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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seven immortalized B cell clones, five of which secreted specific human monoclonal antibodies (MAbs) against hepatitis B, tetanus toxoid, and Rhesus D antigens, were evaluated for their susceptibility to infection by human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2). Infection was confirmed in three human MAb-producing lines by detection of infectious virus and p24 antigen in culture supernates, by immunofluorescence, and by detection of viral DNA in cells by polymerase chain reaction. The infectable lines were as susceptible to HIV-1 infection as several T cell lines and remained persistently infected for several months, but in contrast to T cell controls, viral cytopathic effects were not observed. Levels of unintegrated viral DNA in the HB1 B cell line were significantly lower than in the HUT78 T cell line. Cell lines that were susceptible to HIV expressed HLA DR, CD20, and CD21, whereas the uninfectable cell lines did not express any of the markers tested. CD4 was undetectable or present on a small percentage of cells in two of the infectable cell lines. However, infection with HIV-1 was blocked more efficiently in B cells than in T cells by soluble CD4, anti-CD4 MAb, and dextran sulphate. The effect of HIV infection on human MAb secretion was variable, being reduced on a per-cell basis in one line, increased in another, and unchanged in a third.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Susceptibility of human monoclonal antibody-producing B cell lines to infection by human immunodeficiency virus. 133 86

The myeloid-monocytic cells ML-1, HL-60, THP-1, and U-937 were chronically infected (for > 2 years) with the lymphotropic human immunodeficiency virus type 1 (HIV-1) strain HTLV-IIIB. Reinfection experiments revealed that viruses obtained from chronically infected ML-1/HIV-1 and HL-60/HIV-1 cells showed a low infectivity if tested with uninfected ML-1 and HL-60 cells in contrast to virus preparations from chronically infected THP-1/HIV-1 and U-937/HIV-1 with their corresponding uninfected cell lines. Analyses of selected cell surface markers revealed a differential expression of CD4, CD8, CD11c, CD14, CD15, CD20, HLA-DR, and HLA-DQ in non- or chronically infected cells. In chronically infected cells, the steady-state levels for tumor necrosis factor-alpha, interleukin (IL)-1 beta, and granulocyte-macrophage colony-stimulating factor mRNA remained unchanged whereas the one for IL-6 dropped.
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PMID:Characterization of human immunodeficiency virus-1-infected cells of myeloid-monocytic lineage (ML-1, HL-60, THP-1, U-937). 145 15

As part of the multidisciplinary effort to characterize the natural history of human immunodeficiency virus type 1 (HIV-1) infection, the cell-surface phenotypes of lymphocytes from a cohort of homosexual men were analyzed in detail and related to clinical and laboratory parameters associated with HIV-1 infection. The present study represents a cross-sectional analysis of coded specimens from 153 homosexual men, of whom 74 were seronegative and 79 seropositive for HIV-1. Fewer circulating B lymphocytes (CD19+) were found in HIV-1-seropositive subjects relative to a seronegative reference group. HIV seropositivity was not associated with decreased numbers of CD8+ T cells or activated T cells, which suggests that the number of circulating B cells specifically decreased. In addition to CD19, B cells were measured by CD20 and CD21 in a subset of subjects, and decreases in circulating CD20+ and CD21+ B cells were also apparent in HIV-1-seropositive subjects. The decrease in B-cell numbers was present at the earliest stages of HIV-1 infection (asymptomatic, clinically silent) and became more pronounced at more advanced stages of HIV-1 infection. The absolute B-cell numbers correlated with absolute CD4+ cell numbers (r = 0.59, p less than 0.001). These data suggest that HIV-1 infection is associated with progressive, selective decreases in the numbers of circulating CD4+ T cells and B cells.
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PMID:Human immunodeficiency virus type-1 infection of homosexual men is accompanied by a decrease in circulating B cells. 170 70

Retinoic acid (RA) has been demonstrated to drive both phenotypic and functional in vitro differentiation of B cell hybridomas from patients with common variable immunodeficiency (CVI) who manifest an "intrinsic" defect in terminal B cell differentiation (J Exp Med 1988;168: 55-71). Therefore, we conducted an open trial to determine the effects of oral 13-cis RA (0.5 mg/kg/day; 12 weeks receiving and 12 weeks without drug) on in vivo B cell differentiation in subjects with CVI. At various times before, during, and after drug administration, patients' B cells were tested for changes in cell-surface phenotype and in vitro immunoglobulin production in response to recombinant cytokines. Before 13-cis RA, all patients had decreased Leu-8 coexpression on CD20+ cells. Seven of eight subjects demonstrated "normalization" of this phenotype after 8 to 16 weeks of 13-cis RA administration. Patients whose B cells demonstrated more than normal CD20 display also had a fall toward normal in this parameter. These effects persisted for 6 to 12 weeks after drug was stopped. It appears that 13-cis RA drives B cells of patients with CVI to express a more differentiated cell-surface phenotype and may promote functional differentiation in some patients.
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PMID:13-cis retinoic acid enhances in vivo B-lymphocyte differentiation in patients with common variable immunodeficiency. 172 Jan 49

Primates infected with simian immunodeficiency virus (SIV) develop a condition similar to the human acquired immunodeficiency syndrome (AIDS). The close resemblance between the simian acquired immunodeficiency syndrome (SAIDS) and the human disease has led to the widespread use of SIV-infected monkeys as an animal model in the study of acquired immunodeficiency. We have investigated the use of standard anti-human antibodies for the immunohistochemical analysis of formalin-fixed, paraffin-embedded tissues from monkeys with SAIDS. With the exception of antibodies UCHL1 (CD45RO), MT1 (CD43), 4KB5 (CD45RA), and Ber H2 (CD30), our routine (human) lymphoma panel of markers worked successfully on the animal tissues. Using the anti-human antibodies, we were able to analyse the phenotypes of two cases of malignant lymphoma arising in a study group of 26 SIV-infected rhesus monkeys. Both of the cases stained with the antibodies WR16 (CD45RA) and L26 (CD20), and the B-cell lineage of the lymphomas was confirmed by the detection of IgA lambda immunoglobulin expression in one case, and IgM heavy chain in the other. We therefore report the successful use of anti-human antibodies in the immunohistochemical analysis of lymphomas arising in non-human primates infected with SIV.
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PMID:Phenotypic analysis of malignant lymphoma in simian immunodeficiency virus infection using anti-human antibodies. 191 70

A murine monoclonal antibody (MoAb) F101.01 reacting with the T cell receptor (TCR)-T3 complex is presented. Immunohistological studies showed that F101.01 specifically stains T-zone lymphocytes in lymph nodes, tonsils, and splenic tissue. Two-colour immunofluorescence and flow cytometry demonstrated co-expression of the antigen defined by F101.01 and the pan-T cell antigens defined by CD2, CD3, CD5, and CD7 antibodies. Cells stained with CD4 and CD8 antibodies were both included in the F101.01-positive population, whereas CD16-positive natural killer cells (NK), B cells (CD19 and CD20), and myeloid cells (CD13 and CD33) were excluded. The target antigen of F101.01 co-modulated with the CD3-defined antigen (T3) and the TCR recognized by the MoAb WT-31. CD3 antibody and WT-31 both blocked binding of F101.01. F101.01 precipitated the TCR-T3 complex from lysates of 125I-labelled peripheral blood mononuclear cells (PBMC) and HPB-ALL, when the lysate was prepared with a detergent (digitonin) that conserves the TCR-T3 complex. FACS analysis of T cells from a patient with a T cell immunodeficiency demonstrated that delta-TCS-1-CD3+CD4+ and delta-TCS-1-CD3+CD8+ cells were brightly F101.01+, whereas a large subpopulation of delta-TCS-1+CD3+CD4-CD8- cells were weakly F101.01+. We conclude that F101.01 recognizes a conformational epitope of the TCR-T3 complex and that it reacts with the alpha beta TCR-T3 and the gamma delta TCR-T3 complexes with different intensities.
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PMID:Characterization and expression of the human T cell receptor-T3 complex by monoclonal antibody F101.01. 296 42

Circadian variations in the number of circulating lymphocytes and their subpopulations have been observed in healthy subjects. These cyclic changes are characterized by a trough at 8:00 a.m. and a peak at midnight. Using multiple peripheral blood samplings, we were able to confirm that this cycle applied to CD4 T-cells (helpers) and to B-cells (CD20). No cycle of CD8 lymphocytes was observed. In a second stage, for greater comfort of the patient the number of samplings was reduced to two: one at 8:00 a.m. (trough) and one at midnight (peak). This method enabled us to calculate the amplitude of lymphocytes cycles in 18 controls and 74 human immunodeficiency virus (HIV) seropositive patients. In asymptomatic HIV carriers the amplitude of CD4 cycles was normal in 6/26 cases and that of B-cell cycles in 2/17 cases. In the group of asymptomatic HIV carriers the mean amplitude of the cycles was much less reduced than in the other two groups. These results incite us to believe that the loss of the CD4 T-cell cycles is an early sign of HIV infection antedating the decrease observed in the number of these cells.
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PMID:[Early anomalies of CD4 and CD20 lymphocyte cycles in human immunodeficiency virus]. 297 76

A novel human T cell line (SALT-3) was established from the pleural effusion of a patient with adult T cell leukemia (ATL) of lymphoma type. SALT-3 showed atypical T cell markers such as CD1-CD2-CD3-CD4+CD5+CD7+CD8-CD19-CD20-CD25+HLA-DR+. T cell receptor alpha/beta and gamma/delta were undetectable. Human T cell lymphotropic virus type 1 (HTLV-I) particles were seen on SALT-3 cells by electron microscopic analysis. HTLV-I gag p19, proviral DNA and mRNA of HTLV-I genes were also detected in the cells. Chromosome analysis showed abnormal karyotypes as 47, XY, partial trisomy of No.3 chromosome, and trisomy of No. 7 chromosome. Furthermore, SALT-3 were susceptible to the infection of human immunodeficiency virus type 1 (HIV-1) and the cells were rapidly killed after HIV-1 infection. This newly established HTLV-I-infected human T cell line would be a useful tool to study biological activities of atypical type of ATL cells and to examine the cytotoxic effects of HIV-1 and it's modulators.
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PMID:A novel adult T cell leukemia-derived cell line (SALT-3) susceptible to human immunodeficiency virus type 1 infection. 747 53

We have analyzed PBL from 7 children exposed to CsA in utero and 4 children exposed to AZA in utero. Expression of CD3, CD4, CD8, and CD20 were normal for both groups of children; however, significant differences were detected in the expression of CD45RA, CD45R0, and CD29. While CsA-exposed children had higher density of CD45RA, and a higher proportion of CD45RA+R0- T cells, than did unexposed children, those exposed to AZA alone had decreased CD45RA+ and a large increase in CD45RA-R0+ T cells. It appears the exposure to CsA slightly delays T cell development, whereas exposure to AZA, without concomitant exposure to CsA, accelerates development to that of an adult. The effects of CsA abrogated the effects of AZA when both were present during pregnancy. The expression of CD29, the beta 1-integrin, on T cells has been linked to enhanced ability to respond to recall antigens and to home to sites of infection. Among children exposed to CsA, T cells from cord blood and a 5-month-old infant have a normal CD29 profile. However from 1 to 6 years of age the proportion of T cells expressing a high density of CD29 is significantly lower (4-fold) than that of T cells from unexposed children. Because these children have no outward signs of immunodeficiency, we postulate that this low proportion is still sufficient for normal immune responsiveness. The distribution of CD29 on T cells was different for the 3 study groups. Among CsA-exposed children, although the proportion of CD29hi T cells was much reduced, all were CD45RA+, as was also the case for unexposed children. In contrast, among children exposed only to AZA, the majority of CD29hi T cells were CD45R0+. Serological testing indicated that immunoglobulin and complement levels, as well as seroconversion in response to vaccination, were normal among CsA-exposed children, with no detectable autoantibodies to cellular or tissue components, including parietal cells. Unlike T cell development in inbred rodents, the immune system in humans appears to be remarkably resilient, and successfully adapts to the presence of CsA during its early developmental stages. This work suggests that the presence of CsA throughout pregnancy has only a minimal effect on fetal immune development and appears to have less impact on T cells than does exposure to AZA only. We conclude that children exposed to CsA in utero are not likely to be at risk of immunodeficiency or autoimmunity.
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PMID:Analysis of peripheral blood lymphocyte populations and immune function from children exposed to cyclosporine or to azathioprine in utero. 750 70

CD40 is expressed on both normal and neoplastic B lymphocytes. Signal transduction through CD40 in vitro has been shown to exert stimulatory effects on normal B cells and inhibitory effects on Epstein-Barr virus (EBV)-induced B-cell lymphoma lines and some other cell lines derived from patients with aggressive histology lymphoma. The transfer of normal human peripheral blood lymphocytes (huPBL) from EBV-seropositive donors into severe combined immune deficient (SCID) mice has been previously shown to result in the generation of human B-cell lymphomas. These tumors are similar to the highly aggressive EBV-induced lymphomas that can arise clinically after transplantation or in the setting of immunodeficiency. Treatment of huPBL-SCID chimeric mice with anti-CD40 or anti-CD20 monoclonal antibodies (MoAb) significantly delayed the development of EBV-induced B-cell lymphoma. However, the effects of the two MoAb were mechanistically distinct. Anti-CD40 treatment prevented lymphoma generation, while still allowing for functional human B-cell engraftment in the huPBL-SCID mice compared with mice receiving no treatment, all of which succumbed to lymphoma. By contrast, treatment with anti-CD20 significantly inhibited total human B-cell engraftment in the SCID recipients, which accounted for the absence of lymphomas. In vitro assays examining the transformation of human B cells by EBV also indicated that anti-CD40 could directly inhibit EBV-transformation, whereas anti-CD20 antibodies had no effect. Thus, anti-CD40 exerts selective effects to allow for the engraftment of normal human B cells and prevent the emergence of EBV lymphomas. Stimulation of CD40 by antibodies or its physiologic ligand may, therefore, be of significant clinical use in the prevention of EBV-induced B lymphomas that may arise when EBV-seropositive individuals receive immunosuppressive regimens after transplantation or in immune deficiency states, such as acquired immune deficiency syndrome.
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PMID:Antibodies to CD40 prevent Epstein-Barr virus-mediated human B-cell lymphomagenesis in severe combined immune deficient mice given human peripheral blood lymphocytes. 754 49


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