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Biomedical subjects

P Rieber

Publications and source records attributed to P Rieber.

At least 37 records · Page 2Linked to original sources
PubMed1989

Anti-CD4 antibody treatment of patients with rheumatoid arthritis: II. Effect of in vivo treatment on in vitro proliferative response of CD4 cells.

In treating rheumatoid arthritis (RA) patients with anti-CD4 antibodies (MT151 10 mg/day, 7 d) we observed diminished skin-test response to recall antigens and reduced proliferative response to antigens and mitogens (in vitro) 2-4 h following the injection. To investigate whether this diminished response is due to functional impairment of CD4+ cells, we analyzed the proliferative response of CD4+ cells to various stimuli, in conditions where the CD4 structure was either cross-linked or not. We found that in vivo anti-CD4-antibody-coated cells could be induced to proliferate if the anti-CD4 antibody was cross-linked with an anti-CD3 antibody [BMA030-F(ab')2] added in vitro and per se non-mitogenic. Also, without cross-linking the cell-bound anti-CD4 antibodies, no impairment of the proliferative capacity of CD4-antibody-coated cells could be detected; double fluorescence analyses of phytohaemagglutinin (PHA)- or CD3-stimulated cells showed that a similar proportion of CD4+ cells proliferated before and after anti-CD4-antibody treatment. The diminished proliferation observed following anti-CD4 treatment correlated to the reduced number of CD3+ and CD4+ cells in culture, which suggests that altered cell distribution might be one factor contributing to the impaired immune response.

Antibodies, Monoclonal↗
PubMed1989

In vitro IgE-secretion in atopic eczema: influence of allergens and mitogens and role of CD8 T cell subpopulation.

In cultures of peripheral blood mononuclear cells (PBMC) from 23 atopic patients and 14 controls the influence of mitogens, allergens and CD8 suppressor T lymphocytes on the in vitro IgE response was studied. The in vitro IgE levels in lymphocyte culture supernatants reached a plateau after 6 days of culture, whereby low levels of IgE could be reproducibly measured down to 0.5 ng/ml. The spontaneous in vitro IgE secretion from PBMC of atopic eczema patients was elevated in comparison to the control group and showed a direct correlation (r = 0.72) to the serum IgE levels. Pokeweed mitogen rather suppressed the in vitro IgE production. After removal of the CD8 subpopulation of T lymphocytes by using an indirect erythrocytes rosetting technique we found increased in vitro levels pointing to a role of IgE regulating T suppressor subpopulations.

Allergens↗
PubMed1989

CD antigens 1989.

Explore the source record for details and available documents.

Antigens, Differentiation↗
PubMed1988

Selective stimulation of human T lymphocyte subsets by heteroconjugates of antibodies to the T cell receptor and to subset-specific differentiation antigens.

Ligand binding under conditions that generate microaggregates of the T cell receptor complex (Ti/CD3) with the membrane molecules CD4 or CD8 can induce activation of small resting T lymphocytes. We demonstrate this by using soluble dimeric heteroconjugates consisting of monoclonal antibodies to CD4/CD8 and of a novel anti-CD3 monoclonal antibody (BMA030) which even in aggregated form is not stimulatory on its own under limiting conditions in the absence of accessory cells. Using combinations of BMA030 with either anti-CD4 or anti-CD8, the corresponding T cell subpopulation could be selectively expanded in vitro. Selective expansion of T cell subpopulations in vitro or in vivo might be helpful for certain therapeutical manipulations. In addition, this finding may contribute to a better understanding of major histocompatibility complex-restricted T cell activation.

Antibodies, Monoclonal↗
PubMed1987

A new ELISA-based assay for quantitation of human T-lymphocyte subpopulations.

In order to circumvent the problems associated with the available methods, we have developed a simple, reliable ELISA for quantitation of T-cells and their subpopulations, T-helper/inducer and T-suppressor/cytotoxic cells. Standard curves with three concentrations of sheep anti-mouse IgG-coupled beads for each T-cell population were used for the determination of the T-cell content in blood. Enzyme-labelled monoclonal antibodies against T-Pan, T-S and T-H cell surface markers were readily able to bind to such beads and the test system was calibrated with T-lymphocytes by comparing cytofluorographic and enzyme immunometric results. Purified preparations of monocytes and granulocytes were negative in the test. Lymphocytes from 50 healthy blood donors gave results which correlated closely with cytofluorograph determinations.

Antigens, Surface↗
PubMed1987

Prostaglandin E2 (PGE2)-dependent suppression of interleukin alpha (IL-2) production in patients with major trauma.

The depression of interleukin-2 synthesis represents a major dysfunction within the cascade of immunologic defects induced by mechanical and thermal trauma. This study was undertaken to elucidate the negative control mechanisms that were responsible for the deficiency of IL-2 production in polytraumatized patients. Peripheral blood mononuclear cells (PBMC's) from 29 patients (average age, 35.8 years; average ISS, 35) were separated on post-trauma days 1, 3, 5, 7, 10, 14, and 21 and cultured as untreated cells (C), cells treated with indomethacin (C + INDO), and cells depleted of adherent cells (C-AC). Cell cultures were assayed for proliferative responses to PHA, IL-2 synthesis, PGE2 production, gamma-interferon levels, and phenotyping studies. On all days post-trauma there was found a marked reduction of IL-2 production compared to controls with a highly significant nadir from day 5 to day 10 with an almost 80% inhibition of IL-2 (p less than 0.005). C + INDO cells showed increases of IL-2 synthesis over untreated cells ranging from 48% (Day 1) to 220% (Day 7). Removal of adherent cells (C-AC) did not reverse the suppression of IL-2 production. gamma-interferon levels were depressed in parallel with IL-2 levels but did not increase with C + INDO. The phenotyping of the PBMC's showed highly significant suppression of OKT3+, OKT4+, and IL-2R+ lymphocytes as well as a highly significant elevation of the monocyte (p less than 0.005) count. There was a highly significant increase of PGE2 synthesis from monocytes, due to the monocytosis and to a higher capacity of synthesis of the individual cells following trauma. PGE2 levels peaked on Day 5 and 7 post-trauma at 400% of control (p less than 0.005). These data suggest that the suppression of IL-2 synthesis post trauma is caused mainly by two factors: the excessive PGE2 output of inhibitory monocytes and inadequate function in immature and/or blocked lymphocytes. The partial restoration of IL-2 synthesis by indomethacin suggests that blockade of the cyclo-oxygenase pathway as an immunomodulating therapy may reverse some of the immunologic abnormalities in multiple trauma patients.

Adult↗
PubMed1986

Cytolytic T cell clones derived from liver tissue of patients with chronic hepatitis B.

To study the role of cell-mediated immunity in chronic hepatitis B (cHB) we have cloned T cells from liver biopsies of 14 patients with cHB. As a first step, T cell lines were established from lymphocytes infiltrating the liver by culturing the biopsied specimens with autologous feeder cells and interleukin 2 (IL2). Fifty-eight clones obtained by limiting dilution showed phenotypic stability over periods of 2-26 weeks. Of the 58 clones 50 were of the "cytotoxic/suppressor" T cell subset (CD8) as defined by the monoclonal antibody T811. Only 8 of 58 clones were of the "helper/inducer" phenotype (CD4) as defined by the monoclonal antibody T151. Functional studies on 9 clones (7 of CD8+ phenotype, 2 of CD4+ phenotype) revealed high cytotoxic activity of all of these clones in a lectin-dependent cell-mediated cytotoxicity assay reflecting the killing capacity of cytotoxic T lymphocytes. All 9 clones lacked significant natural killer activity, while two additional CD8+ clones that also expressed the VEP13 antigen showed significant natural killer activity. For none of the clones tested could killer cell activity (ADCC) be demonstrated. The studies demonstrate that the clonal expansion of T lymphocytes from liver biopsies of patients with cHB in the absence of detectable antigen is possible. The propagation of in vivo activated cytolytic T lymphocytes points to an active role of these cells in the pathogenesis of this disease.

Adult↗
PubMed1986

Acquired immune haemolysis by anti A 1 antibody following bone marrow transplantation.

In ABO mismatched organ or bone marrow transplants recently some cases of acquired immune hemolysis have been reported. It was felt that these life threatening complications were due to immunosuppressive treatment with cyclosporin-A. A case of severe hemolysis following mismatched BMT is reported. Here no cyclosporin-A treatment was given since the bone marrow was T-cell deprived by an E-rosetting technique. Apparently T-cell purging can under these conditions become dangerous.

ABO Blood-Group System↗
PubMed1986

Reactivity of monoclonal antibody BE 2 in different stages of mycosis fungoides and in benign dermal infiltrates.

The cutaneous infiltrate in mycosis fungoides (MF) is predominantly composed of T4-positive T-cells. Attempts to distinguish the early stages of this condition from benign inflammatory infiltrates using anti-T3, T4 and other T-cell-associated antibodies have hitherto been unsuccessful. Recently a monoclonal antibody BE 2 has been described as selectively reacting against leukemic cells in patients with cutaneous T-cell lymphoma. To investigate whether the BE 2 antigen is differentially expressed in different stages of MF and benign dermatoses, thus facilitating diagnosis, especially of early MF, the reactivity of monoclonal antibody BE 2 against cutaneous infiltrates from such conditions was assessed. In the early stages of MF only a small number of reactive cells was present. In benign inflammatory infiltrates, especially in those that clinically and histologically were hardly distinguishable from early MF, BE 2 reactivity was essentially the same as in eczematous-stage MF. Lesions from plaque and tumor stage MF contained large numbers of BE 2-reactive cells. Our results indicate that expression of BE 2 is associated with the stage of a given MF lesion and is essentially identical in early MF and eczematous lesions with a similar histopathological appearance.

Antibodies, Monoclonal↗
PubMed1985

Infiltrating mononuclear cells in human breast carcinoma: predominance of T4+ monocytic cells in the tumor stroma.

Frozen sections of 52 breast carcinomas were examined for the presence and nature of a leukocytic infiltrate. The number of "common leukocyte (T200-) antigen"-bearing cells was remarkably high in the stromal compartment of the carcinomas, whereas the tumor foci themselves were usually infiltrated only sparsely. Approximately 80% of these T200+ stromal cells carried the myelomonocyte lineage-associated antigens M-M522 and 63D3 and exhibited "non-specific esterase" activity. More than 2/3 of the stromal monocytic cells expressed the T4 antigen as verified by monoclonal antibodies (MAbs) directed against different T4-associated epitopes. A T-cell analysis showed that T4+ cells clearly outweighed the total number of T cells as defined by anti-T3 and anti-TII antibodies. In addition, a correlation became apparent between the HLA-DR phenotype and the T lymphocyte content of tumor cell areas in the sense that densely infiltrated tumor areas were invariably HLA-DR+.

Animals↗
PubMed1985

Epidermal synthesis and expression of HLA-DR on keratinocytes in lupus erythematosus.

It has been suggested that aberrant expression of HLA-DR plays an important role in the induction of an autoimmune reaction. In lupus erythematosus (LE), skin represents a major target for autoimmune attack. We therefore tested lesional and nonlesional skin from 11 patients with different clinical subtypes of LE for the presence of HLA-DR molecules on keratinocytes using a monoclonal antibody against a non-polymorphic HLA-DR determinant. In all lesions tested, HLA-DR-positive keratinocytes were present, whereas in nonlesional skin, these cells remained HLA-DR negative. To exclude the possibility of passive absorption of DR molecules, the de novo synthesis of HLA-DR was demonstrated by the presence of cytoplasmic HLA-DR gamma chains in keratinocytes. If aberrant HLA-DR expression is a primary event, it could facilitate the recognition of autoantigens on keratinocytes by immunocompetent cells. Alternatively, the synthesis of DR molecules could be induced as a secondary event by mediators derived from the inflammatory infiltrate.

Adult↗
PubMed1985

Antigenic relationship between the alpha-chain of C3, a leucocyte-surface antigen involved in the activation of phagocytic cells, and a 50,000 MW B-cell antigen.

A monoclonal antibody, M522, reacting with human monocytes, neutrophils and a proportion of non-adherent PBL in a pattern similar to OKM-1 and anti-Mo-1, and precipitating a dimer of MW 165,000 and 100,000 from neutrophils, was shown to react with C3 at an epitope localized on the alpha-chain of C3. F(ab)2-fragments of M522 stimulate the respiratory burst of neutrophils and monocytes. M522 differs from two monoclonal antibodies against the Mo-1 molecule with respect to the capacity to inhibit the binding of sheep erythrocytes coated with different C3-fragments to C-receptor carrying cells. It inhibited the binding of H-coated particles to B-lymphoid cells and precipitated a 50,000 MW molecule from RAJI cells and tonsil lymphocytes. The results obtained suggest an antigenic relationship between the alpha-chain of C3, the heavy chain of a membrane molecule involved in neutrophil/monocyte activation, and a B-cell molecule of MW 50,000.

Antibodies, Monoclonal↗
PubMed1985

Monoclonal antibody to human cytotoxic-suppressor T-lymphocytes cross-reacts with canine lymphocytes and inhibits cell-mediated lympholysis of canine cells.

Of 19 murine antihuman Tp32 (T8) monoclonal antibodies tested, only antibody T811 showed cross-reactivity with canine lymphoid cells. It recognized an antigen expressed on 19%-27% of peripheral blood mononuclear cells (PBMC), 20%-30% of peripheral Thy 1+ T-lymphocytes, 40% of puppy thymocytes, 35%-45% of alloantigen-activated peripheral lymphocytes, and 100% of PBMC from a dog with acute T-cell leukemia. The antigen was not expressed on peripheral Thy 1- cells, bronchoalveolar cells, or null-type acute leukemia cells. The antibody inhibited cell-mediated lympholysis in the absence of complement, while antibody F3-20-7 directed at the canine Thy 1 antigen did not. It was not possible to precipitate a corresponding cell surface antigen on canine cells using standard 125I radioimmunoprecipitation techniques nor did the antibody cause antigenic modulation. Our data suggest that monoclonal antibody T811 reacts with a functional subset of canine T-lymphocytes similar to that of human cells; however, significant differences may exist between the antigens recognized on these cells in the two species.

Animals↗
PubMed1984

Distribution of T-cell subsets as defined by monoclonal antibodies in skin lesions of psoriasis vulgaris.

Cryostat tissue sections from skin lesions of 16 patients suffering from chronic stationary psoriasis vulgaris were assayed for the presence of distinct T-cell subpopulations with monoclonal antibodies. Using two pan-T surface markers (M-T 4-11 and Lyt 3) the total number of infiltrating T-cells was measured. This cell population was further dissected into Leu 3a (helper/inducer) and M-T 8-11 (cytotoxic/suppressor) positive subsets. Percentages of T-cell subpopulations were within the ranges found in healthy peripheral blood and were thus regarded as normal.

Antibodies, Monoclonal↗
PubMed1984

Immunological aspects of retinoids in humans. I. Analysis of retinoic acid enhancement of thymocyte responses to PHA.

We previously reported that retinoic acid (RA) enhances the blastogenic responses of human thymocytes. In this study, we explored the mechanism(s) of this effect by determining the phenotype of cells that show augmented responses to PHA and by analyzing RA effects on regulatory events mediated by interleukin-2 (IL-2). Our results indicate that RA is required early in the PHA activation process and that thymocytes affected by RA treatment already express the "mature" T3 antigen but lack T6 and Fc mu receptors. In the presence of saturating concentrations of exogeneous IL-2, RA caused further enhancement of both unfractionated and T3+ thymocyte proliferation, but could not induce immature T3- cells to become PHA responsive. RA treatment of thymus cells did not affect IL-2 production nor IL-2-dependent T-cell blast growth. RA-induced enhancement appears to induce increased sensitivity of T3+T6-Fc mu- thymocytes to PHA activation, but does not alter either IL-2-dependent proliferation or the accessory cells involved in IL-2 production.

Cell Differentiation↗