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At least 739 records · Page 41Linked to original sources
PubMed1989

"Lysostrip" experiments with HLA class II antigens. II. Incomplete interdependence of surface mobility of supertypic DR and narrow DR specificities.

Utilizing the lysostrip technique we analyzed the relations between the mobility of supertypic HLA-DRw52 and DRw53, and narrow DR specificities. Different types of determinants were found, the one removed only by supertypic anti-DR allosera, the second removed by narrow anti-DR allosera, and the third removed by supertypic anti-DR and narrow anti-DR allosera as well. The results are discussed in terms of intermolecular complexes formed on cell surface by HLA class II antigens.

B-Lymphocytes↗
PubMed1989

"Lysostrip" experiments with HLA class-II antigens. I. Independent surface mobility of DQ and DR molecules.

We report on results of lysostrip experiments designated to analyse the molecular relations between DQ and DR antigens. The purpose of lysostrip application was to determine whether these antigens can independently be redistributed on B-cell surface by incubation with a specific antibody followed by incubation with F(ab')2 fragments of rabbit antihuman Ig. The obtained results have clearly shown that DQ antigens, and supertypic and narrow DR antigens, move independently, indicating that they are located on separate molecules, supporting the concept of different DQ and DR loci.

B-Lymphocytes↗
PubMed1985

Delineation of three subsets of class I human T antigens (HTA) on Molt-4 cells: serologic and regulatory relationship to HLA class I antigens.

Three subsets of class I human T antigens (HTA) were serologically identified on the surface of the Molt-4 T lymphoma cell line. The HTA 1 subset is defined by NAI/34, D47, or 10H3.9 cross-reactive m.Ab. and by BL6 m.Ab. The HTA 2 and HTA 3 subsets are defined by M241 and 4A7.6 m.Ab., respectively. We obtained no evidence of any additional HTA subset. The different HTA antigens share only few epitopes with human leukocyte antigens (HLA-A, -B, and -C). Interestingly, these epitopes all belong to the same cluster defined on HLA class I molecules, but differ from one HTA subset to another. These results would therefore suggest that HTA and HLA class I antigens display a limited structural homology, but have a conserved epitopic area whose detailed structure differs for each HTA subset. Furthermore, the cell surface expression of each HTA class I molecule type is differently enhanced by natural interferon (IFN)-alpha or -gamma. This result additionally supports the serologic delineation of HTA subsets, and suggests that the corresponding genes in Molt-4 cells, are subjected to distinct regulations.

Animals↗
PubMed1989

Functional characterization of mononuclear cells of normal and hypercholesterolemic rabbits.

Cholesterol-fed rabbits are more susceptible to respiratory and skin infections, and show a higher index of mortality than rabbits given a normal diet. Several tests were employed to estimate the proportion of T and B lymphocytes (L-T and L-B) and aspects of their physiology in rabbits with hypercholesterolemia. The proportion of L-T and L-B in hypercholesterolemic rabbits (HChR) was found to be similar to that of normal rabbits (NR). The proliferative response of mononuclear cells (MNC) from peripheral blood stimulated with mitogens in HChR decreased during the first ten days of the cholesterol rich-diet, being variable afterwards. The addition of HChR serum to the culture media decreased the proliferative response of MNC isolated from both HChR and NR and stimulated by Con A and PWM. A similar antibody response to sheep red blood cells (SRBC) and bovine serum albumin (BSA) antigens was found in HChR and NR.

Animals↗
PubMed1987

T3-T cell receptor (Ti) complex-independent activation of T cells by wheat germ agglutinin.

The T3-Ti complex appears to play a central role in the activation of T cells by antigens and mitogens. Wheat germ agglutinin (WGA) is a unique lectin which inhibits T cell proliferation induced by mitogens, but it also induces marked IL 2 production by peripheral blood T cells. The pattern of responses induced by WGA suggests that this lectin may use a different mechanism of T cell activation other than the mechanism employed by the common T cell stimulants. We first investigated the production of IL 2 by Jurkat cells (E6-1) stimulated with WGA, before and after modulation of the surface T3-Ti complex. IL 2 production was markedly reduced after modulation of the T3 antigen from the cell surface when these cells were stimulated with PHA. In contrast, little change was observed in WGA-induced IL 2 production after modulation. Furthermore, we examined the effect of WGA on a T3-mutant of E6-1 cells (T3.1) which does not produce IL 2 in response to PHA or PHA plus PMA. WGA-stimulated T3.1 cells produced a significant amount of IL 2 with or without added PMA. In addition, a small but consistent rise in intracytoplasmic free calcium was observed when these cells were stimulated with WGA. These results demonstrate the presence of an alternative mechanism of T cell activation independent of the T3-Ti complex.

Acetylglucosamine↗
PubMed1987

Induction of calcium flux and enhancement of cytolytic activity in natural killer cells by cross-linking of the sheep erythrocyte binding protein (CD2) and the Fc-receptor (CD16).

Binding of the anti-cluster of differentiation (CD) 2 monoclonal antibody 9-1 causes an increase in the concentration of cytoplasmic-free calcium ([Ca2+]i) in cultured CD3-/CD16+ natural killer (NK) cells. This response did not occur in cultured CD3+/CD16- cytotoxic T lymphocytes (CTL). Anti-CD16 antibodies could partially block the calcium response when NK cells were stimulated with intact antibody 9-1, and antigen-binding fragment F(ab')2 of antibody 9-1 did not produce a calcium response. Thus an interaction of the 9-1 antibody with CD16 Fc receptors was required for the functional effect. The dual interaction of antibody 9-1 with both CD2 and CD16 was demonstrated by comodulation experiments. The cytolytic activity of cultured NK cells was increased by antibody 9-1 but not by F(ab')2 fragments of antibody 9-1. The enhanced lytic activity was blocked by anti-CD16 antibody, anti-CD18 antibody, and anti-CD2 antibodies that do not block the binding of antibody 9-1. This pattern was distinct from antibody-dependent cell-mediated cytotoxicity which was blocked only by the anti-CD16 antibody. Thus antibody 9-1 enhanced cytotoxicity by activating effector cells. There was no enhancement of lytic activity when F(ab')2 of antibody 9-1 were cross-linked with a polyclonal antiglobulin, even though [Ca2+]i was increased. These results show that induction of a [Ca2+]i response is not sufficient to enhance lytic activity in NK cells, and suggest that signals delivered through CD16 are necessary.

Antibodies, Monoclonal↗
PubMed1987

Human T cell clones use a CD3-associated surface antigen recognition structure to exhibit both NK-like and allogeneic cytotoxic reactivity.

In the present study, we developed human non-MHC-restricted CTL clones from human peripheral blood mononuclear cells activated in vitro with recombinant IL 2 and subsequently expended with PHA. The CD3/Ti+ clones were selected for their ability to exhibit non-MHC-restricted CTL reactivity by killing various tumor cell lines in culture, including the line K562 which does not express MHC antigens. We report that, at least for some of the NK-like T cell clones, it is possible to establish an allo-CTL activity, and that the CD3-associated surface antigen recognition structure might be involved in both reactivities.

Antibodies, Monoclonal↗
PubMed1987

Redistribution of platelet glycoproteins induced by allo- and autoantibodies.

The redistribution of platelet glycoproteins (GP) Ib, IIb and IIIa in response to stimulation with human platelet specific alloantibodies, autoantibodies and a quinidine-dependent antibody was investigated using immunofluorescence and a quantitative radioimmunoassay. The platelet GPs carrying the corresponding epitopes were determined using immunoblot technique or radioimmunoprecipitation. In accordance with previous results obtained with murine monoclonal platelet specific antibodies, redistribution upon stimulation with human platelet reactive antibodies was observed only due to reactions with epitopes on GP IIb, IIIa, respectively, but not on GP Ib. We therefore believe that membrane redistribution of human platelets induced by various antibodies is a function of the GP recognized by those antibodies rather than the source of the platelet reactive antibody.

Antibody Specificity↗
PubMed1987

Concanavalin A-induced electrokinetic changes and redistribution of receptors in mouse thymocytes.

Thymocytes are known to consist of mature and immature cells. The assessment of Con A-induced changes in electrophoretic mobilities (EPM) and receptor redistribution in thymocytes of AKR mice revealed two distinct sub-populations of cells. Sub-population A showed receptor redistribution and increase in EPM at low concentrations of Con A (5 micrograms/ml). Majority of these cells showed two sets of sequentially reacting receptor sites for the lectin. Cells belonging to sub-population B, in contrast, required higher concentrations (15-25 micrograms/ml) of Con A for the redistribution of receptors. Second set of receptors, reacting with Con A after the redistribution of the first set, could not be detected on these cells. High concentrations of Con A inhibited receptor mobility on all the thymocytes. The receptor redistributional profile of cells in the sub-population A was similar to that of mature splenic T-cells while cells in sub-population B resembled the immature leukaemic cells in this respect. These investigations provide an additional parameter to study cellular heterogeneity in thymus.

Animals↗
PubMed1987

Myasthenogenicity of human acetylcholine receptor synthetic alpha-subunit peptide 125-147 does not require intramolecular disulfide cyclization.

This study reports the synthesis of a disulfide-looped peptide corresponding to residues 125-147 (Cys 128-Cys 142) of the nicotinic acetylcholine receptor (AChR) of human skeletal muscle, H alpha 125-147 (Lys-Ser-Tyr-Cys-Glu-Ile-Ile-Val-Thr-His-Phe-Pro-Phe-Asp-Glu-Gln- Asn-Cys-Ser-Nle-Lys Leu-Gly), and a nondisulfide-looped analogue, H alpha 125-147(S) (Lys-Ser-Tyr-Ser-Glu-Ile-Ile-Val-Thr-His-Phe-Pro-Phe-Asp-Glu- Gln-Asn-Cys-Ser-Nle-Lys-Leu-Gly), in which the amino acid Cys 128 was replaced with serine. Both peptides induced antigen-specific helper T cell responses, as evidenced in vitro by lymph node cell proliferation and in vivo by production of anti-AChR antibodies. Rats immunized with 100 micrograms of either synthetic peptide, without conjugation to a carrier, produced anti-peptide antibodies which bound to native AChR in immunoprecipitation assays and induced modulation of membrane-bound AChR from cultured human myotubes. Both peptides also induced electrophysiologic and biochemical signs of experimental autoimmune myasthenia gravis. Thus, region 125-147 of the AChR alpha-subunit is at least partly exposed extracellularly in human muscle and contains one or more autoantigenic sites capable of stimulating T cells and B cells. Disulfide-linkage between residues Cys 128 and Cys 142 is not essential for myasthenogenicity.

Animals↗