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Biomedical subjects

D Juy

Publications and source records attributed to D Juy.

31 records · Page 2Linked to original sources

Damage of liposomes in antibody-dependent cell-mediated cytotoxicity.

Lymphoid cells bearing Fc receptors are able to lyse antibody-coated animal target cells in an antibody-dependent cell-mediated cytotoxicity reaction. The results presented here show that liposomes consisting of sphingomyelin, cholesterol, and cardiolipid and coated by cardiolipidic antibodies could be destroyed by spleen or thymus cells. No alteration of liposomes was observed when normal rabbit serum was used or when the effector cell population was depleted of cells bearing Fc receptors. The lysis of antibody-coated liposomes by effector cells could be carried out in two steps. In the first step, the fixation of antibodies on the cardiolipidic antigens could lead to a reorganization of the liposomal membrane. In the second step, the effector Fc-receptor-bearing cells might amplify this alteration of the liposomes.

Animals↗

Failure of endotoxin to increase nonspecific resistance to infection of lipopolysaccharide low-responder mice.

In vitro and in vivo responses to lipopolysaccharide (LPS) and various other bacterial immunostimulants were compared in c3H/He low-responder mice. The principal findings were as follows. (i) Their splenic lymphocytes were stimulated by various gram-negative mitogens such as an Escherichia coli peptidoglycan, a detoxified derivative of LPS, and even endotoxins extracted by trichloroacetic acid that are known to contain protein; spleen cells of these mice were also transformed by two other B-cell mitogens extracted from acid-fast organisms. (ii) Their macrophages were refractory to LPS and weakly responsive to a mycobacterial prepartion. (iii) LPS failed to elicit nonspecific resistance in these mice against Klebsiella pneumoniae infection. (iv) Endotoxin extracted by trichloroacetic acid and a mycobacterial preparation that could increase nonspecific resistance to infection in other strains did not protect C3H/He mice against a challenge by K. pneumoniae, although both prepartions could evoke nonspecific responses of B cells in this low-responder subline.

Animals↗

Cell suppression in PPD-induced blast specific response of human peripheral blood lymphocytes.

Secific stimulation of T-cells by PPD was inhibited by their autologous B cells. This inhibition was obtained with B cells separated either by depletion of E-RFC or by elution, with human IgG of lymphocytes bound to Sephadex beads coated with rabbit antibodies anti-human Fab fragments. The suppression was proportional to the number of B cells added to 10(6) T cells incubated with PPD and as previously reported was more marked in the case of B or T cells from BCG-vaccinated subjects with negative skin tests. The suppressive phenomenon required viable B cells and was inhibited by cycloheximide but was not altered by pretreatment of suppressor cells with actinomycin D or colchicine. It seems that B-suppressor cells interfere with recognition of PPD by T cells rather than with the proliferative phase of the specific blast response. Using various surface markers (i.e. Ig, C3 and Fc receptors) it was shown that the suppressor cells represent a subset of Ig-bearing B cells which do not carry Fc receptors.

Antigens↗

Human lymphoblast cell lines: antibody-dependent cytotoxicity.

Five cell lines were isolated after prolonged culture of human buffy coat leukocytes. The cells consisted for the most part of lymphoblasts morphologically similar to those produced by in vivo or in vitro stimulation of small lymphocytes by antigens or mitogens. One of the lines possessed virus-like particles of the Epstein-Barr type. All the established lines were capable of mediating antibody-dependent cytotoxicity (LADC) quantitatively at a level not significantly different from that mediated by freshly isolated, normal human peripheral blood lymphocytes (PBL). The LADC of the lymphoblasts was inhibited by all the human IgG subclasses tested (IgG1, IgG2, IgG3, IgG4) as was the LADC of PBL. It is concluded that, at least so far, the lymphoblasts have retained the properties of the lymphocytes from which they were originally derived as regards their ability to mediate LADC.

Antibodies↗

Comparison between macrophage activation and enhancement of nonspecific resistance to tumors by mycobacterial immunoadjuvants.

It has repeatedly been observed that various bacterial preparations could increase the host's resistance to tumors. It has also been shown that after nonspecific activation by BCG (bacillus Calmette-Guérin), peritoneal macrophages could inhibit in vitro the growth of neoplastic target cells. In the present study a fraction extracted from Myobacterium smegmatis and referred to as interphase material was tested in view of measuring its ability to activate macrophages in vitro and in vivo. This preparation was previously shown to protect mice against a syngeneic leukemia and to increase the immune response of the guinea pig. Other water-soluble adjuvants devoid of demonstrable antitumor activity in vivo were also assayed. The results argue in favor of a correlation between adjuvant activity and the capacity of activating macrophages. Moreover, interphase material administered in vivo consistently induced stronger and more persistent stimulations of macrophages than the other preparations assayed.

Adjuvants, Immunologic↗

Polyclonal B-cell activation by influenza A/Texas virus-specific human T-cell clones.

A previously described proliferating class-II-restricted CD4+ human T-cell clone (TA4) specific for the N2 neuraminidase of the influenza A/Texas virus was tested for its ability to induce B cells to polyclonal immunoglobulin (Ig) production. The data reported in the present study show that, when stimulated by T-depleted autologous peripheral blood mononuclear cells (E-) and A/T virus, the TA4 clone was able to induce B cells to polyclonal Ig production. This effect was also seen using another class II-restricted human T-cell clone specific for the H3 haemagglutinin of the A/Texas virus and autologous polyclonal T cells. This Ig production was MHC-restricted at the inductive level, i.e., the stimulating-virus-treated E- population and the clones or the T cells had to share the same HLA-DR determinants. However, the responding B cells could be allogeneic provided the helper T cells were activated in the presence of autologous irradiated virus-infected E- cells.

Antibodies, Viral↗

[Influence of injection of cortisone acetate on blast transformation and antibody-dependent cell-mediated cytotoxicity in rabbit (author's transl)].

Inhibition of circulating antibody production by steroids has been repeatedly shown in steroid-sensitive animals such as mice or rabbits. It is well known that after a single injection of 5 mg of cortisone acetate, mouse spleen cells loose their ability to be transformed by B cell mitogens such as lipopolysaccharides or Nocardia water soluble mitogen. Therefore it was of interest to study in the rabbit the influence of cortisone on the reactivity of spleen cells to a B cell mitogen (blast transformation and polyclonal strimulation) and their ability to be cytotoxic in the antibody-dependent cell-mediated cytotoxicity assay. Our data demonstrate that the cells which mediate such a cytotoxicity are cortisone-resistant whereas the B lymphocytes--which can be transformed and polyclonally activated by these mitogens--are sensitive to cortisone treatment.

Animals↗