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Results for “Immunologic Capping”

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PubMed1981

Interaction of reovirus with cell surface receptors. III. Reovirus type 3 induces capping of viral receptors on murine lymphocytes.

We have previously shown that there are receptors for the hemagglutinin of reovirus type 3 on a subset of both murine T and B cells. Using purified reovirus type 3 particles as a ligand, followed by FITC-labeled antiviral antibody we have now been able to demonstrate viral induced capping of the reovirus receptor on both B and T cells. Kinetic studies and inhibition experiments using cytochalasin B and colchicine demonstrate that reovirus-induced capping of the viral receptor on both B and T cells has characteristics identical to the capping of immunoglobulin on B cells by anti-immunoglobulin reagents. Removal of the viral receptor and reexpression after overnight culture was demonstrated after membrane treatment by proteolytic enzymes (trypsin, pronase) or after viral induced modulation of receptor. Protein synthesis was required for reexpression since cyclohexamide prevented the reexpression of receptor in culture. Co-capping studies utilizing 2-color immunofluorescence failed to identify and association between the reovirus receptor and a variety of known surface structures on either B or T cells, but demonstrated independent modulation of the viral receptor from other surface structures. These studies suggest that the lymphocyte surface binding site for reovirus type 3 is a distinct structure that behaves identically in capping studies of both B and T cells, is protein in nature, and is intimately linked to the cell cytoskeleton.

Animals↗
PubMed1992

Lymphocyte adhesion can be regulated by cytoskeleton-associated, PMA-induced capping of surface receptors.

Intercellular adhesion in lymphocytes is mediated in part by the interaction of the integrin lymphocyte function-associated antigen-1 (LFA-1) with intercellular adhesion molecule-1 (ICAM-1). The B lymphoblastoid line JY expresses both LFA-1 and ICAM-1, and intercellular adhesion is enhanced by treatment with the phorbol ester phorbol 12-myristate 13-acetate (PMA), which also induced capping of LFA-1, ICAM-1, and human leukocyte antigen. Capping of LFA-1 is likely to result from protein kinase C (PKC) activation because receptor-mediated stimulation of PKC also led to capping. Additionally, adhesion mediated by PMA or lipopolysaccharide was blocked by either of two PKC inhibitors, calphostin C and staurosporine. PMA induced the apparent condensation of cytoskeletal elements that colocalized with the membrane protein cap. Cytoskeletal condensation and capping occurred in the absence of intercellular adhesion. Alteration in the distribution of cytoskeletal components and membrane redistribution of LFA-1 were inhibited by cytochalasin D, which also abolished intercellular adhesion. Taken together, these data suggest that intercellular adhesion is the result of PKC-mediated membrane redistribution of LFA-1 and ICAM-1, which is in turn associated with modification of the actin-based cytoskeleton.

Actins↗
PubMed1985

Sheep-erythrocyte-capping by human T-lymphocytes. Pharmacological inhibition by phenothiazine drugs.

In our previous studies it was found that E-rosette dissociation and sheep-erythrocyte capping were active processes involving the cytoskeleton. These cellular functions are now shown to be very sensitive to phenothiazine-drugs whose activities can be differentiated as follows: trifluoperazine greater than chlorpromazine greater than sulfoxide derivatives, suggesting a role for calmodulin-mediated events. These findings are in contradiction to prior reports pointing to the inefficacy of chlorpromazine to inhibit slow kinetic capping. However, no co-capping of trifluoperazine fluorescence (as a probe of calmodulin) and sheep erythrocytes could be observed. No requirement in extracellular calcium was evident for E-rosette formation and dissociation.

Adult↗
PubMed1982

Lymphocyte capping in muscular dystrophies.

Since reports of lymphocyte capping in muscular dystrophies of various authors revealed controversial results, we investigated 47 patients and carriers with Duchenne or Becker-Kiener muscular dystrophy according to different methods. There was no significant reduction of cap formation compared to 64 healthy controls, both groups showing a mean of about 75% caps. Reduced numbers of caps, however, could be demonstrated in three otherwise healthy probands aged 70 years or more, two patients under interferon treatment, four patients under high dose methotrexate therapy as well as one patient with untreated chronic myeloic leukemia. Thus lymphocyte capping in our experience is far from being a valid method for carrier detection or prenatal diagnosis of muscular dystrophies.

Adolescent↗
PubMed1978

Two distinct mechanisms for redistribution of lymphocyte surface macromolecules. I. Relationship to cytoplasmic myosin.

A detailed kinetic analysis of the distribution of cytoplasmic myosin during the capping of various lymphocytic surface molecules revealed two distinct capping mechanisms. (a) Some cell surface molecules, including immunoglobulin, Fc receptor, and thymus leukemia antigen, all cap spontaneously in a small fraction of lymphocytes during locomotion. Cytoplasmic myosin becomes concentrated in the cytoplasm underlying these spontaneous caps. Exposure to specific antibodies causes all three of these surface molecules to cap rapidly with a concomitant redistribution of cytoplasmic myosin to the area of the cap. These antibodies also stimulate cell locomotion. (b) Other lymphocyte surface molecules, including H2 and Thy.1, do not cap spontaneously. Moreover, exposure to antibodies to these molecules causes them to cap slowly without a redistribution of cytoplasmic myosin or stimulation of cell locomotion. Exposure to concanavalin A gives a response intermediate between these two extremes. We believe that the first type of capping is active and may involve a direct link between the surface molecules and the cytoplasmic contractile apparatus. The second type of capping appears to result simply from aggregation of cross-linked molecules in the plane of the membrane.

Animals↗
PubMed1989

Capping of HLA antigens in human lymphocytes as followed by immunogold label-fracture.

We used immunogold label-fracture to follow the migration of HLA I class and HLA II class antigens during capping as induced by specific monoclonal antibodies. Capping is achieved through a process of clustering and "consolidation" of clusters into larger patches and, finally, a single cap. All receptors appear to cluster from the very start, with no "stray" molecules joining already formed patches. Characterization of exoplasmic and protoplasmic fracture-faces of capping cells fails to reveal any corresponding accumulation of intramembrane particles and/or subtler rugosities. Our results are consistent with the concepts that view the migration of capping molecules as contemporaneous with the efflux of noncapping integral membrane proteins.

Antibodies, Monoclonal↗
PubMed1984

Anomalous function of vimentin in chronic lymphocytic leukemia lymphocytes.

Chronic lymphocytic leukemia (CLL) lymphocytes manifest anomalous motility and cap formation. Since these processes involve cytoskeletal proteins, vimentin from intermediate filaments of normal and CLL lymphocytes was investigated using hetero- and monoclonal antisera. The antisera reacted predominantly with a 60-kD polypeptide, following sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of total lymphocyte proteins. When lymphocytes were stained by indirect immunofluorescence, normal lymphocytes demonstrated well defined cytoplasmic fibrils that capped spontaneously after contact with a glass surface and incubation at 37 degrees C. This capping was dependent on energy and intact microfilaments. Lymphocytes from patients with CLL showed several patterns. In one group, the initial staining was weak, and few capped cells were present after incubation. Lymphocytes from other patients had either normal or aberrantly organized fibrils in which capping was diminished. In another group, a fibrillar pattern with normal or increased capping was seen. In total, 47% +/- 5.1% (mean +/- SE) of normal lymphocytes capped after a 1-hr incubation at 37 degrees C (n = 12) compared to 21% +/- 5.1% for CLL lymphocytes (n = 20, p less than 0.002). Purified subpopulations of normal B and T cells did not differ from unfractionated normal lymphocyte populations. These results demonstrate an anomalous vimentin capping response in CLL lymphocytes. They also show that the arrangement of vimentin in these cells differs from that of normal lymphocytes.

Antibodies, Monoclonal↗
PubMed1989

Poliovirus translation: a paradigm for a novel initiation mechanism.

All eukaryotic cellular mRNAs, and most viral mRNAs, are blocked at their 5' ends with a cap structure (m7GpppX, where X is any nucleotide). Poliovirus, along with a small number of other animal and plant viral mRNAs, does not contain a 5' cap structure. Since the cap structure functions to facilitate ribosome binding to mRNA, translation of polio-virus must proceed by a cap-independent mechanism. Consistent with this, recent studies have shown that ribosomes can bind to an internal region within the long 5' noncoding sequence of poliovirus RNA. Possible mechanisms for cap-independent translation are discussed. Cap-independent translation of poliovirus RNA is of major importance to the mechanism of shut-off of host protein synthesis after infection. Moreover, it is likely to play a role in determining poliovirus neurovirulence and attenuation.

Humans↗
PubMed1985

Significance of number of HLA determinants in HLA capping in childhood acute lymphoblastic leukemia.

The density of HLA determinants on the cell surface was studied in relation to HLA capping in childhood acute lymphoblastic leukemia (ALL). Analysis was performed with flow cytometry (FACS) and a subjective labeling score. These two methods gave comparable results. In T-ALL high percentages of capped cells were related to low numbers of HLA determinants. In c-ALL we found the opposite. This study shows that capping capacity and number of HLA determinants in childhood ALL are inversely related.

Antibodies, Monoclonal↗
PubMed1983

Impaired T cell capping and receptor regeneration in active systemic lupus erythematosus. Evidence for a disorder intrinsic to the T lymphocyte.

It is currently unclear whether the T cell dysfunctions observed during active systemic lupus erythematosus (SLE) reflect a disorder intrinsic to the T cell or defects that result from interaction with anti-T cell autoantibody. To determine whether a disorder intrinsic to the T cell exists in SLE, the T cell capping mechanism was selected as a model of cellular function. The normal T cell capping mechanism is a rapid, energy-dependent and coordinated sequence of membrane events that consists of microaggregation, capping, endocytosis, and regeneration of the surface molecule. The monoclonal antibodies OKT3, OKT4, and OKT8, directed against the T cell-specific membrane glycoproteins T-3, T-4, T-8, served as specific probes of the glycoproteins' mobility within the membrane and membrane glycoprotein regeneration. When compared with greater than 91% T cell capping in normal and control subjects with active Sjögren's syndrome, active rheumatoid arthritis and active tuberculosis, only 49-60% of T cells from active SLE patients completed the capping sequence (SLE vs. healthy controls; T-3, P less than 0.002; T-4, P less than 0.004; T-8, P less than 0.002). Colchicine (10(-5) M), which inhibits microtuble polymerization and augments the rate of normal T cell capping, failed to restore the abnormal capping. However, as judged by the elapsed time intervals to half-maximal capping, the capping kinetics of the T cells able to initiate capping were not significantly different from controls. Fluorescence microscopy demonstrated an abnormal staining pattern characterized by microaggregation of ligand-glycoprotein complexes on resting T cells, coarse aggregation of ligand-glycoprotein complexes over the surfaces of cells that failed to cap, and cleaved or disrupted caps. After clearance of determinants by capping, greater than 94% of T cells from healthy controls regenerated T-3, -4, and -8 within 24 h. In contrast, only 20-40% of capped T cells from active SLE patients reexpressed new determinants. With improving disease activity, the proportion of cells capping and regenerating T-3, -4, and -8 increased, but remained significantly below control levels. In conclusion, this study has identified a disorder of T cell surface glycoprotein mobility and regeneration affecting the majority (60-80%) of both the T-3+, T-4+, (inducer/helper), and T-3+, T-8+ (suppressor) subsets during active SLE. Although the impaired capping and reexpression improve with disease remission, a residual defect persists. The data support the concept of a disorder intrinsic to the T cell in SLE.

Adult↗
PubMed1990

High-resolution surface views of human lymphocytes during capping of CD4 and HLA antigens as revealed by immunogold fracture-flip.

The surface ultrastructure of lymphocytes during capping of two transmembrane proteins is shown. As seen by fracture-flip the plasma membranes of human lymphocytes are covered by a high density of surface particles. Incubation in 30% glycerol leads to aggregation of these surface particles. Immunogold labelling shows that the transmembrane proteins bearing HLA class I and CD4 antigens are confined to the particle aggregates. These results indicate that surface particles revealed by fracture-flip represent surface protrusions of integral membrane proteins seen as intramembrane particles in freeze-fractured lymphocytes. During capping HLA or CD4 antigens aggregate into progressively larger patches and, finally, into single caps. As revealed by fracture-flip the patches/caps are seen as clearly differentiated raised platforms that are clearly and sharply demarcated relative to contiguous areas of the surface. In non-patched (non-capped) regions, the pattern of distribution and apparent density of surface particles remain unaltered. Immunogold labelling clearly demarcates patches and caps, and shows that virtually no antigen molecules remain dispersed over the non-patched (non-capped) regions. Estimates of the surface density of either HLA or CD4 antigens over the capped areas point to high planar concentrations of the transmembrane proteins that bear these antigens.

Antigens, Surface↗
PubMed1983

[Effect of cytoskeleton-disrupting on the redistribution of the surface receptors of cultured cells].

The capacity of cap-formation in cultured cells was shown to increase from 2 to 20 fold upon treating them with ligands in the presence of a conditioned medium. This permitted us to compare the influence of cytoskeleton-disrupting agents on the process of cap-formation in cultured cells of different origin. Cytochalasin was shown to inhibit cap-formation, induced with concanavalin A or anti-H2-serum, both in cells of lymphoid and fibroblastic origin. In contrast, vinblastin did not inhibit cap-formation in cells of lymphoid origin, but caused inhibition in cells of fibroblastic origin twice as strong as did cytochalasin B.

Animals↗
PubMed1983

Receptor capping in mouse T-lymphoma cells: a Ca2+ and calmodulin-stimulated ATP-dependent process.

The roles that Ca2+, calmodulin, and ATP play in the redistribution of concanavalin A (Con A) binding sites on the surface of mouse T-lymphoma cells were examined. Membranes of cells labeled with fluorescein-conjugated Con A (Fl-Con A) were made permeable ("skinned") to ions and proteins by incubation in a solution containing no added Ca2+, 7 mM EGTA, and ATP. The intracellular ionic and protein concentrations could then be varied, and the degree of Con A receptor capping monitored simultaneously. A graded increase (9.0 to 30%) was found in the number of capped cells with increasing Ca2+ concentration from 10(-6)-10(-4.9) M. Increasing concentrations of trifluoperazine, chlorpromazine, and promethazine (1.5 x 10(-6) to 1.0 x 10(-4) M) in cell suspensions containing 10(-4) M Ca2+ produced graded inhibition of capping in the same order that the drugs bind to calmodulin. Removal of extracellular Ca2+ dissociated (reversed) some of the caps into patches, thus reducing their number (12%). ATP was required for either capping or cap dissociation to occur. Addition of calmodulin (3.9 x 10(-8)-6.3 x 10(-7) M) to the cell suspension increased the Ca2+ sensitivity. These results provide direct evidence that capping of Con A receptors is a reversible process (i) regulated by intracellular Ca2+ concentrations, (ii) requiring ATP as an energy source, and (iii) susceptible to the influence of calmodulin. These findings are consistent with the hypothesis that the collection of surface receptor patches into cap structures is controlled by the interaction of actomyosin filaments, which in turn is regulated by a Ca2+-calmodulin-activated control system.

Adenosine Triphosphate↗
PubMed1981

Characterization of class II histocompatibility antigens in pigs.

The D region of the SLA complex in the pig has been studied by immunochemical and sequential immunoprecipitation techniques as well as the redistribution of membranous antigens (capping). The molecules identifies by the anti-Ia sera were solubilized by NP 40, purified on lectin and precipitated. Polyacrylamide gel electrophoresis under dissociating conditions shows that these molecules are made up of two chains whose molecular weights are 32000 and 26000 daltons respectively. Sequential immunoprecipitation and capping experiments indicate that two distinct types of Ia molecules exist. At least a part of the nylon-wood-adherent lymphocyte population express both types of molecules.

Animals↗
PubMed1991

CD45 is not involved in the processing of spatial information required for chemotaxis.

To examine the possible role of CD45 (a cell surface tyrosine phosphatase) in processing spatial information leading to the orientation of neutrophils in a gradient of chemoattractant, we used antibodies to cap CD45. If the phosphatase activity of CD45 was processing spatial information coming from occupied receptors and leading to the directional cell response, sequestering CD45 in one region of the cell surface should lead to a decreased ability of the cells to orient in a gradient of chemoattractant. CD45 was capped by sequential addition of KC56, a mAb against CD45, and a rabbit anti-mouse antiserum. Cells with capped CD45 were able to orient toward N-formylnorleucylleucylphenylalanine and C5a at levels similar to those achieved by cells processed simultaneously but without capping CD45. This indicates that the spatial arrangement of CD45 is not critical for the ability of cells to orient in a gradient of chemoattractant.

Antigens, CD↗
PubMed1987

Cap formation in a B-lymphocyte cell line is inhibited by pertussis toxin and phorbol ester.

We have examined concanavalin A (Con A)-induced cap formation in a B-lymphocyte derived cell line, LAZ-559. Treatment with pertussis toxin (PT) or phorbol-12-myristate-13-acetate (PMA) prior to exposure of the cells to Con A abolished the capping reaction. The possible role of calcium mobilization was tested using cells pre-loaded with the fluorescent dye Quin2. Both PT and PMA caused inhibition of calcium mobilization at concentrations similar to those observed for the inhibition of capping. The possible identity of the substrate for pertussis toxin was examined by carrying out ADP-ribosylation of the isolated plasma membranes using [alpha-32P]NAD and pertussis toxin. Several bands were observed at molecular weights of 109,000, 43,000, 34,000 and 22,000. Comparative labelling with cholera toxin revealed a separate band at 42,000. The bands at 43,000 and 34,000 are PT specific. Of these, the 43,000 band comigrated with the PT substrate that has been shown to regulate capping in human neutrophils (Lad et al., 1985a, 1986b). PMA-induced phosphorylation was examined in 32P-loaded cells, and multiple bands were observed to be labelled in a dose-dependent manner, at least two of which were very similar in mobility to the PT substrate. Our results suggest that regulation of calcium mobilization and the control of capping via a PMA-sensitive, GTP-binding protein are probably general phenomena observable in multiple cell systems.

B-Lymphocytes↗
PubMed1980

Autosomal dominant cerebrovascular amyloidosis: properties of peripheral blood lymphocytes.

Selected properties of peripheral blood lymphocytes (PBLs) from five ambulatory affected individuals of a kindred with autosomal dominant cerebrovascular amyloidosis were studied. The percentage of PBLs bearing surface membrane immunoglobulin (SmIg+ cells) was increased in the patient group (30 +/- 3% versus 20 +/- 2%; p less than 0.05). The percentage of PBLs forming early and total E-rosettes was comparable in patient and control groups. Mitogenic response to concanavalin A (Con A) was suggestively reduced in the patient group, measured both by total 3H-thymidine incorporation and by comparison of stimulation indices. Mitogenic response to phytohemagglutinin and pokeweed was comparable in the two groups. Capping of Con A by PBLs was significantly reduced in the patient group compared with the controls (13 +/- 1% versus 26 +/- 2%; p less than 0.01). The findings of reduced Con A response and increased SmIg+ cells support the hypothesis that immune dysfunction contributes to the development of amyloidosis. The reduced capping suggests altered membrane properties in this autosomal dominant disorder.

Adult↗
PubMed1981

Capping of peripheral blood lymphocyte C3 receptors in chronic lymphocytic leukemia: relationship to chemotherapy.

The data show that in chronic lymphocytic leukemia (CLL) there are elevated numbers of peripheral blood lymphocytes (PBL) capable of rosette formation (complement-rosetting lymphocytes, CRL) with bacteria (B)-antibody-(A)-complement (C) (BAC) complexes. In most of the CLL patients studied, large percentages of CRL were impaired in their ability to undergo BAC-C3R cap formation compared to normal donors. The degree of impairment varied from one patient to the next. A consideration of clinical information suggested that the variation was related to the clinical response of patients to chemotherapy. Four categories of CLL patients could be identified on the basis of clinical data: (1) patients never received therapy for CLL; (2) those whose clinical history indicated a failure to respond to ongoing chemotherapy; (3) patients who had received successful prior chemotherapy and who were asymptomatic or stable and were receiving no therapy at the time of study; and (4) those who were undergoing therapy at the time of study and who subsequently became stable or asymptomatic and were removed from therapy. The first two categories of patients failed to show significant BAC-C3R capping, whereas the last two were able to form C3R caps on significant percentages of CRL. No direct relationship could be discerned between C3R capping and currently accepted classifications on stages (Rai) of CLL. These results suggest that monitoring the percentages of BAC-C3R cap-forming CRL may be useful in determining the success of chemotherapy of CLL patients. The microtubule-disrupting agent colchicine enhanced BAC-C3R capping in all CLL patients to normal levels, whereas the microfilament-disrupting agents cytochalasin B(CB) had no effect on CLL RBL C3R capping. CB totally abolished C3R capping of CRL from normal donors. These results suggest that abnormalities exist in both cytoskeletal and contractile systems of CR from CLL peripheral blood.

Antineoplastic Agents↗