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At least 235 records · Page 13Linked to original sources
PubMed1998

NK cell granule exocytosis and cytokine production inhibited by Ly-49A engagement.

MHC class I-specific NK cell receptors inhibit natural killing, and presumably granule exocytosis, when engaged by target cell ligands but it is not yet known which specific activation receptor pathway for natural killing is inhibited or if these receptors influence other NK cell activities such as cytokine production. Moreover, an individual NK cell may express multiple inhibitory MHC class I receptors; these NK cell receptors may cooperate in inhibiting NK cell activity. To address these issues, we examined whether the murine Ly-49A NK cell receptor, specific for H-2Dd, can regulate granule exocytosis and NK cell cytokine responses. Expression of transfected H-2Dd on tumor targets specifically inhibited granule release from Ly-49A+ NK cells. Importantly, Ly-49A engagement also inhibited target cell-induced cytokine (GM-CSF) secretion. Using a target cell-free system, we next determined that anti-Ly49A mAb can regulate NK cell responses induced by specific stimuli. Cross-linking of NK1.1 with immobilized mAb induced granule release and TNF-alpha, IFN-gamma, and GM-CSF secretion; all were inhibited by coimmobilized anti-Ly-49A. These effects were specific because an isotype-matched control mAb did not alter NK1.1-mediated responses. Therefore, these results demonstrate that the Ly-49A receptor can regulate granule exocytosis and cytokine secretion in response to targets and NK1.1 signaling, consistent with its function as an inhibitory receptor for MHC class I molecules in NK cell-mediated cytotoxicity. In addition, these results strongly support the thesis that signals transduced from Ly-49A alone are sufficient for mediating the inhibitory effects against target cells.

Animals↗
PubMed1980

Capping revisited. I. Inhibition by some thiols.

The capping, but not the clustering (spotting), of membrane immunoglobulins and of other lymphocyte membrane macromolecules is inhibited when the medium contains some reducing agents, principally cysteine. The inhibition is easily reversible, being rather a retardation of capping than its blockage. The mechanism of inhibition is still unclear, but it definitely depends on the sulfhydryl moiety of the thiols.

Amino Acids↗
PubMedDate not supplied

Lymphocyte capping in hereditary muscular dystrophic chickens and mice: no evidence for a systemic membrane defect.

Splenic lymphocytes from both the Storrs and Davis strains of muscular dystrophic chickens and the C57BL/6J-2J strain of muscular dystrophic mice cap FITC-Con A and FITC-Ig in a manner similar to normal controls. In analyses of testcross progeny of Storrs muscular dystrophic chickens, no difference in the ability of lymphocytes to cap were observed among the segregating progeny. Neither were any significant differences observed in lymphocyte capping among F2 segregating progeny of C57BL/6J-2J mice. These studies do not support the systemic membrane defect hypothesis for muscular dystrophy.

Animals↗
PubMed1989

Capping and co-capping of membrane immunoglobulin and lipid-conjugated immunoglobulin inserted in the cell membrane of B lymphocytes.

Human and mouse immunoglobulins (Ig) or F(ab')2 fragments of rabbit Ig were conjugated to lipids and the conjugates inserted into the membrane of mouse spleen cells. It was found that nearly all B cells, but not T cells, became decorated with lipid immunoglobulin. Both endogenous Ig receptors and inserted Ig capped after the addition of cross-linking F(ab')2 antibodies and in both cases capping required energy. Capping of endogenous mouse Ig led to co-capping of inserted human Ig, but the reverse was not true.

Animals↗
PubMedDate not supplied

[Use of the direct capping technic in lymphocytes for the detection of women carrying the Duchenne type muscular dystrophy].

Duchenne muscular dystrophy (DMD) is a progressive X-linked recessive condition. The detection of female carriers is important for genetic counseling but no precise method is available in our country. Based on the demonstration by other authors of an impaired lymphocyte "capping" in DMD patients and carriers, we evaluated the usefulness of this method in the detection of DMD carriers. Nineteen control subjects, 9 obligate carriers, 6 DMD patients, and 10 probable carriers, were studied. The analysis of variability intra and interobserver of the results of "capping" showed variation coefficients of 17% and 19%, respectively. The comparison of groups (F test) showed no difference between controls, obligate carriers and DMD patients. When a diagnostic value of 30 was chosen, we obtained 78% specificity and 40% sensitivity. It was concluded that, under the conditions of this study, we were unable to demonstrate a diminished lymphocyte "capping" in DMD patients and carriers as compared with normal subjects.

Adult↗
PubMed1978

Cell surface changes in capping studied by correlated fluorescence and scanning electron microscopy.

A simple method has been devised for correlating fluorescence microscopy and scanning electron microscopy, whereby the identical cell observed by the former can be observed by the latter. With this methodology, we have studied the sequence of cell surface changes which occur when mouse B lymphocytes, bearing immunoglobulin (Ig) on their surfaces, interact with fluoresceinated anti-Ig antibodies. Initially, the pattern of staining is diffuse; then, rapidly, patching occurs, followed by the sweeping of the patches into a cap. Accompanying these events are: the disappearance of microvilli, the formation of ruffles and lamellipodia at the pole of the cell opposite the capped pole, the presence of a constriction ring beneath the cap, ameboid shapes, and the translocation of the cell in a direction opposite the cap. Whereas the cell body is smooth, the capped pole frequently shows the presence of numerous microvilli. However, not all capping cells show the changes, and cells capped in the presence of cytochalasin B usually show none of them, except that their surfaces are smooth. Furthermore, T-cells undergoing translocation show the same cell surface changes as do B-cells. Whereas the contractile apparatus of the cell is considered to underlie all these phenomena, it is concluded that the cell surface changes do not result from patching and capping per se, but rather are an expression of the cell translocation also induced by the anti-Ig antibody.

Animals↗
PubMed1977

Transmembrane interactions and the mechanism of capping of surface receptors by their specific ligands.

The mechanism of capping of cell surface receptors has been examined by a double fluorescence staining procedure that permitted simultaneous observations of the distribution of a surface-bound ligand together with intracellular actin or myosin. At an early stage in the capping of the T-25 antigen or the H2 histocompatibility antigens on mouse splenic T lymphocytes, or of concanavalin A receptors on HeLa cells, when the specific receptors in question were collected into patches that were distributed over the entire cell surface, the intracellular membrane-associated actin or myosin was also accumulated into patches that were located directly under the receptor patches. These and other results have led us to propose a general molecular mechanism for the process of capping, in which actin and myosin are directly involved. It is suggested that membrane-associated actin is directly or indirectly bound to an integral protein or class of proteins, X, in the plasma membranes of eukaryotic cells. When any receptor in the membrane is aggregated by an external multivalent ligand, the aggregate binds effectively to X, whereas unaggregated receptors do not bind to X. The receptor aggregates, linked to actin (and myosin) through X, are then actively collected into a cap by an analogue of the actin--myosin sliding filament mechanism of muscle contraction.

Actins↗
PubMed1983

Lymphocyte capping in myotonic dystrophy.

Lymphocyte capping with antihuman immunoglobulin was studied in 16 cases of myotonic dystrophy, including two cases with the congenital form. Percentage capping after 1 hour incubation was reduced and the time course of the capping sequence was apparently delayed. The significance of these findings remains to be determined.

Adolescent↗
PubMed1979

Mobility and density of AgB, "Ia", and Fc receptors on the surface of lymphocytes from young and old rats.

Analysis of spleen cell populations from old Lewis rats (greater than 24 months) and from young Lewis rats (3 to 4 months) in a fluorescence-activated cell sorter indicated that with aging there is a loss of brightly stained Ia and Fc receptor- (FcR) positive cells. The density of AgB, Ia, and FcR was diminished on the surface of cells from old rats. The rate of capping of all three membrane proteins was slower on cells from old rats. Colchicine treatment allows capping of AgB with a single ligand only in young rats. Fluorescence photobleach recovery experiments (FPR) show that the fluidity of the lymphocyte membrane from old rats is diminished and the lateral diffusion of AgB is decreased. The colchicine and FPR experiments suggest that the changes in capping in old rats are due to, in part, alterations in membrane fluidity and cytoskeletal function.

Aging↗
PubMed1983

Hyperthermic enhancement of antibody-complement cytotoxicity against normal mouse B lymphocytes and its relation to capping.

Normal mouse B lymphocytes were exposed to water-bath hyperthermia in vitro and examined for susceptibility to antibody-complement (Ab-C) cytotoxicity. Enhancement of Ab-C cytotoxicity was observed during heat treatment at 42 or 43 degrees C. Sensitivity to Ab-C cytotoxicity returned to normal levels by 2-3 hr post exposure to 42 degrees C. No such recovery was observed when cells were preheated at 43 degrees C for 40 min. The mechanism responsible for heat-induced enhancement of Ab-C cytotoxicity may be related to the way heat affects the redistribution of membrane-bound antigen-antibody (Ag-Ab) complexes. To investigate this possibility, cells were preheated at 37, 42, or 43 degrees C. The Ab-C assay was then performed at 37 degrees C immediately or 2.5 hr after hyperthermia. The distribution of Ag-Ab complexes was evaluated by immunofluorescence. A direct correlation was found between the hyperthermic enhancement of Ab-C cytotoxicity and the hyperthermic inhibition of capping, a process where membrane-bound Ag-Ab complexes coalesce into a polar cap on the cell surface. Sensitivity to Ab-C cytotoxicity returned to normal levels when cells restored the ability to cap Ag-Ab complexes following 42 degrees C hyperthermia. Cells heated at 43 degrees C were still sensitive to Ab-C cytotoxicity and did not recover the capping ability even 2.5 hr after heat treatment.

Animals↗
PubMed1983

Redistribution of mouse spleen cell Fc receptors following treatment with mouse or human aggregated immunoglobulin G.

Mouse spleen cells treated with the Fc receptor ligands mouse IgG2b and human IgG, followed or not by a second antibody, exhibit different patterns of redistribution. In the work reported here we have examined the redistribution of Fc receptors (FcR) after binding of aggregated mouse IgG2b (Alg) or of Alg followed by anti-lg. We were particularly interested in learning whether binding of isologous Alg to FcR is followed by significant redistribution and shedding of Alg-FcR complexes. Mouse IgG2b alone will not induce capping even after 60 min at 37 degrees C. Human IgG induces some capping with minor shedding of complexes. Human IgG followed by anti-IgG readily induces capping by 15 min on 70% of the cells. This treatment also induces capping by 60 min at 20 degrees C on about 80% of the cells with a moderate degree of shedding of complexes. This is in agreement with the concept that the crosslinking required for FcR capping can be best induced with a second antibody. It is of interest, however, that heterologous IgG, unlike isologous, can induce a modest degree of capping and slight shedding even without the second antibody, suggesting that some crosslinking occurs with heterologous IgG.

Animals↗
PubMedDate not supplied

[Study of influenza virus interaction with T- and B-lymphocytes].

B and T lymphocytes of a healthy and immune donor inactivate influenza virus and form "caps" in the presence of the latter. The process of "cap formation" by lymphocytes of a healthy donor terminated in separation of the "cap" with virions adsorbed on multiple microspikes. The virions attached to lymphocytes of the immune donor concentrate in the area of the "cap" which apparently is not rejected from the cell. B lymphocytes of normal and T lymphocytes of immune donors seem to form the "caps" more actively. Influenza virions penetrate lymphocytes of immune donors more rapidly and in greater numbers.

B-Lymphocytes↗
PubMed1984

Acanthamoeba castellanii capping protein: properties, mechanism of action, immunologic cross-reactivity, and localization.

We report further characterization of the physical and immunologic properties, mechanism of action, and intracellular localization of Acanthamoeba castellanii capping protein, an actin regulatory protein discovered by Isenberg (Isenberg, G., U. Aebi, and T. D. Pollard, 1980, Nature (Lond.) 288:455-459). The native molecular weight calculated from measurements of Stokes' radius (3.8 nm by gel filtration chromatography) and sedimentation coefficient (4.8 S by sucrose gradient velocity sedimentation) was 74,000 daltons. The subunit molecular weights were 31,000 and 28,000 daltons, so the native molecule is a heterodimer. The two subunits did not immunologically cross-react with each other or with any other proteins from Acanthamoeba or several other organisms. In studies of the mechanism of action, Isenberg (see above reference) found that capping protein blocked polymerization from the barbed end of actin filaments and sedimented with actin filaments. We confirmed that capping protein binds to actin filaments with a gel filtration assay. Capping protein decreased the length distribution and high shear viscosity of actin filaments. Capping protein did not bundle or cross-link actin filaments. Low concentrations of capping protein increased the critical concentration for muscle and ameba actin polymerization from 0.1 to 0.6 microM in Mg++ and EGTA. Increasing amounts of capping protein did not increase the critical concentration further. In Ca++ capping protein did not change the critical concentration for muscle actin, but did increase the critical concentration for ameba actin. Ca++ had no effect on the ability of capping protein to decrease the low or high shear viscosity of actin filaments. By indirect fluorescent antibody staining, capping protein was localized to the cell cortex, an area rich in actin filaments. During subcellular fractionation of homogenates, about 1/3 of cellular capping protein banded with a crude membrane fraction. The other 2/3 of cellular capping protein was soluble, with a Stokes' radius equal to that of the purified protein. The molar ratio of capping protein to actin in the cell was 1:150.

Actin Depolymerizing Factors↗
PubMed1995

Myosin II is involved in capping and uroid formation in the human pathogen Entamoeba histolytica.

The redistribution and capping of surface receptors on the human pathogen Entamoeba histolytica was observed in the presence of concanavalin A (ConA). Capping was correlated with plasma membrane folding towards the rear of the amoeba and with uroid formation. The uroid is thought to play a role in the escape of amoebae from the host immune response. To localize myosin II during capping, amoebae were incubated in the presence of ConA and then analyzed by microscopy. Myosin II was three times more concentrated within the uroid compared with the rest of the cell, suggesting that the release of caps may depend upon mechanical contraction driven by myosin II activity. The use of drugs that disrupt cytoskeletal structure or that inhibit myosin heavy chain phosphorylation demonstrated that inhibition of capping prevents uroid formation. Biochemical analysis allowed the identification of two ConA receptors which have been previously described as major pathogenic antigens of this parasite: the 96-kDa antigen, which carries alcohol dehydrogenase 2 activity and binds extracellular matrix proteins, and the Gal-GalNAc-inhibitable surface lectin, which is involved in amoeba-cell interactions and in the degradation of complement particles attached to the parasite.

Amino Acid Sequence↗
PubMed1989

Impairment of capping in lymphoblastoid cell lines of Duchenne patients indicates an intrinsic cellular defect.

Duchenne muscular dystrophy (DMD) is a lethal sex-linked degenerative disorder of the muscle in man. Generalized cell membrane abnormalities seem to be involved in the pathogenesis of the disease; in particular, the impairment of lymphocyte capping capacities has been repeatedly confirmed. To clarify whether capping impairment is a consequence of factors related to the activity of the disease or an expression of an intrinsic cellular defect, we have investigated the capping capacities of DMD EBV-transformed cell lines. The results indicate a significant impairment of capping capacity in cultured cell lines, providing evidence for an intrinsic cell deficiency in DMD.

Antibodies, Monoclonal↗
PubMed1979

Functional studies of hairy cell leukemia (leukemic reticuloendotheliosis).

Reports proposing that the cell or origin of "hairy cell" leukemia (leukemic reticuloendotheliosis) is a B lymphocyte have been based primarily on the presence of surface immunoglobulin markers, frequently in "cap" form. Most of the immunoglobulin markers in this series of patients with hairy cell leukemia were multiclass, but were present in cap form under conditions not usually inducing cap formation in normal or leukemic human lymphocytes. In five cases the authors were able to remove these surface immunoglobulins by trypsinization or overnight incubation in serum-free tissue-culture medium. There was no evidence of synthesis of surface immunoglobulins in these cases following incubation in serum-free tissue-culture medium; however, surface immunoglobulins could again be detected after subsequent reintroduction of these hairy cells into the patients' own sera. The peculiar cap formation could not be prevented with sodium azide, a standard inhibitor of cap formation. Phagocytized latex particles and neutral red dye produced similar caplike structures. These findings suggest that hairy cells readily adsorb and pinocytose circulating immunoglobulins, but do not synthesize them.

Azides↗
PubMed1980

Permanent inhibition of capping of spleen lymphocytes from neonatally oestrogen-treated female mice.

Female mice of the NMRI strain were injected with 5 microgram diethylstilboestrol (DES) or oestradiol-17 beta for the first 5 days after birth. Controls were given olive oil only. At the age of 4-6 months, the spleen lymphocyte population from the DES females had about half the percentage of cells undergoing capping after exposure to concanavalin A (Con A) as controls. The results from the oestradiol-injected females varied. After treatment of lymphocytes from DES females with colchicine, the percentage cells capping was as in control females. Binding studies did not reveal any difference in Con A receptor affinity or receptor number between DES females and controls.

Animals↗