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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe functional simplified T cell and Fc receptor chimeras that are capable of directing CD8+ cytotoxic T lymphocytes (CTLs) to specifically recognize and lyse cells expressing HIV envelope proteins. Target cells bearing HLA-DR molecules are not recognized by CTL armed with the chimeras. The variety of cell types in which the native receptors are active suggests multiple possibilities for antiviral intervention through genetic means.
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PMID:Cellular immunity to HIV activated by CD4 fused to T cell or Fc receptor polypeptides. 190 Apr 56

Cells from the human monocytic cell-line THP1 were incubated prior to activation with IFN-gamma or LPS with varying amounts of p24, the main product of the HIV gag gene and the major component of the virus core. The IFN-gamma-dependent increase of mRNA for HLA-DR and for the heavy chain of cytochrome b was markedly decreased by p24 but not by gp120. This effect was abrogated by anti-p24 antibodies. On the other hand, preincubation of THP1 cells with p24 did not affect the accumulation of the LPS-dependent mRNA for TNF alpha and IL1-beta. These results indicate that p24 at concentrations similar to those found in the serum of HIV-infected individuals specifically affects IFN-gamma-induced activation markers.
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PMID:The HIV core protein p24 inhibits interferon-gamma-induced increase of HLA-DR and cytochrome b heavy chain mRNA levels in the human monocyte-like cell line THP1. 190 83

Cryostat sections of human normal term placentae were studied for evidence of immunopathology by using antibodies to lymphocytes, macrophages, platelets, and coagulation factors. Areas of so-called chronic villitis of unestablished etiology were identified in all placentae. The same tissues were examined for HIV protein antigens gp120, p17, p24, and gp41. No evidence for gp41 was found. Antigens gp120 and p17 were identified in normal chorionic villi in vimentin-positive fibroblast-like cells and in endothelium, respectively. Antigen p24 was localized to HLA-DR positive cells that morphologically resembled macrophages in areas of villitis. The distribution of gp120 and p17 was similar to that observed for tissue factor. These findings prompted speculation that retroviral proto-oncogenes that are known to encode for certain placental receptors could be involved in the presentation of tissue factor, and that gp120 may be a hitherto unrecognized immunobiological mechanism for the blockade of CD4 on maternal lymphocytes if and when such cells gain entrance to chorionic villi.
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PMID:HIV proteins in normal human placentae. 193 Jun 45

The human immunodeficiency virus (HIV-1) preferentially infects cells that express the CD4 molecule, including monocytes and cells of the monocyte lineage. The monocyte-like cell line U937 and monocytes isolated from peripheral blood lymphocytes (PBL) were infected with HIV-1. Cell surface antigen expression was determined in infected and noninfected cells as was the ability to stimulate in mixed lymphocyte reaction. The CD4 antigen decreased in infected cells U937 and PBL monocytes. MHC class II antigens HLA-DR, HLA-DQ, and HLA-DP increased in HIV-1 infected U937 cells. In infected PBL-derived monocytes, HLA-DR increased, HLA-DQ decreased, and HLA-DP was unchanged. Infected U937 and PBL monocytes were capable of stimulating allogeneic lymphocytes, thus demonstrating retention of the alloantigen presentation function of HIV-1-infected monocytes.
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PMID:Cell surface antigens and function of monocytes and a monocyte-like cell line before and after infection with HIV. 196 31

Relationships among four serologic activation markers and T cell subsets were measured in HIV-seropositive former blood donors (N = 64) and seronegative controls (N = 61). Significant correlations were observed for the HIV group in pairwise comparisons of soluble IL-2 receptor (sIL-2R), beta 2-microglobulin (beta 2M), neopterin (NEOP), and soluble CD8 (sCD8). CD4 cell levels (number/microliter) in the HIV group showed significant negative correlation with all four serologic markers; CD8 cell levels, in contrast, showed no significant correlation with any serologic activation marker measured. Significant correlations were observed, however, among various cell surface activation markers and serologic activation markers. Specifically, the proportion of CD8 cells expressing CD45RA showed significant negative correlations with NEOP and B2M levels, whereas the proportion of CD8 cells expressing HLA-DR showed significant positive correlations with B2M and sIL-2R levels. Further, the proportion of CD8 cells expressing CD38 showed significant positive correlations with all four serologic activation markers. These findings indicate that sIL-2R, B2M, NEOP, and sCD8 show similar quantitative changes and correlational relationships to CD4 cell destruction in HIV infection; they differ, however, in their relationships to proportional changes in activated CD8 cell subsets.
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PMID:Interrelationships between serologic markers of immune activation and T lymphocyte subsets in HIV infection. 196 60

We have developed CD4+, tetanus antigen-specific T cell clones that proliferate in the presence of tetanus antigen and autologous irradiated peripheral blood leucocytes (PBL) as antigen-presenting cells (APC). There have been several reports that T cells can present antigen themselves. We have used tetanus antigen-specific T cell clones to examine the effects of envelope glycoproteins of HIV-1 on processing and presentation of antigen to T cells. Cloned T cells were pre-incubated with soluble crude preparation of tetanus antigen for 4 h at 37 degrees C, irradiated, and used as APC (T-APC). These cells could present antigen, as assessed by the ability of the autologous cloned T cells to proliferate. Resting T cells and phytohaemagglutinin-activated T cell blasts from autologous PBL could not present tetanus antigen to the responder cloned T cells. Antigen presentation by T-APC was abrogated by treating cells with anti-HLA-DR but not by anti-HLA-DQ monoclonal antibodies; treatment of tetanus antigen-pulsed T-APC with anti-tetanus antibody also blocked the ability of these cells to induce proliferation in responder T cells. Antigen presentation by cloned T cells was by a chloroquine-resistant pathway. Pretreatment of T-APC with envelope glycoprotein of HIV-1, gp120, did not affect the proliferative responses of the responder T cells. These data suggest that gp120 does not inhibit the antigen-presenting function while suppressing antigen-specific responses.
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PMID:Requirement of the T cell receptor for antigen presentation by T lymphocytes. Effect of envelope glycoproteins of HIV-1 on antigen presentation by T cells. 197 70

Factor VIII concentrate inhibits T-cell function in vitro and in vivo. The mechanisms underlying the phenomenon were investigated. Factor VIII concentrate has a direct effect on lymphocytes, uninfluenced by haemophilic monocyte dysfunction, since it inhibited lymphocyte transformation with phorbol myristate acetate, a reaction unaffected by monocyte depletion. Inhibition of lymphocyte transformation by factor VIII concentrate is not corrected by the addition of exogenous IL2, suggesting that it does not inhibit lymphocyte function by suppression of IL2 secretion alone. Factor VIII concentrate causes profound inhibition of IL2-receptor expression (CD25); with an 89% reduction in CD25-positive CD4 cells and a 50% reduction in CD25-antigen molecules per cell. CD8 lymphocytes are similarly affected. Smaller reductions in CD71 and HLA-DR expression are also observed. Down modulation of CD25-antigen may explain the reduced IL2 secretion observed by others, and may be an important cause of immunodeficiency in HIV-seronegative haemophiliacs.
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PMID:Inhibition of lymphocyte IL2-receptor expression by factor VIII concentrate: a possible cause of immunosuppression in haemophiliacs. 211 76

An increased incidence of tumors and B-cell lymphomas development has been reported in persons with or at risk for acquired immunodeficiency syndrome (AIDS). This report focuses on a 50-year-old homosexual man with HIV antibodies who met the established criteria for the diagnosis of multiple myeloma: an IgG monoclonal spike greater than 2 g/dl and a plasma cell count greater than 20% in the bone marrow aspirate. Serum protein immunoelectrophoresis showed monoclonal IgG kappa, and in the urine no excess of kappa chains was found. Laboratory data revealed a total IgG of 38 g/l, IgA of 5.2 g/l, and IgM of 2.3 g/l; the calcium level was normal; ESR was 119/130, and no plasmocytoid cells were seen in the differential count. No lytic lesions were found in the skeletal survey. The helper/suppressor T-cell ratio was depleted with 0.1 and HLA-DR was highly elevated with 56% in the immunofluorescent analysis. The development of the most differentiated B-cell tumor broadens the spectrum of B-cell neoplasias in patients with a predominant helper T-cell defect and focuses on the role of disordered immunoregulation and chronic antigenic stimulation in predisposing to B-cell malignant transformation associated with AIDS.
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PMID:Multiple myeloma in a patient at risk for AIDS. 211 86

The expression of HLA class II glycoproteins by monocytes from HIV-infected individuals was evaluated. We found no differences in HLA-DR, HLA-DQ, or HLA-DP expression by freshly isolated monocytes from patients with clinical AIDS, HIV-infected patients without AIDS or from uninfected individuals. However, monocytes from HIV-infected individuals without AIDS responded better to stimulation with recombinant human interferon-gamma (IFN-gamma) than did monocytes from patients with clinical AIDS or from uninfected individuals. The response to IFN-gamma stimulation by monocytes from patients with clinical AIDS was different. Thus, the largest increases in the percentage of cells expressing HLA-DR was associated with the smallest changes in the fluorescence intensity of the population that is observed following stimulation of monocytes from other patient populations.
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PMID:HLA class II glycoprotein expression by monocytes from HIV-infected individuals: differences in response to interferon-gamma. 212 60

Human cell lines (the T-cell lines H9, Jurkat, and HUT102, the myeloid lines U937 and HL60, and the Raji B cell line) were infected with HIV-1. HIV-1 antigen could be detected by immunofluorescence analysis in more than 50% of T cells and myeloid cells 15 days after infection. Infection of Raji cells took more than 2-3 months. Studies of cell surface marker expression revealed remarkable changes after HIV-1 infection of Raji cells: expression of CR2 (C3d/EBV receptor, CD19, CD20, CD22, CD23, CD10, and surface IgM) were highly reduced, in the case of CR2 and membrane-IgM from 100 to 0%, whereas levels of CD37 and CD38 remained unaltered by HIV-1 infection. U937 cells showed a reduction of CD4 expression from 14 to 5% after HIV-1 infection; the CR3 expression slightly increased from 25 to 30%. In contrast, HLA-DR was only expressed (21%) after HIV-1 infection but not in uninfected U937 cells. Expression of HLA-DR could be detected also in HL60 cells (33%) after HIV-1 infection. In H9 cells, CD4 was reduced from 60 to 30% after HIV-1 infection, whereas HLA-DR and CD25/IL-2 receptor expression increased from 16 to 90% and from 0 to 50%, respectively. CD4 was reduced from 70 to 0% from Jurkat cells after HIV-1 infection, whereas expression of CR2 was only slightly diminished from 8 to 4%. Expression of CR1 and HLA-DR was slightly increased in these cells (1 to 3%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of the C3d/EBV receptor and of other cell membrane surface markers is altered upon HIV-1 infection of myeloid, T, and B cells. 213 11


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