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PubMed1986

Role of adenylate cyclase in human T-lymphocyte surface antigen capping.

Our recent studies indicated that capping of T3, T4 and T8 surface antigens on human T lymphocytes is augmented by interaction of adenosine with a purinergic receptor. We suggested that the T-cell capping process was mediated by an adenylate cyclase-coupled purinergic receptor that resulted in the generation of cAMP and occupancy of cAMP receptors. The present study was undertaken to examine whether activation of adenylate cyclase in the absence of purinergic stimulation is sufficient to regulate surface antigen capping. Treatment of T lymphocytes with forskolin or cholera toxin caused activation of adenylate cyclase and occupancy of intracellular types I and II regulatory subunits of protein kinase by cAMP, as demonstrated by photoaffinity labeling with [8-3H]N3-cAMP. Such treatment augmented the rate of capping of the T3, T4, and T8 antigens, which resulted in a significant decrement in the elapsed time to half-maximal capping of each antigen. These observations support the proposition that the normal T-lymphocyte capping mechanism of both T3+, T4+ (inducer/helper) and T3+, T8+ (suppressor) subsets can be augmented by activation of adenylate cyclase.

Adenosine↗
PubMed1982

Anti-immunoglobulin, cytoplasmic free calcium, and capping in B lymphocytes.

This paper examines, in mouse spleen lymphocytes, the effect of anti-immunoglobulin (anti-Ig) on the cytoplasmic free calcium concentration, [Ca2+]i, measured with the fluorescent indicator quin2, and the relationship of [Ca2+]i to the capping of surface Ig. Anti-Ig causes a rapid rise of [Ca2+], which precedes capping. Assuming that only those 40-50% of the cells which can bind anti-Ig (the B cells) undergo a [Ca2+]i response, [Ca2+]i in those cells approaches 500 nM. It declines to resting levels over many minutes, roughly paralleling the formation of caps. Part of the [Ca2+]i signal is due to stimulated influx across the plasma membrane, since in Ca2+-free medium, anti-Ig gives a smaller and shorter [Ca2+]i rise. The amplitude of this reduced transient now varies inversely with quin2 content, as if some 0.25 mmol Ca per liter of cells was released into the cytoplasm from internal stores. These stores are probably sequestered in organelles since A23187 in Ca2+-free medium also causes a transient [Ca2+]i rise after which anti-Ig has no effect. These organelles seem not to be mitochondria because uncouplers have hardly any effect on [Ca2+]i. Though anti-Ig normally raises [Ca2+]i before causing capping, there seems to be no causal link between the two events. Cells in Ca2+-free medium whose stores have been emptied by A23187, still cap with anti-Ig even though there is no [Ca2+]i rise. Cells loaded with quin2 in the absence of external Ca2+ still cap anti-Ig normally even though their [Ca2+]i remains steady at below 30 nM, four times lower than normal resting [Ca2+]i.

Adenosine Triphosphate↗
PubMed1981

Mechanism of T cell activation. II. Antigen- and lectin-dependent acquisition of responsiveness to TCGF is a nonmitogenic, active response of resting T cells.

Small resting T cells, which do not respond to T cell growth factor (TCGF), acquire responsiveness upon a short (4-hr) pulse of specific ligands by presenting growth receptors for TCGF. The results demonstrate that the same mechanisms operate in the specific induction of primary MLR in that a 5-hr MLR is sufficient to render the responder cells reactive to TCGF. Furthermore, the results demonstrate that an active "response" by the resting T cells is required for expression of functional growth receptors, as demonstrated by the fact that: 1) a 4-hr pulse of concanavalin A (Con A) at 4 degrees C did not result in gain of reactivity to TCGF, whereas a 4-hr pulse at 37 degrees C did; 2) this metabolic requirement for acquisition of responsiveness to TCGF was not due to a secondary requirement for cap-formation of Con A-binding membrane structures, as normal responses were observed in the presence of cytochalasin B (cyt B); 3) the process of Con A-induced acquisition of susceptibility to TCGF was puromycin sensitive.

Animals↗
PubMed1978

Shedding of anti-IgM from antibody-coated human lymphoma lines: differences between Epstein-Barr virus-negative lines and their virus-converted sublines.

In vitro converted, Epstein-Barr (EBV) genome-carrying cell lines showed a reduced ability to shed surface-bound antibodies, compared to their EBV-free parental B lymphoma lines. On the other hand, antibody degradation was higher with EBV-positive cells. Analysis of antibody-coated single cells revealed that cells which failed to redistribute or cap their ligand-bound surface components at 37 degrees C, were also capable of shedding bound antibody. This suggests that capping and shedding are essentially independent phenomena, although both may be influenced by the same virally induced change in the lateral mobility of membrane constituents.

Antibodies, Anti-Idiotypic↗
PubMed1980

Relationship between membrane fluidity and capping of receptors for concanavalin A.

The activities of a range of phenylalaninol-related compounds on capping of concanavalin A and induction of rounding of Chinese hamster ovary tsHl cells, as well as on the fluidity of phosphatidylcholine-cholesterol (1:1) liposomes, have been examined. These compounds include phenylalaninol, histidinol, leucinol, benzyl alcohol, benzylamine, 2-phenylethanol, 2-phenylamine, 3-phenyl-1-propanol, 3-phenyl-1-propylamine, and 3-phenylpropionic acid. The results indicate a strong correlation between the capacities of these compounds to enhance fluidity and their capacities to inhibit capping of concanavalin A. The specificity of this correlation is suggested by the finding that both types of capacities are poorly correlated with the capacities of the various compounds to induce cell rounding.

Animals↗
PubMed1990

Microfilament-disrupting Clostridium difficile toxin B causes multinucleation of transformed cells but does not block capping of membrane Ig.

The effects of Clostridium difficile toxin B on some actin-dependent cellular functions were studied. A three-day incubation of intoxicated B-lymphocytes and transformed 3T3 fibroblasts resulted in dose-dependent multinucleation. Using vimentin-negative Daudi cells we showed that this effect of toxin B does not involve vimentin. As DNA and protein syntheses are not impaired in the cells used, the results suggest that toxin B has an effect on the actin-containing contractile ring during mitosis, in a manner similar to that of the microfilament-disrupting agent cytochalasin B. Toxin B is the first bacterial toxin shown to have this effect. It was also found that the capping of surface IgM on B-lymphocytes was not inhibited by toxin B, whereas cytochalasin B did inhibit capping. These results suggest that capping is dependent on a specific membrane-associated actin structure, which is not affected by toxin B.

Actin Cytoskeleton↗
PubMed1990

Polarization and capping of lymphocytes in HIV infection.

The present study was undertaken to assess the locomotor capacity of lymphocytes from patients with human immunodeficiency virus (HIV) infection by a polarization assay. In addition, the capping phenomenon of lymphocytes from HIV-infected patients or in vitro preincubation of lymphocytes with HIV-envelope glycoproteins, gp41 and gp120 was evaluated. A significant decrease in polarized lymphocytes from patients with acquired immunodeficiency syndrome (AIDS) was observed. On the other hand, the capping phenomenon either of lymphocytes from AIDS patients or of lymphocytes from healthy donors preincubated with gp41 and gp120 was reduced but not significantly.

Chemotaxis, Leukocyte↗
PubMed1984

Regulation of human T lymphocyte surface antigen mobility by purinergic receptors.

The present study was undertaken to establish whether the capping mechanism of normal human T lymphocytes is regulated by a purinergic receptor. Interaction of T lymphocytes with adenosine significantly increased the mobility of the T3, T4, and T8 surface antigens. This enhanced rate of capping was reflected by a significant decrement in the time intervals to achieve half-maximal capping. T lymphocytes preincubated with theophylline or isobutylmethylxanthine did not exhibit accelerated capping or a decrease in the time required for half-maximal capping in response to adenosine, suggesting that these agents inhibited the binding of adenosine to its receptor. A role for a cAMP-dependent pathway in capping was suggested by the observation that the phosphodiesterase inhibitor RO-201724 caused a decrease in the concentration of adenosine required to accelerate the capping process. Moreover, exposure of T lymphocytes to the cyclic nucleotide derivatives 8-N3-cAMP and 8-Br-cAMP mimicked the effect of adenosine, significantly reducing the time to half-maximal capping. Photoaffinity labeling of intracellular cAMP receptors with 32P-8-N3-cAMP indicated that adenosine caused occupancy of the receptors. This effect of adenosine was inhibited by theophylline, a known purinergic receptor blocker. The data support the concept that the T cell capping mechanism is mediated by an adenylate cyclase-coupled purinergic receptor that activates a cAMP-dependent pathway, and that this pathway is functional in the T3+, T4+, (inducer) and T3+, T8+ (suppressor) subsets.

Adenosine↗
PubMed1994

Ligation of CD45 on B cells can facilitate production of secondary Ig isotypes.

The possibility that isotype switching in B cells may be affected by engagement of the CD45 molecule on B cells has been investigated in microcultures containing limiting numbers of B cells and nonlimiting numbers of both alloreactive Th cells and purified dendritic cells (DC). Addition of Abs to the B cell-specific isoform, B220, to the microcultures leads to an increase in the proportion of B cell clones that secrete secondary Ig isotypes. In the presence of anti-CD45 Ab, microculture wells show a 39% frequency of secondary isotypes (560/1440) compared with a 11% frequency in control microcultures (89/780). Cross-linking appears to enhance this effect. Even in cultures of B cells and DC without T cells, addition of anti-B220 induces isotype switching in a significant number of microwells. Cross-linking and capping B220 molecules results in co-capping of surface Ig and MHC class II molecules. The results suggest that signal transduction through the CD45 molecule may affect pathways involved in isotype switching.

Animals↗
PubMed1998

Colon carcinoma cells use different mechanisms to escape CD95-mediated apoptosis.

CD95(APO-1/Fas) is a cell surface receptor that, when oligomerized by natural ligand, CD95L, or antibody, confers an apoptotic signal to apoptosis-sensitive cells. Whereas CD95 is expressed in every colonocyte of normal colon mucosa, CD95 is down-regulated or lost in the majority of colon carcinomas. To investigate the sensitivity to CD95-mediated apoptosis of normal and neoplastic colonocytes, we applied cross-linking CD95(anti-APO-1) monoclonal antibody to freshly isolated colon crypts and colon carcinoma cell lines and monitored apoptosis by DNA fragmentation and morphology. Normal colonocytes were constitutively sensitive to CD95-mediated apoptosis. All carcinoma lines were constitutively resistant but were sensitized upon pretreatment with IFN-gamma. Transcription blocking, protein synthesis, and export in carcinoma cells indicated that even low surface levels of CD95 were sufficient to efficiently transmit the signal. Despite low CD95 surface levels of non-IFNgamma-treated cells, actinomycin D, cycloheximide, and brefeldin A each sensitized all cell lines, but at different rates and kinetics. In this context, it was observed that a greatly delayed apoptotic response of SW620 cells was associated with the absence of antibody-induced CD95 capping. Phorbol 12-myristate 13-acetate inhibited CD95-mediated apoptosis by counteracting the IFNgamma-, actinomycin D-, and cycloheximide-mediated but not the brefeldin A-mediated sensitization. This phorbol 12-myristate 13-acetate-induced protection against apoptosis was completely abolished by staurosporine and by a selective protein kinase C inhibitor, Goe 6983. We conclude that, during malignant transformation, colonocytes acquire different mechanisms to escape CD95-mediated apoptosis. These include abrogation of CD95, inhibition of CD95 capping, and activation of antiapoptotic programs, both governed by and independent of protein kinase C.

Antigens, Neoplasm↗
PubMed1997

Antibody-induced and cytoskeleton-mediated redistribution and shedding of viral glycoproteins, expressed on pseudorabies virus-infected cells.

Fluorescein isothiocyanate-labeled porcine pseudorabies virus (PrV) polyclonal antibodies were added to PrV-infected swine kidney cells in vitro at 37 degrees C. In approximately 47% of the infected cells, the addition induced passive patching and subsequent energy- and microtubule-dependent capping of all viral envelope glycoproteins, expressed on the plasma membranes of the infected cells. Further contraction and extrusion of the capped viral glycoproteins occurred in approximately 30% of the capped cells 2 h after the addition of antibodies and was accompanied by a concentration of F-actin beneath the caps. At that time, about 18% of the extruded caps were shed spontaneously into the surrounding medium. Mechanical force released 85% of the extruded caps, leaving viable cells with no microscopically detectable levels of viral glycoproteins on their plasma membranes. Experiments with PrV deletion mutants showed that viral glycoproteins gE and gI are important in triggering viral glycoprotein redistribution. Since the PrV gE-gI complex exhibits Fc receptor activity which facilitates capping, the importance of gE and gI may be partially explained by antibody bipolar bridging.

Actin Cytoskeleton↗
PubMed1988

Motility of leukaemic cells in acute leukaemia related to tumour mass, maturation and FAB classification.

In a group of 56 patients with acute leukaemia, the relation between leukaemic cell motility and peripheral leukaemic cell count, degree of organomegaly, maturation and FAB classification was investigated. Cell motility was studied by means of directly observed motility and scoring of handmirror cells and anti-HLA-capping. The percentage of moving cells in the peripheral blood was higher than in the bone marrow. A positive correlation was found between the percentage of moving cells in the peripheral blood and the peripheral leukaemic cell count. In acute myeloid leukaemia, the percentage of moving cells in the bone marrow and the degree of organomegaly were higher in the monoblastic groups than in the myeloblastic groups. No correlation was found between directly observed motility, handmirror cells and capping. Leukaemic cell motility can play a role in the egress of leukaemic cells from the bone marrow, resulting in a higher tumour mass, thereby influencing prognosis.

Acute Disease↗
PubMed1978

Independent mobility of cholera toxin binding sites and Thy-1 alloantigen on mouse thymocytes.

The hypothesis that Thy-1.2 carries a carbohydrate antigenic determinant with the same specificity as the monosialoganglioside GM1 was tested by attempting to co-cap Thy-1.2 and GM1 in CBA thymocytes using anti-Thy-1.2 alloantiserum and cholera toxin. Co-capping of these determinants was not observed suggesting that they are on separate molecules. We do not therefore confirm the previous reported association between Thy-1 and GM1 (Thiele, Arndt & Stark, 1977).

Animals↗
PubMed1980

Human lymphocyte capping in Duchenne muscular dystrophy.

We have confirmed the observation that, in patients with Duchenne muscular dystrophy, there is a significant reduction in lymphocyte capping. However, our results indicated that this may be related to the degree of muscle damage in these boys, since it was correlated to both age and serum creatine kinase activity and could therefore be a secondary phenomenon.

Adolescent↗
PubMed1982

"Pseudo-cap" formation in Ehrlich ascites tumor cells induced by cytochalasin B.

Cytochalasin B (CB) treatment induces or accelerates the capping phenomenon in some cells. In Ehrlich ascites tumor cells (EATC) CB treatment apparently induced the capping of Con A binding sites as observed under a fluorescent microscope. However, electron microscopic examinations revealed that the CB treatment did not induce a rearrangement of Con A binding sites, but rather it only induced a change in cell shape. On the contrary, CB treatment inhibited the capping phenomenon induced by treatment with Con A. Electron microscopic observations may give exact information on the distribution of lectin binding sites.

Animals↗
PubMed1979

Lymphocyte surface modulation and glycosphingolipids.

Using the fluorescent antibody method, identical localization of ligand and glycosphingolipids was found in human peripheral blood B lymphocytes patched and capped with polyvalent anti-immunoglobulin. cAMP also showed the same pattern of localization. It is suggested that glycosphingolipids are hydrogen bonded to receptor-bearing membrane macromolecules and are borne with them into the ligand-induced patches and caps. Here the asymmetric carbon chains of the glycosphingolipids modify the local lipid environment, leading to activation of the adenyl cyclase in the membrane which produces the cAMP.

Antibodies, Anti-Idiotypic↗
PubMed1985

Chediak-Higashi syndrome: studies in long-term bone marrow culture.

The granulocyte defects of Chediak-Higashi syndrome (CHS) include neutropenia, characteristic giant lysosomal granule morphology, and functionally abnormal cell motility, degranulation, and bacterial killing. Findings of elevated levels of adenosine 3', 5' cyclic monophosphate nucleotide (cAMP) and of concanavalin A (Con A) capping have suggested a pathogenic role of a cyclic-nucleotide-related defect in microtubule polymerization, but not all patients exhibit these abnormalities. In order to test which defects derive from the cells' genetic program and which from the host environment, we examined granulocytes produced by CHS bone marrow progenitors in long-term in vitro bone marrow cultures. These cells exhibited the characteristic giant-granule morphology and defective cell motility of CHS. However, culture-derived CHS granulocytes had normal cAMP contents and normal spontaneous capping of Con A. Granulopoiesis diminished dramatically after five weeks in culture, with accompanying autophagocytosis by mononuclear phagocytes. In mixing experiments, the phenotype of the mature granulocytes corresponded to the genotype of the hematopoietic component of the culture rather than the stroma. These results indicate that the hallmark giant-granule morphology and cell motility defect of CHS are expressions of the genetic program of the hematopoietic cells. However the abnormalities in resting cyclic nucleotide levels and in Con-A capping may be secondary manifestations of the disease and are not essential to the pathogenesis of the chemotactic defect.

Autophagy↗
PubMed1981

Immune reactive measles virus polypeptides on the cell's surface: turnover and relationship of the glycoproteins to each other and to HLA determinants.

To better understand the mechanism(s) whereby antibody and complement and cytotoxic lymphocytes lyse infected cells, we studied the structure, interrelationship and turnover of measles virus polypeptides expressed on the cell's surface. Of the 6 major viral structural polypeptides, L, HA, P, NC, F, and M, found in purified virions or infected cells, only 2, the HA and F, resided on the surface of infected cells. The HA was present primarily in the form of a 160k dimer, and F was identified as a 64k polypeptide migrating distinct from other viral polypeptides. With reduction, the HA migrated as a 80k monomer, and F0, after cleavage, was found to be composed of a 42k nonglycosylated polypeptide, F1, and a 24k glycosylated protein, F2. The relationship between F0 and F1 and between the HA dimer and monomer was verified by tryptic peptide mapping. The turnover of HA and F from the cell's surface was 10 and 9 hr, respectively. However, in the presence of specific antibody after a marked loss of viral antigen from the surface, the turnover for HA and F was 15 and 12 hr, respectively. Despite being independent molecules, HA and F were closely linked, as they moved together (co-capped) over the plasma membrane when incubated with monospecific or monoclonal antibody. In contrast, neither HA nor F co-capped with the major histocompatibility antigens or with other host cell proteins, which indicates a separation between these host cell proteins and measles viral glycoproteins on the cell's surface.

Antibodies, Viral↗