIDS patients: modulation by IFN-gamma. 829 Aug 92