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)

Certain immunological parameters (i.e. low CD4+ T cell numbers, high serum soluble CD8) have been described as prognostic factors for the progression of human immunodeficiency virus (HIV) infection to later clinical stages. In the present study we have found in one hundred HIV-infected Spanish patients (81% drug abusers, 7% homosexuals, 6% heterosexuals, and 6% other or unknown risk groups) that CD11b+ peripheral blood mononuclear cells are increased in those with persistent lymphadenopathy as compared to other clinical stages (asymptomatic, AIDS-related complex and AIDS). Serum IgA was significantly increased in AIDS patients, and in patients at any other clinical stage who had concomitant infections (mainly mycobacterial and fungal). CD11b (an integrin with complement receptor functions) may thus be of clinical interest for the staging of HIV-infected patients, and reflect stage-selective immunological changes in mononuclear cell biology during HIV infection. High IgA on the other hand, would be a marker of concomitant infection as well as of disease progression. The results concern mostly drug addicts (the main risk group in Spain), but may apply to the other risk groups because no significant differences were detected between drug addicts (n = 81) and non-drug addicts (n = 19) for the studied variables (p greater than 0.05).
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PMID:CD11b-bearing mononuclear leucocytes and IgA levels in the staging of human immunodeficiency virus infection. 134 66

The ability of complement to inactivate human immunodeficiency virus (HIV) in the presence of specific antibody was evaluated. HIV was treated with complement and/or antibody, and then its titer was determined on the CD4+ H9 cell line. While complement alone had no effect on the HIV titer, complement plus subneutralizing levels of antibody resulted in titer reductions. Complement sources deficient in membrane attack component C5 or C8 did not inactivate antibody-treated HIV, suggesting that neutralization occurred via lysis. This possibility was investigated by assessing release of reverse transcriptase (RT) from the virion. Antibody plus complement, but neither reagent alone, released RT from HIV in a dose-dependent manner. Release of RT did not occur with C5- or C8-deficient sera, also indicating a requirement for membrane attack components. These studies show that complement can neutralize HIV via the classical complement pathway and that this neutralization occurs via C5b-9-mediated viral lysis. Thus, complement may play a major role in resistance to disease by lysing HIV and preventing infection of Fc- and complement receptor-positive cells, as well as CD4+ cells.
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PMID:Neutralization of human immunodeficiency virus type 1 by complement occurs by viral lysis. 170 Aug 28

A human Epstein-Barr virus-transformed B-cell line (IC.1) was characterized for cell surface antigen profile and permissivity to immunodeficiency virus (HIV) infection. According to cocultivation assay with MT2 cells, P24 release, and immunofluorescence assay, complement-sufficient serum enhanced in vitro infection of IC.1 cells. Enhancement occurs independently of the presence of HIV type 1-specific antibodies, although more efficiently when they are present. Blocking experiments with monoclonal antibodies demonstrated that complement receptor type 2 mediates this phenomenon and that the CD4 molecule is required for infection. Enhancement of in vitro infection on IC.1 cells appears closely related to previously described complement-mediated, antibody-dependent enhancement of HIV infection on the T-lymphoblastoid cell line MT2 (W. E. Robinson, Jr., D. C. Montefiori, and W. M. Mitchell, Lancet i:790-794, 1988).
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PMID:Antibody-dependent and antibody-independent complement-mediated enhancement of human immunodeficiency virus type 1 infection in a human, Epstein-Barr virus-transformed B-lymphocytic cell line. 184 8

Patients infected with the human immunodeficiency virus (HIV) may have an antibody deficiency and a deficiency of cellular immunity. Intravenous immunoglobulin (IVIG) preparations may benefit HIV-infected children and adults with recurrent bacterial infections at doses of 200 to 400 mg/kg every 2 to 4 weeks. In addition, IVIG (1 to 2 g/kg) is effective at raising platelet counts to hemostatic levels in HIV-infected patients with idiopathic thrombocytopenic purpura and life-threatening bleeding. Indirect evidence also suggests that IVIG may be effective in preventing Pneumocystis carinii pneumonia. Finally, recent studies suggest that specific anti-HIV antibody preparations may have a therapeutic role, either as immunoglobulin concentrates or as immunoadhesions and immunotoxins. However, further investigations are needed to exclude antibody enhancement of HIV infection by the Fc receptor or the complement receptor.
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PMID:Use of intravenous immunoglobulin in acquired immune deficiency syndrome. 187 43

Antibody-dependent enhancement (ADE) of human immunodeficiency virus type 1 (HIV-1) infection in vitro has been described recently and was shown to occur by two mechanisms: either participation of the alternative pathway of complement or to involve an Fc receptor-mediated, complement-independent mechanism. Complement-mediated ADE results in an accelerated cytopathic effect in target cells that can abrogate the protective properties of neutralizing antibodies. This study characterizes the surface antigens of MT-2 cells using flow cytometric analysis and shows that these cells express high levels of both CD4 and complement receptor type 2 (CR2) while several CD4+ cell lines that do not demonstrate complement-mediated ADE lack high levels of complement receptors. Further, utilizing MT-2 cell cultures, it is demonstrated that complement-mediated ADE of HIV-1 infection is conferred by the sera from more than 80% of HIV-1 antibody-positive individuals (N = 85). Complement-mediated ADE of HIV-1 infection causes an acceleration of several parameters indicative of HIV-1 infection in vitro including increased HIV-1 antigen synthesis as detected by indirect immunofluorescence, RNA accumulation as measured by a solution hybridization protocol, reverse transcriptase release, and progeny virus production.
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PMID:Complement-mediated, antibody-dependent enhancement of HIV-1 infection in vitro is characterized by increased protein and RNA syntheses and infectious virus release. 246 4

A sensitive enhancing system was developed for detecting low density cell surface antigen by flow cytometry. The system termed the 'super avidin-biotin system' (SABS) uses biotinylated antibody, phycoerythrin-streptavidin (StreptA-PE), biotinylated goat anti-streptavidin antibody, and StreptA-PE. CR1 complement receptor antigenic sites were quantified on erythrocytes from healthy individuals and patients with antibodies against human immunodeficiency virus (HIV) using SABS and a conventional radioimmunoassay (RIA) with monoclonal anti-CR1 antibody. As little as 50 sites/cell were detected using either SABS or RIA. Accurate quantification of CR1 antigenic sites was achieved within the range of 100-1300 sites/cell. Similar results were obtained using either of the two methods. Intra-assay and day-to-day reproducibilities using SABS were 2% and 12% respectively, comparable to those of conventional RIA measurements. In addition to enumeration of CR1 on erythrocytes for clinical purposes, the use of SABS may probably be extended to a wide number of situations where a sensitive detection of low density cell surface antigen is needed.
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PMID:Enumeration of CR1 complement receptors on erythrocytes using a new method for detecting low density cell surface antigens by flow cytometry. 295 33

Blood monocytes were analyzed in 28 patients with chronic lymphocytic leukemia without previous cytotoxic therapy and without recent infection. Using monoclonal antibodies and flow cytometry, monocytes identified by LeuM3 or My4 were low in percentage (2.3%), but absolute numbers were increased in many patients with values exceeding the normal range (120 to 510/microliter) in seven of 28 patients. Monocytosis was more prominent in patients with high leukemic counts, but there was no correlation to clinical stages. Monocytopenia was evident with less than 50 LeuM3+ cells/microliter in three patients. Two-color fluorescence was used for the analysis of cell surface expression of major histocompatibility complex (MHC) Class II molecules, complement receptors, and Fc receptors on the LeuM3+ monocytes. Compared to cells from control donors, there was an increase for MHC class II antigens, complement receptors, and Fc receptors on the monocytes in chronic lymphocytic leukemia, in terms of both the percentage of positive cells among the LeuM3+ monocytes and of fluorescence intensity. This increase was not restricted to patients with monocytosis nor were the molecules always upregulated concomitantly. The increase of antigen expression on LeuM3+ monocytes was more than 50% (1.5-fold) in seven of 22 patients for MHC Class II antigens, in seven of 16 patients for complement receptor and in six of 12 patients for Fc receptor. A similar decrease of antigen expression was observed only in one patient for MHC Class II and in one patient for complement receptor expression. Monocytosis and increased expression of monocyte cell surface antigens described for a large portion of patients might be causally involved in the immunodeficiency in chronic lymphocytic leukemia.
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PMID:Abnormal blood monocytes in chronic lymphocytic leukemia. 340 22

The lymphocytes from the patients with primary immunodeficiency diseases and those under immunosuppressive conditions such as viral infection or administration of antimetabolites were studied by various parameters of T- and B-lymphocytes. T-lymphocyte specific antigen, spontaneous rosette formation with sheep erythrocytes, phytohaemagglutinin response of the lymphocytes and delayed hypersensivity skin reaction were used to assess T-lymphocytes, while complement receptor, surface immunoglobulin, serum immunoglobulin levels and antibody response to antigens were estimated as parameters of B-lymphocytes. 9 of infantile agammaglobulinemia, 8 severe combined immunodeficiency, 5 ataxia telangiectasia, d Di-George syndrome, 11 common variable immunodeficiency, 3 isolated IgA deficiency and 4 cases thymectomized more than 10 years previously were studied and discussed for the results. The peripheral blood lymphocytes, especially T-lymphocytes were reduced in the acute stage of measles infection, while they were increased in infectious mononucleosis caused by EB (Epstein-Barr) virus. Atypical lymphocytes observed in the later disease seemed to originate from mainly T-lymphocytes. Cyclophosphamide had suppressive effect selectively on B-lymphocytes.
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PMID:T- and B-lymphocytes in immunological disorders. 437 62

Microglia, the resident tissue macrophages of the central nervous system, have a highly differentiated morphology and do not express many of the antigens typically associated with other tissue macrophages. Activation of microglia is associated with a change in morphology and an increase in their repertoire of antigen expression. Microglia become activated in many neuropathological conditions including chronic neurodegenerative diseases and human immunodeficiency virus neuropathology, yet little is known of the mechanisms involved. Here we demonstrate for the first time that microglia can be activated and induced to divide and/or undergo apoptosis via a beta 2-integrin (complement receptor type 3, CR3, Mac-1 or CD11b/CD18) using an anti-CR3 monoclonal antibody (McAb5C6). This antibody, which has been shown to block myelomonocytic recruitment during central nervous system inflammation, is unique in that it can cross the intact blood-brain barrier to activate microglia. Since CR3 not only binds the iC3b component of the alternative complement cascade but also denatured proteins this suggests a potential route for microglia activation in neuropathological conditions.
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PMID:Mitosis and apoptosis of microglia in vivo induced by an anti-CR3 antibody which crosses the blood-brain barrier. 825 20

Patients with human immunodeficiency virus-type 1-immune thrombocytopenic purpura (HIV-1-ITP) have elevated polyethylene glycol (PEG)-precipitable immune complexes (ICs) composed of IgG, IgM, and complement that are threefold to sevenfold higher than in healthy control subjects. These complexes contain anti-F (ab')2 as well as anti-idiotype antibodies versus anti-HIV-1gp120. Because anti-F (ab')2 and anti-idiotype antibodies correlate with thrombocytopenia (r = .83 [J Clin Invest 77:1756, 1986] and r = .90 [J Clin Invest 89:356, 1992], respectively) we studied the binding of ICs to platelets and monocytes as well as their role in platelet-monocyte rosette formation. ICs bind to platelets in a saturation-dependent manner (optimum at 10 micrograms/mL; 0.5% of serum conc). Binding to platelets could not be inhibited with platelet saturating concentrations of aggregated IgG or with monoclonal antibody (MoAb) IV.3 versus FcR gamma II. Platelet binding could be inhibited with Fab anti-C3, anti-Clq, or anti-C4 by 57%, 40%, and 46% respectively, not with control Fab (P < .001). Monocytes from HIV-1-ITP patients form rosettes with normal platelets 16.8 +/- 5.2 rosettes/100 monocytes compared with 4.8 +/- 0.8 control monocytes plus normal platelets (P = .009). Gel-washed HIV-1-ITP platelets formed 19 +/- 2.0 rosettes with U937 cells compared to 6.3 +/- 1.0 for normal platelets (P = 0.001). Arming of U937 cells with HIV-1-ITP ICs (5 micrograms/mL) formed 36.7 +/- 2.5 rosettes compared with 10.6 +/- 1.2 for control ICs (P < .01). Rosetting of armed U937 cells could be inhibited with MoAbs versus the alpha chains of CD11a (LFA-1), 11b (Mac-1), or 11c (p150,95) by 67%, 70%, and 61%, respectively (P < .007), whereas binding of ICs to U937 cells was unaffected. Isotype-matched control as well as MoAbs versus antigens on U937 cells (CD13, CD33) or the anti-FcR gamma II receptor had no effect. However, Fab fragments of polyclonal anti-C3 inhibited rosette formation by 78% (P < .01); control Fab had no effect. Thus, platelet-monocyte rosette formation is not Fc dependent. It is complement receptor dependent and requires the cooperation of all three leuCAM integrins.
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PMID:Role of leuCAM integrins and complement in platelet-monocyte rosette formation induced by immune complexes of human immunodeficiency virus-type 1-immune thrombocytopenic purpura patients. 848 17


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