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)

We have developed a flow cytometric method for demonstrating cell fusion between human immunodeficiency virus type 1 (HIV-1)- or HIV-2-infected HUT-78 cells and uninfected CD4-bearing MOLT-4 cells. Syncytium formation due to an interaction between the gp120 glycoprotein expressed on HIV-infected HUT-78 cells and the CD4 receptor present on MOLT-4 cells, resulted in an immediate decrease in the number of MOLT-4 cells; after a 24 h incubation period almost all MOLT-4 cells had disappeared from the culture. To show that the target MOLT-4 cells and not the aggressor HUT-78 cells were destroyed, specific monoclonal antibodies (MAbs) that reacted with antigens expressed on either MOLT-4 or HUT-78 cells were used. The formation of giant cells and the concomitant disappearance of MOLT-4 cells was blocked by MAbs specific for OKT4A and Leu3a, and, to a much lower level, by the MAbs specific of OKT4 and gp120. MAbs specific for OKT3, Leu2a, HLA-DR, Leu18 and LeuM3 did not prevent the disappearance of MOLT-4 cells. Sera from two AIDS patients containing antibodies to the HIV envelope glycoproteins did not protect MOLT-4 cells against the destructive effect of the HIV-infected HUT-78 cells. The fusion index, the percentage fusion inhibition and the 50% fusion inhibitory concentration of the MAbs can be accurately determined with the flow cytometric assay. The method can be readily implemented to evaluate any therapeutic treatment by examining its capacity to block cell-to-cell fusion, and hence destruction of the target bystander cells. Five anti-HIV compounds which have been previously shown to interfere with HIV binding to cells (namely pentosan polysulphate, heparin, suramin, aurintricarboxylic acid and Evans Blue) were further evaluated by this new method. With the exception of heparin, all of these compounds were found to inhibit cell-to-cell fusion and the concomitant destruction of the target bystander cells. Azidothymidine failed to inhibit fusion or bystander T cell destruction.
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PMID:Syncytium formation and destruction of bystander CD4+ cells cocultured with T cells persistently infected with human immunodeficiency virus as demonstrated by flow cytometry. 278 68

The phenotype and functions of monocytes in patients with haemophilia A and age-matched controls were studied. Fourteen male haemophiliacs were classified in three categories according to the mean number of units of factor VIII received during the last 5 years. Eleven patients were positive for antibodies to human immunodeficiency virus but none of our patients were homosexuals or drug abusers, nor do they fulfill the criteria of acquired immunodeficiency syndrome. Patients treated with high amounts of factor VIII concentrates (greater than 3 x 10(5) U/year) showed a significantly lower percentage of monocytes expressing HLA-DR, LFA-1 and CR3 antigens as compared with patients receiving lower amounts of factor VIII (less than 2 x 10(6) U/year) or controls. Kinetics of DR, LFA-1 and CR3 in cultured monocytes showed tht they were lost faster by monocytes from haemophiliacs treated with large amounts of factor VIII than by control monocytes. Adherence ability and chemotactic response of monocytes from patients treated with less than 3 x 10(5) U/year of factor VIII were also impaired. Although phagocytic indices were in normal ranges in haemophiliacs, a significant difference was observed between percentages of phagocytic monocytes from haemophiliacs treated with the largest doses of factor VIII and normal controls. Tests for respiratory burst activity, measured by chemiluminescence and superoxide anion generation, and Staphylococcus aureus killing were in normal ranges in haemophiliacs' monocytes.
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PMID:Phenotypic and functional abnormalities in monocytes from patients with haemophilia A treated with factor VIII concentrates. 282 91

The histopathological and immunopathological features of peripheral neuropathy were investigated in 21 patients with the acquired immunopathological syndrome (AIDS) or AIDS-related complex (ARC). Clinical syndromes observed in the 11 (52%) symptomatic patients included distal symmetrical polyneuropathy (DSPN) and chronic inflammatory demyelinative polyneuropathy (CIDP). Specimens from 19 of 20 patients (95%), both symptomatic and asymptomatic, had histopathological evidence of moderate or severe demyelination (79%), axonal degeneration (36%), and mononuclear cell inflammation (37%). Nerves from patients with CIDP and DSPN showed similar degrees of demyelination and axonal degeneration, but inflammation was more intense in CIDP. Immunohistochemical staining identified the majority of inflammatory cells as T lymphocytes or macrophages, with a predominance of CD8+ cytotoxic/suppressor cells. Diffuse immunostaining for human leukocyte antigen (HLA)-DR was present on endothelial cells, mononuclear inflammatory cells, and Schwann cells, and variable patchy immunostaining for HLA-DR was present on nerve fibers. Control nerve specimens showed staining for HLA-DR limited to endothelial, and a few mononuclear cells. The patterns of immunostaining were similar for AIDS and ARC patients. Human immunodeficiency virus (HIV) was cultured from peripheral nerve in 3 patients, but HIV antigen was not detected by immunohistochemical staining of 8 specimens. The findings implicate HIV infection in nerve, with T cell- and macrophage-mediated tissue destruction as the pathogenetic mechanism of the AIDS/ARC neuropathy.
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PMID:Peripheral neuropathy in the acquired immunodeficiency syndrome. 283 6

Fifteen patients and their respective bone marrow donors were entered in this study 1 to 5 yr after allogeneic bone marrow transplantation. Peripheral blood E rosetting (T) cells were analyzed for their phenotypic characteristics as well as for their ability to regulate Ig synthesis in the in vitro PWM system. A close relationship was found between a high proportion of T8+/HNK-1+ cells and/or T8+/HLA-DR+ cells and a strong (greater than or equal to 50%) inhibition of the antibody response. It was noteworthy that even the patients without suppressor activity had high proportions of such cells when compared with normal marrow donors. Moreover, the suppression occurred irrespective of the presence or absence of chronic GVHD. Through negative selection experiments (with MAb and complement) and through immunofluorescence cell sorting, it was shown that the suppressor cells expressed the T8+, HNK-1+, HLA-DR- phenotype. They did not carry the Leu-11, NKH1A, or NKH2 determinants, which are expressed on mature functional NK cells. When examined by electron microscopy, they exhibited a morphology of resting agranular lymphocytes. The significant increase of these suppressor cells among the BMT patients was not correlated with clinical syndromes such as chronic GVHD or opportunistic viral infections, which argues against the notion of in vivo profound immunodeficiency coexisting with these cells.
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PMID:Persistence of T8+/HNK-1+ suppressor lymphocytes in the blood of long-term surviving patients after allogeneic bone marrow transplantation. 294 51

As part of a larger study to characterize immune alterations in blood donors seropositive for human immunodeficiency virus (HIV), we measured subsets of CD4 (T helper/inducer) and CD8 (T suppressor/cytotoxic) cells by 2-color cytofluorometry. Alterations observed in asymptomatic seropositive donors (ASP) included: 1) decreased mean levels of Leu 8+ CD4 cells, although the proportion of Leu 8+ cells within the CD4 population was unchanged; 2) a selective increase in Leu 8- CD8 and Leu 18- CD8 cell levels; and 3) increased levels of both CD8 subsets defined by Leu 7, Leu 17, or HLA-DR expression. Alterations observed in symptomatic seropositive donors (SSP) were: 1) a further decrease in Leu 8+ CD4 cell levels, with a decrease in the proportion of Leu 8+ CD4 cells; 2) decreased levels of both Leu 18- and Leu 18+ CD4 subsets; 3) selective increases in Leu 8- and Leu 18- CD8 cell levels; and 4) increases in Leu 7+ CD8, Leu 17+ CD8, and HLA-DR+ CD8 subsets but not the reciprocal negative CD8 subsets. Thus, changes merely reflective of HIV infection included decreased levels of Leu 8+ CD4 cells and increased levels of Leu 8- CD8, Leu 18- CD8, Leu 7+ CD8, Leu 17+ CD8, and HLA-DR+ CD8 cells. Development of symptoms were associated with a further, preferential loss of Leu 8+ CD4 cells, proportional losses of both CD4 subsets defined by Leu 18 expression, and a return to normal levels of Leu 7- CD8, Leu 17- CD8, and HLA-DR- CD8 cells.
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PMID:CD4 and CD8 subsets defined by dual-color cytofluorometry which distinguish symptomatic from asymptomatic blood donors seropositive for human immunodeficiency virus. 296 80

The degree of clinical severity in human immunodeficiency virus infected patients, ranging from asymptomatic seropositive subjects to acquired immune deficiency syndrome, as well as in individuals at risk was assessed in relation to: (1) T-cell subset balance and expression of markers of T-cell activation; (2) natural killer activity; and (3) interferon gamma production. A decrease in the CD4/CD8 (helper/suppressor) ratio and an increase in the percentage of CD8+ (suppressor/cytotoxic) cells coexpressing markers of activation (HLA-DR or CD25) were closely correlated with the clinical severity of the human immunodeficiency virus infection. Natural killer activity was significantly impaired in patients with acquired immune deficiency syndrome and acquired immune deficiency syndrome-related complex but normal in asymptomatic seropositive individuals and subjects at risk. Interferon gamma production, either in response to mitogens or the antigens from infectious agents commonly affecting human immunodeficiency virus-positive individuals, was decreased in patients with acquired immune deficiency syndrome or acquired immune deficiency syndrome-related complex, with lesser involvement in human immunodeficiency virus-seropositive subjects or individuals at risk. Four of the six persons in the last group seroconverted during the ten months subsequent to evaluation of their immune status. Since production of interferon gamma was diminished in these patients while other assays of immunity were normal, measurement of this lymphokine may be a useful determinant of infection with the human immunodeficiency virus.
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PMID:Diminished interferon gamma production may be the earliest indicator of infection with the human immunodeficiency virus. 297 56

The relationship between hemophiliac immunodeficiency and exposures to factor VIII concentrate, LAV/HTLV-III retrovirus, and infection with Epstein-Barr virus and cytomegalovirus was examined. Exposure to factor VIII concentrate was significantly correlated with decreased percentages of T helper/inducer cells, decreased T helper/suppressor cell ratios, and decreased proliferative responses to plant mitogens. LAV/HTLV-III seropositivity was the primary predictor of increased percentages of HLA-DR-bearing mononuclear cells and decreased proliferative responses to pokeweed mitogen. Epstein-Barr virus and cytomegalovirus infections acted in a synergistic manner with LAV/HTLV-III to produce immunoregulatory defects. Increased percentages of T suppressor cells and decreased delayed cutaneous hypersensitivity skin test responses were observed in LAV/HTLV-III seropositive hemophiliacs infected with Epstein-Barr or cytomegalovirus. We conclude that hemophiliacs receiving commercial factor VIII concentrate experience several stepwise incremental insults to the immune system: alloantigens in factor VIII concentrate, LAV/HTLV-III infections, and herpesvirus infections.
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PMID:Hemophiliac immunodeficiency: influence of exposure to factor VIII concentrate, LAV/HTLV-III, and herpesviruses. 300 15

The CD4 (T4) antigen was originally described as a phenotypic marker specific for helper T cells, and has recently been shown to be the receptor for the human immunodeficiency virus (HIV). Functional studies using monoclonal antibodies directed at CD4 and major histocompatibility complex (MHC) class II molecules led to the suggestion that CD4 binds to the MHC class II molecules expressed on stimulator cells, enhancing T-cell responsiveness by increasing the avidity of T cell-stimulator cell interaction and/or by transmitting a positive intracellular signal. But recent evidence that antibodies to CD4 inhibit T-cell responsiveness in the absence of any putative ligand for CD4 has been interpreted as suggesting that antibody-mediated inhibition may involve the transmission of a negative signal via the CD4 molecule instead. We have infected a murine T-cell hybridoma that produces interleukin 2 (IL-2) in response to human class II HLA-DR antigens with a retroviral vector containing CD4 cDNA. The resulting CD4-expressing hybridoma cell lines produce 6- to 20-fold more IL-2 in response to HLA-DR antigens than control cell lines. Furthermore, when antigen levels are suboptimal, the response of the cell lines is entirely CD4-dependent. The data presented here clearly demonstrate that CD4 can enhance T-cell responsiveness and may be crucial in the response to suboptimal levels of antigen.
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PMID:Expression and function of CD4 in a murine T-cell hybridoma. 303 88

Oral hairy leukoplakia (HL) is a recently described manifestation of human immunodeficiency virus (HIV) infection in which Epstein-Barr virus (EBV) has been shown to replicate. To seek evidence for a local defect in mucosal immunity, we assessed the presence of epithelial Langerhans cells (LC) in these lesions and in autologous nonlesional mucosa. We used monoclonal antibodies against HLA-DR, HLA-DQ, and T6 antigens to identify LC in biopsy specimens of HL from 23 homosexual men. In all lesion specimens, LC either were not detected or were present only in greatly reduced numbers with at least 1 of the antibodies. In nonlesional oral mucosa from the same patients, LC were detected with all 3 antibodies in 11/12 specimens (92%) and were found in approximately normal numbers with at least 1 antibody. There was close correlation between the absence of LC and positive staining for EBV, human papillomavirus antigens, and candidal hyphae in the epithelium. We conclude that LC are absent or greatly reduced in the lesions of HL. Absence of normal LC function may be important in the pathogenesis of HL and may reflect an event in the pathogenesis of other features of the acquired immune deficiency syndrome.
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PMID:Absence of Langerhans cells in oral hairy leukoplakia, an AIDS-associated lesion. 311 Mar

Various aspects of monocyte-associated function were evaluated in the peripheral blood mononuclear cells of male homosexuals who were infected with the human immunodeficiency disease virus (HIV). The functional assessments included indomethacin-sensitive regulation of blastogenesis and lymphokine-activated killer (LAK)-cell induction, chemiluminescent responses of mononuclear leukocytes to opsonized zymosan, and the expression of HLA-DR antigen on CD-14-positive monocytes. The results obtained demonstrate that each of these functions is abnormal in asymptomatic individuals who have HIV core antigen (p24) in their circulation. These results suggest that monocyte abnormalities which could contribute to immune dysfunction in HIV-infected patients can be detected early during the course of HIV infection and are associated with the expression of serum HIV antigen.
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PMID:Monocyte functional studies in asymptomatic, human immunodeficiency disease virus (HIV)-infected individuals. 314 85


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