PubMed Health⌕ Search

Biomedical subjects

G Masucci

Publications and source records attributed to G Masucci.

66 records · Page 4Linked to original sources
PubMed1982

Human lymphoma-lymphoma hybrids and lymphoma-leukemia hybrids. I. Isolation, characterization, cell surface markers, and B-cell markers.

Four new somatic cell hybrids were obtained by fusion of various Burkitt's lymphoma (BL)-derived cell lines that had different selective markers: Raji-P3HR-1, Daudi-Raji, and a P3HR-1-P3HR-1 "autohybrid" derived from two P3HR-1 sublines. In addition, a hybrid was obtained between the Daudi (BL) line and the human leukemia cell line K562. The hybrids were extensively characterized by means of chromosome, isozyme, and HLA surface markers. The phenotypic differences between the parent cell lines allowed some conclusions with respect to the expression of latent Epstein-Barr virus (EBV) genomes, C3 and EBV receptors, and of immunoglobulin and beta 2-microglobulin-HLA expression as well as the influence of the leukemia cell (K562) genome on B-cell properties in the Daudi-K562 hybrid. B-cell and differentiated markers of these hybrids were characterized. High-level expression dominated for the marker C3 and EBV receptors, which showed a good correlation coefficient of 0.84, as was true for Fc receptors and surface immunoglobulin. The Daudi-K562 hybrid showed loss of all B-cell markers but retention of the leukemia cell markers (e.g., hemoglobin synthesis).

Animals↗
PubMed1981

Cellular immune defects to Epstein-Barr virus-determined antigens in young males.

Three males with the X-linked lymphoproliferative syndrome (XLP) with hypo- or agammaglobulinemia following Epstein-Barr virus (EBV) infection and two males with the chronic mononucleosis syndrome were investigated for immune responses to EBV-determined antigens. Males with XLP showed profound cellular immune defects. Markedly diminished responses of natural killer cell and interferon-activated killer cell activities and impaired leukocyte migration inhibition responses to phytohemagglutinin were determined in patients with XLP. The two patients with chronic mononucleosis showed less severe defects. All patients showed partial or complete impairment of their EBV-specific immune responses as measured by leukocyte migration inhibition. EBV-specific antibodies were markedly diminished against EBV-associated nuclear antigen, early antigen, and viral capsid antigen in males with XLP. In contrast, patients with chronic mononucleosis had elevated antibodies to most EBV-specific antigens. Individuals with life-threatening EBV-induced lymphoproliferative disorders may exhibit multiple defective immune mechanisms against the virus.

Adolescent↗
PubMed1981

T-cell response to B-cells and Epstein-Barr virus antigens in infectious mononucleosis.

After Epstein-Barr virus (EBV) infection in vivo, B-cells with latent virus infection persist indefinitely through life. These cells grow in vitro on explanation and can be established as immortal B-cell lines. To reconcile the unlimited growth potential in vitro with the maintenance of a low proportion of B-cells infected by EBV in vivo, a strict in vivo control mechanism has to be postulated. Certain aspects of this control are apparent when the primary infection is followed by infectious mononucleosis. This is characterized by lymphocytosis and the presence of activated T-cells. The T-cell proliferation is probably the manifestation of the immune response against EBV antigens. However, the reaction of T-cells upon encounter of B-blasts is also likely to contribute to the events. At present, it is difficult to detect an EBV-specific component in the action of the T-cells in the acute phase of mononucleosis exerted on B-cells. However, for the clinical course of the disease the activation of T-cells is important. The activated T-cells may control and also eliminate the B-cells infected by EBV. In addition to the immunity which develops during the disease, th immunoregulatory mechanism is likely to have a role in the inhibition of B-cell proliferation.

Antigens, Viral↗
PubMed1981

Cell-mediated immune reactions in three patients with malignant lymphoproliferative diseases in remission and abnormally high Epstein-Barr virus antibody titers.

Two patients with Hodgkin's disease in remission and one chronic lymphatic leukemia patient with extraordinarily high anti-Epstein-Barr virus (EBV) (viral capsid antigen) antibody titers (greater than 10,000) were selected to study a spectrum of cell-mediated immune responses, including natural killer, interferon-boosted killer, antibody-dependent lymphocytotoxicity, and T-cell-mediated reactions. The purpose was to compare these reactions in patients with immunosuppression and a high EBV load who can hold their EBV-carrying cells under control with the corresponding reactions in patients with EBV-carrying lymphoproliferative disease. In contrast to the latter group, the three patients of the present study showed a less profound and less general suppression of the immune responses. Multiple effector mechanisms probably safeguard against the proliferation of EBV-transformed B-cells. Clinically manifest EBV-carrying lymphoproliferative disease occurs only in very severe immunodeficiencies effecting multiple effectors.

Adolescent↗
PubMed1980

Interferon suppresses antigen- and mitogen-induced leukocyte migration inhibition.

Although first recognized by its effect on virus-cell interactions, interferon (IFN) has a variety of other effects. It can affect cell proliferation, modify the immune response at several levels, enhance the cytotoxic action of lymphocytes, suppress antibody formation and inhibit the development of delayed-type hypersensitivity (DTH) reactions. Therefore we have now tested the effect of interferon on leukocyte migration inhibition (LMI), regarded as the counterpart in vitro of DTH in humans. We have found that IFN suppresses both mitogen-and antigen-induced LMI, acting directly on the granulocytes but also affecting the lymphokine production of the lymphocytes.

Antigens↗
PubMed1980

Somatic hybrids between a high NK-sensitive lymphoid (YACIR) and several low sensitive sarcoma or L-cell-derived mouse lines exhibit low sensitivity.

Mouse somatic cell hybrids between a high NK-sensitive lymphoma line (YACIR) and various sarcoma or L-cell-derived cell lines (all weakly sensitive) all exhibited low NK sensitivity. This was not due to a general resistance to cell-mediated lysis, since these mouse hybrids could be killed by in vitro-sensitized specific T cells. Alloantigens are usually codominantly expressed in somatic cell hybrids, whereas differentiation-related markers are usually suppressed. Because NK sensitivity was found to be suppressed, in contrast to the expression of alloantigens and tumor-associated antigens, we suggest that the target structure may be either a differentiation-related antigen or a differentiation-related "membrane property."

Animals↗
PubMed1980

Target selectivity of interferon-induced human killer lymphocytes related to their Fc receptor expression.

Human blood lymphocytes were fractionated on the basis of surface characteristics such as adherence to nylon wool and expression of erythrocyte (E) and Fc receptors. The various subsets were incubated with interferon for 3 hr. Two cell lines that differ in sensitivity to the natural killer effect, K562 and Daudi, were exposed to these lymphocytes (i.e., their sensitivity to interferon-activated killing was tested.) Cell line Daudi, with a low sensitivity to the natural killer effect, was also affected by interferon-activated killing. The efficiency of the nonadherent subsets, separated according to the expression E receptor, ranked similarly in natural killing (anti-K562) and interferon-activated killing (anti-K562 and anti-Daudi) in the following order: E receptor-negative cells, low-affinity E receptor-positive cells, and high-affinity E receptor-positive cells. Further separation on the basis of Fc receptor expression revealed a difference between the two targets. The Fc receptor-positive and -negative cells that did not express high-affinity E receptors killed K562 with similar efficiency whereas Daudi cells were more sensitive to the effect of cells devoid of Fc receptor. Results obtained with other targets suggested that T cell lines behave similarly to K562 and that the difference may be generally valid for T and B cell lines.

Animals↗
PubMed1980

Hybridization of a myeloid leukemia-derived human cell line (K562) with a human Burkitt's lymphoma line (P3HR-1).

The myeloid leukemia-derived Epstein-Barr virus (EBV)-negative human lymphoid cell line K562 was successfully hybridized with the EBV-carrying Burkitt's lymphoma line P3HR-1. Authenticity of the hybrid PUTKO-1 was established by chromosome and isoenzyme studies. A virtually complete hybrid PUTKO-1 carried the EBV genome derived from the lymphoma parent. It averaged 26 EBV DNA copies per cell and was 100% positive for Epstein-Barr virus-associated nuclear antigen (EBNA). In most respects, the hybrid resembled the K562 parent: It had a high Fc receptor concentration, high sensitivity to natural killer cells, absence of EBV C3 receptors, and deficiency of membrane-associated beta 2-microglobulin (beta 2M) and HLA, in parallel with intracellular synthesis and secretion of beta 2M to the medium. Unlike the P3HR-1 parent, the hybrid was completely nonpermissive for antigens of the EBV cycle, early antigen, and viral capsid antigen. None of the 3 inducing agents, 5-lodo-2'-deoxyuridine, 12-O-tetradecanoyl-phorbol 13-acetate, or sodium butyrate, caused any viral antigen synthesis in PUTKO-1 in contrast to the good inducibility of the parental P3HR-1 subline. Thus the myeloid parent restricted expression of EBV antigens except EBNA. This exception further supports the concept that EBNA is an autonomous function of the viral genome, independent of host cell control that regulates expression of antigens related to the viral cycle. On the contrary, extinction of viral antigens in this hybrid between 2 cell lineages supports our previous concept that the ability to produce viral antigens is similar to a differentiated B-cell property.

Antigens, Surface↗
PubMed1976

Persistence of Epstein-Barr viral nuclear antigen (EBNA) in cells entering the EB viral cycle.

It was shown by double immunofluorescence studies that Epstein-Barr viral nuclear antigen (EBNA) was preserved in EBV-infected cells after they had entered the productive viral cycle, as signalled by the appearance of the early antigen (EA)complex. A nuclear component of the EA comples could be clearly distinguished from EBNA with regard to antigenic specificity.

Antigens, Viral↗