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Biomedical subjects

H T Duc

Publications and source records attributed to H T Duc.

At least 37 records · Page 2Linked to original sources
PubMed1990

Differential modulation of the in vitro lymphocyte activation pathways by soluble and solubilized placental substances.

Soluble and detergent-solubilized placental extracts were studied for their modulatory effects upon the proliferation of lymphocytes stimulated by various activating agents. It was shown that soluble placental extract (SPE) exerted an inhibitory effect on the lymphoproliferation triggered by alloantigen or LPS but not by Con A or the combined action of PMA + calcium ionophore A 23187. This effect was also observed with SPE precipitated by 30% of ammonium sulfate (SPE30). On the other hand, a solubilized placental extract (SzPE) that was obtained by using octyl-beta-D-glucopyranoside inhibited the stimulation triggered by alloantigen, LPS, and Con A but did not affect the protein kinase C pathway. The modulatory effects were observed not only when SPE (or SPE30) and SzPE were added at the time of culture initiation but also at 24 h before or after the activating agents. Preincubation with SPE30 or SzPE immobilized on plastic surface, however, transduced an enhanced lymphoproliferative response to alloantigen and mitogen Con A but not to LPS. The above results suggest that placental substances exerted their modulatory effects by interfering mainly with the antigen or mitogen lymphoproliferation pathways.

Adjuvants, Immunologic↗
PubMed1987

In vitro immunomodulatory effects of placental substances on preparatory MLR and resulting modifications of lymphocyte reactivities.

The immunomodulatory effects of murine placental extracts (PE) were studied in vitro using mixed lymphocyte culture (MLC) and resulting cell-mediated lympholysis (CML). The results showed that preparative cultures in the presence of PE syngeneic to the responding cells led to a low secondary MLR response with a concomitant generation of suppressor cells. At the efferent phase, cells from the same preparative culture showed a weaker cytotoxic activity than controls cultured in the absence of extract. Furthermore, the induction of regulatory cells able to inhibit CTL in vitro activity was also observed. The active substances can be found in the 30% ammonium sulphate precipitate as well as in some gel filtration fractions showing several main bands from 115 to 43 kDa in SDS-PAGE.

Animals↗
PubMed1985

Evolution of alloantibodies and suppressor cells in allografted mice treated for passive enhancement.

The kinetics and quality of the alloimmune reaction were studied in CBA (H-2k) mice treated for passive enhancement of tumor allografts (Sa 1 indigenous of A/J (H-2a or H-2k/d) mice). Serum samples of treated animals were tested for their biological properties relevant to different antibody isotypes in vitro (hemagglutination, complement-dependent cytotoxicity, and anaphylaxis, i.e., mast cell degranulation involving all main Ig isotypes; IgM, IgG2, and IgG1, IgE, respectively) as well as in vivo (allograft enhancement). Spleen cells from these treated animals were examined for their capacity to interfere with the rejection of tumor allografts by adoptive transfers into syngeneic recipients. In vitro, 51Cr release cytolysis assays were performed in order to test their cytolytic and regulatory activities in comparison to rejecting control animals. It has been shown that: grafted mice, pretreated for passive enhancement, kept their grafts longer and synthetized anaphylactic antibodies (mainly IgG1) earlier and at higher titers than normal serum controls, which rejected the same Sa 1 allografts. Mice with enhanced tumors synthetized cytotoxic antibodies (mainly IgG2) later than rejecting controls. Serum samples from treated and control animals, harvested 10 days (early sera) and 30 days (late sera) after grafting, were injected with a "normal dose" (0.2 ml) and a "high" dose (0.4 ml) to new CBA recipients grafted with Sa 1. Early immune sera were only enhancing at high doses when derived from animals previously treated for enhancement (at the low dose both immune sera were enhancing). Late sera, presenting both complement-fixing, cytotoxic (predominantly IgG2), and IgG1 anaphylactic alloantibodies in the two groups, induced enhancement in all cases, but more strongly when derived from the group treated for Sa 1 enhancement. Adoptive transfer of spleen cells from animals treated for passive enhancement were able either to inhibit the accelerated rejection (Day 10) or to promote enhancement of Sa 1 allogeneic cells (Day 30) while similar cells taken (Day 10 and Day 30) from control graft-rejecting mice transferred accelerated rejection. Among the transferred T-cell sub-populations, the suppressive effect was mediated by Lyt 2 T cells. In vitro, these spleen cells showed a weaker cytolytic activity than those of allograft-rejecting mice. Moreover, they were able to regulate the cytolytic activity of cytotoxic effector cells from specifically immunized CBA mice.

Animals↗
PubMed1985

Deviation of humoral and cellular alloimmune reactions by placental extracts.

Modifications of the alloimmune response at both the humoral and the cellular levels by placental extracts (PE) syngeneic to the recipient were studied in the mouse using two different H-2 strain combinations. CBA (H-2k) or C57BL/Ks (H-2d), immunized with A/J (H-2a) spleen cells. The tests included in vivo tumor allograft evolution (accelerated rejection or enhancement reactions), and in vitro analysis of the involved immune agents, both cellular and humoral, using mixed lymphocyte reactions (MLR) and biological activity studies of serum samples. Animals from the recipient strains exhibited a delayed rejection of A/J tumor Sa 1 allografts if preimmunization was carried out with 10(6) A/J spleen cells combined with PE syngeneic to the recipients, as compared to controls immunized with A/J cells only or supplemented with isogeneic liver extracts (LE). The serological analysis revealed that PE treatment did not modify the overall hemagglutinating antibody production but resulted simultaneously in both a decreased production of cytotoxic complement fixing antibodies and an increase of specific anaphylactic mast cell degranulating antibodies, as compared to controls. The sera from PE-treated donors also demonstrated enhancing activity following passive transfer to isogeneic recipients. MLR regulatory activity was exhibited by spleen cells from PE- and immunogen-treated mice although the same or stronger activity was obtained from mice immunized without the addition of PE. However, in vivo transfer of these cells to syngeneic recipients showed that PE treatment erased the accelerated rejection caused by allogeneic immunization in the absence of PE and could even cause some degree of allografted tumor enhancement. The cells responsible for this inhibitory effect were mainly IJ+ lymphocytes, since their elimination with a relevant anti-IJ serum and complement restored a secondary type rejection pattern. These results show that PE present during the onset of immunization can promote the activation of regulatory agents such as enhancing antibodies and suppressor cells favoring allograft survival.

Animals↗
PubMed1985

Activation of the human classical complement pathway by a mouse monoclonal hybrid IgG1-2a monovalent anti-TNP antibody bound to TNP-conjugated cells.

A mouse hybridoma selected and cloned for anti-TNP specificity produced three distinct monoclonal antibody species that were separated on protein A-Sepharose by stepwise acid elution. The IgG1 kappa product of the parental myeloma was eluted at pH 6.0. An IgG2a kappa bivalent anti-TNP antibody was eluted at pH 4.5, whereas elution at pH 5.0 yielded a hybrid IgG1-2a kappa monovalent anti-TNP antibody. The IgG2a molecules agglutinated TNP-conjugated sheep erythrocytes (TNP-ES) and lysed TNP-ES in the presence of normal human serum (NHS). Hybrid IgG1-2a antibody was also capable of lysing the cells in NHS, although it did not agglutinate TNP-ES. A threshold in monovalent antibody input was necessary for the lysis of TNP-ES, indicating a requirement for a minimal density of bound monovalent IgG to trigger complement activation. Lysis occurred in NHS-VBS++ but not in NHS-MgEGTA, and it was associated with a dose-dependent consumption of C1, C4, and C2 hemolytic activities. Quantitation of the antibody bound to TNP-ES when using radiolabeled rabbit anti-mouse Fab antibody demonstrated that for similar inputs, 5.4 times as much bivalent as monovalent antibody bound to TNP-ES. When similar amounts of antibody were effectively bound to TNP-ES, monovalent hybrid IgG1-2a was five times less efficient than bivalent IgG2a to yield 50% cell lysis in the presence of NHS. These results indicate that neither bivalent binding nor the presence of two identical heavy chains are necessary requirements for antibody-dependent activation of the classical complement pathway.

Agglutination↗
PubMed1982

Passive allograft enhancement by subclasses of polyclonal antibodies directed toward restricted regions of the major histocompatibility complex.

Two parameters of enhancing major histocompatibility complex (MHC) antibodies, previously separately studied, namely, Ig class and antigen specificity, have been treated simultaneously. In the experimental model used, Sa 1 tumor cells, indigenous of A/J (H-2a) were grafted on CBA (H-2k) or C57BL/Ks (H-2d) mice. Immune sera specific for the H-2 K/D- or H-2 I coded antigens of the A/J haplotype (anti-Kk, or IAk, IBk, IJk, IEk, or ICd, Sd, Gd, or Dd) and their immunoglobulin fractions (separated on protein A-Sepharose columns) were injected either i.v. or locally as mixture with the challenging Sa 1 cells. Within the limits of the studied system, the following results were obtained: (1) Sa 1 cells do possess Iak antigens at their surface detected by C-dependent cytotoxicity; no ICd, Sd, or Gd products were detected. (2) The bulk of enhancing activity is concentrated in IgG1 anti-K/D antibodies (anti-Dd when Sa 1 was grafted on CBA mice and anti-Kk, on C57BL/Ks). (3) Anti-Iak antibodies have some activity on Sa 1 cells grafted on C57BL/Ks mice. This activity is significant for IgG1 anti-Iak and suggestive for IgG2 of the same specificity. (4) No enhancing activity was detected in the other antibodies: IgG2 anti-Dd, IgG2 anti-Kk, IgG1, or IgG2 anti-ICd, Sd, Gd as well as in fractions containing IgM and IgA antibodies directed against any studied portion of the MHC products. This results are discussed in terms of the mechanisms involved in enhancement.

Animals↗
PubMed1978

Ia versus K/D antigens in immunological enhancement of tumor allografts.

The respective role of anti-H-2 K/D and anti-H-2 Ia antibodies in allotransplanted tumor enhancement was tested in vivo on two experimental tumors. Sa I A/4 (H-2a, i.e., H-2k/d) was enhanced in CBA (H-2k) and C57BL/Ks (H-2d) strains with anti-A/J immune sera prepared in CBA and C57BL/Ks, respectively. EL 4, C57BL/6 (H-2b) lymphoma, was enhanced in DBA/2 (H-2d) and BALB/c (H-2d) with immune sera prepared in DBA/2 and BALB/c. Anti-K/D antibodies were obtrained by elution from glutaraldehyde-treated RBC previously incubated with corresponding alloimmune sera prepared in mice immunized with spleen cells, thymocytes, or two consecutive skin grafts syngeneic to the RBC. The residual complement-dependent serocytotoxicity for target lymphocytes observed after complete hemagglutinin absorption on corresponding RBC was attributed to anti-Ia antibodies. RBC eluates (anti-K/D) were found to be enhancing for both experimental tumors and for all studied sera. After RBC absorption, the sera lost all enhancing activity when they were prepared by immunization with spleen or thymus cells, but remained enhancing in some sera prepared by immunization with skin grafts. Both types of antibodies (anti-K/D and anti-Ia) therefore appear able to enhance allografts. These results are compatible with the in vitro correlates of the two phases of the transplantation reaction: initiation phase (mixed lymphocyte reaction) inhibitable by anti-Ia and effector phase (cell-mediated cytotoxicity) inhibitable by anti-K/D.

Animals↗
PubMed1978

Evaluation of in vitro and in vivo activities of isoantibodies directed against idiotypes and recognition structures for transplantation antigens.

Anti-idiotype sera were prepared by injection of CBA anti-A/JAX serum with or without adjuvant into CBA mice. These sera were tested in allocluster inhibition and passive enhancement-facilitation. While the anti-idiotype sera inhibited allocluster formation, particularly when prepared with complete Freund's adjuvant, they had virtually no effect on enhancement of Sa I grafted in CBA mice except for a marginal prolongation of graft survival in one out of three experiments. Anti-RS serum was prepared by immunizing (CBA X A)F1 mice with CBA thymus or spleen cells. The sera were tested in local graft-versus-host inhibition and passive enhancement. F1 anti-CBA thymus serum inhibited the local graft-versus-host reaction but had no enhancing effect. F1 anti-CBA spleen serum was virtually ineffective in both tests although a slight tendency to graft-versus-host inhibition was noted. The relative contribution of anti-idiotype and/or anti-RS antibodies to transplantation reactions is discussed.

Animals↗
PubMed1976

An ultrastructural study of two different responses of mouse mast cells to transplantation antibodies directed against the same transplantation antigens.

The present paper describes an ultrastructural study of two different kinds of behavior of mouse mast cells during two immunological reactions induced by transplantation antibodies: the direct allogeneic anaphylactic degranulation and the serocytotoxicity. In both situations, the same alloantigens, born by the mast cells themselves, are the targets of the reaction, but the first one is mediated by anaphylactic alloantibodies whereas the second one is mediated by cytotoxic alloantibodies in the presence of complement. The comparison of the ultrastructural aspects of the cells in these two systems demonstrated that mast cells can behave in two different ways depending on the nature of the immunological agents utilized. First, a physiological degranulation process with active granule expulsion was observed. This process was shown to be identical to the one induced in classical in vitro anaphylaxis or by histamine releasers such as compound 48/80. A second type of behavior was a lethal, complement-dependent, cell lysis without active granule expulsion.

Anaphylaxis↗
PubMed1975

Biologic properties of transplantation immune sera. IV. Influence of the course of immunization, dilution and complexing to antigen on enhancing activity of Ig classes.

The influence of the course of immunization on the facilitating-enhancing activity of antibody classes has been studied by passive enhancement of growth of A/JAX sarcomas in CBA and IC mice and of C57BL/6 EL 4 leukemia in BALB/c mice. The influence of dilution of antibodies and complexing to antigens was also studied. During immunization (with several boosters), the enhancing capacity of sera increased together with 7S IgG antibody activity, but showed no correlation with 19S IgM antibody activity. It also was mercaptoethanol resistant. IgG1 to be more enhancing than an equal number of hemagglutinating units of IgG2a. When concentrated on a small amount (10(5)) of target sarcoma I cells, complement-fixing IC anti-A antibodies were even inhibitory on Sa I allografted to IC recipients. Progressive dilutions reversed this situation, IgG1 activity disappearing and IgG2 acquiring enhancing activity. After complexing to corresponding antigens IgG2 also (and immune sera with inhibitory properties) acquired enhancing properties. These results may provide a basis for understanding the discrepancies between the results of several groups of authors studying the class(es) of enhancing anibodies.

Animals↗