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Biomedical subjects

H T Duc

Publications and source records attributed to H T Duc.

53 records · Page 3Linked to original sources
PubMed1972

Immune status of mice tolerant of living cells. II. Continuous presence and nature of facilitation-enhancing antibodies in tolerant animals.

CBA mice were rendered highly tolerant to A/Jax cells by neonatal intravenous injections of (CBA x A)F(1) spleen cells. The high degree of tolerance was ascertained by the absence of circulating antibodies detected in the sera by the usual tests and by the perfect state of A skin grafts during all the experiments. Tolerant sera (sera from tolerant animals) were studied at three periods of tolerance: before skin test grafting, from 2 to 11 wk after grafting, and at time of sacrifice at almost 6 months of age. The tolerant sera were shown to have specific facilitation-enhancing properties promoting the take and growth of A/Jax sarcoma (SaI and /Sa 15091a grafted on normal CBA mice. These properties were present throughout the duration of the experiments, showing that they were not the result of a beginning interruption of tolerance. The tolerant sera, although lacking the usual serological properties (hemagglutination, hemolysis, cytotoxicity, passive cutaneous anaphylaxis) had, however, specific synergistic hemagglutinating properties (increasing the hemagglutinating titer of a reference immune serum). Antibodies giving direct specific hemagglutination could be extracted from spleens of 20% of highly tolerant mice. The tolerant sera were also found to contain more IgG1 and more IgA than normal sera while they contained normal quantities of the complement-fixing immunoglobulins IgG2 and IgM. Fractionation of tolerant sera on DEAE chromatography column confirmed the data concerning immunoglobulin classes and demonstrated direct specific serological activities undetected in unfractionated sera: a weak hemolysis in the most cationic fractions and a weak hemagglutination in the middle fractions. Synergistic hemagglutination, detected in unfractionated serum, was localized in fast anionic fractions containing high IgA concentration, along with facilitation-enhancing activity, thus confirming a link suggested previously between these three properties. The relation between immunological tolerance and facilitating antibodies was discussed in the light of the fact that antibodies, possibly of a particular class continuously present at low dose in the sera of highly tolerant animals, are able to transfer (at least partly) this state of tolerance provided a sensitive test system is utilized.

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Effects of placental extracts on the immune response to histocompatibility antigens: class deviation of alloantibody response and allograft enhancement.

Placental extracts obtained from CBA (H-2k) mice during syngeneic (CBA female X CBA male) pregnancy were evaluated for their capacity to deviate the immune reaction of CBA mice toward A/J(H-2a) immunizing spleen cells, as tested by alloantibody subclass formation and Sa 1 allograft accelerated rejection-or enhancement. The immunomodulatory activity appeared to be located in the soluble and in the insoluble extracts of placenta. The sodium deoxycholate (SDO) solubilized proteinic material, fractionated on Concanavalin A [Con A] and injected to CBA mice simultaneously with A/J spleen cells caused a suppression of the hemagglutinating titer and C-mediated cytotoxicity (IgG2). However, it also favoured antibody-mediated mast cell degranulation (IgG1) and Sa 1 allograft enhancement. The presence and role of IgG1 antibodies in both tumor enhancement and gestation has been described. It is concluded that placenta contains Con A-binding glycoproteins which are located in the membranes and released in soluble form. They exert their immunomodulatory effect in a way which might help the successful outcome of pregnancy as it helps to enhance the development of allografted sarcoma.

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In vitro and in vivo comparative studies on immunosuppressive properties of cyclosporines A, C, D and metabolites M1, M17 and M21.

Cyclosporine A (CsA) and its major metabolites: M1, M17 and M21 and two analogues: cyclosporines C (CsC) and D (CsD), were studied for their capacity to interfere with different in vitro activation pathways. Their inhibition potentials against the reaction of Graft-versus-Host (GvH) were also studied. The results showed: CsA, CsC and metabolite M17 were the most active compounds upon the inhibition of lymphocyte proliferation induced by different mitogens (ConA, PHA, PWM) and also on the proliferation of mixed lymphocyte cultures (MLC). The same results were observed concerning the direct activation by protein kinase C using a combined action of phorbol ester + calcium ionophore. In vivo using local GvH reaction, CsA and CsC proved more active than M17 in the two different combinations: H-2d --> (H-2b x H-2d)F1 and H-2k --> (H-2b x H-2k)F1 CsD and two metabolites M1 and M21 showed no or weak immunosuppressive effects. Overall, the immunosuppressive potency of six compounds could be schematized as: CsA > or = CsC > M17 > M1 > or = CsD > M21.

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IGF-I triple helix strategy in hepatoma treatment.

BACKGROUND/AIMS: To investigate the effect of gene therapy for hepatocellular carcinoma based on inhibition of cellular IGF-I expression, the technique of IGF-I triple helix was investigated in mice developing programmed hepatoma. METHODOLOGY: mhAT1F1 mouse hepatoma cell line was transfected in vitro with IGF-I triple helix expression vector (pMT-AG-TH) or with IGF-I antisense expression vector (pMT-Anti-IGF-I). 10 x 10(6) transfected cells of either triple helix or antisense type were inoculated intraperitonealy into transgenic ATIIITB6 mice developing genetically programmed hepatoma (mice die between the age of 6 and 7 months). In parallel, human cell cultures established from surgically removed hepatomas were investigated. RESULTS: mhAT1F1 and human primary cell cultures, transfected with pMT-AG-TH or pMT-Anti-IGF-I vectors resulted in total inhibition of IGF-I demonstrated by immunocytochemical and Northern blot techniques. Transfected cells changed their phenotype and recovered major histocompatibility complex I expression showed by fluorescence-activated cell sorting analysis and Western blot. Moreover, two phenomena were observed in IGF-I "antisense" or "triple helix" transfected cells: 1) the apoptosis, demonstrated by TUNEL technique; 2) the presence of IL-6 simultaneously with disappearance of tumor necrosis factor-alpha and IL-10, investigated by reverse transcriptase-polymerase chain reaction technique. In in vivo experiments, injection of murine transfected cells into mice in terminal-phase prolonged their survival 3-4 months in 100% of cases, as well in "antisense" group (8/8) as in "triple helix" group (10/10). CONCLUSIONS: Injection of hepatoma cells transfected with IGF-I triple helix expression vector, and showing immunogenic and apoptotic characteristics, can constitute an effective cellular therapy against hepatocellular carcinoma.

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[Antigenic sites implicated in tumour allograft enhancement].

Allo-immune sera were prepared by injecting CBA mice with spleen or thymus cells, or by two consecutive skin grafts of A/Jax origin. When absorbed 6 to 8 times on glutaradahyde treated A/Jax red blood cells (RBC), these sera lost all their haemagglutinating activity (anti- "SD" antibodies, predominantly H-2D) While their cytotoxic activities on A/Jax lymphocytes (anti-LD antibodies, perdominantly Ia, H-2IC) were partially preserved. Antibodies (anti-"XD") eluted form A/Jax RBC treated with an 0.5 M NaCl--HCL glycincing activity of these preparations was tested using SaI (A/Jax) grafts in CBA mice. Our results suggest that SD antigens are the main target of the enhancing effect. Further results obtained with DBA/2 anti-EL4 (C57Bl/6) sera confirmed this interpretation. Experiments performed with anti-idiotype and anti-recognition structure sera using tumor allograft targets, did not reveal any clear cut effect. Their relevance in tumor enhancement appears therefore doubtful.

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PubMedDate not supplied

Ia versus K/D antigens in immunological enhancement of tumour allografts. II. Studies with alloimmune sera prepared in recombinant strains.

Previous studies have demonstrated that anti-K/D antibodies obtained by specific absorption on and elution from relevant red blood cells were capable of inducing enhancement of tumour cells in allogeneic hosts. Anti-Ia antibodies were not found enhancing except when alloimmune sera prepared by skin grafts were used. In the present report, anti-H-2K and anti-H-2D or anti-H-2I sera were obtained in mouse recombinant strains, in order to obviate such absorption and elution procedures. It has been shown that SaI-tumour cells (H-2a, i.e. H-2k/d) can be enhanced in allogeneic recipients, CBA (H-2k) or C57BL/Ks (H-2d) by antisera directed towards H-2Dd or H-2Kk. Alloimmune sera directed towards H2i-coded antigens prepared by immunization with spleen cells had no enhancing activity on the same tumour allografts in the CBA-A/J strain combination anti-IC'D,Sd,Gd) but caused a transitory effect in the C57BL/Ks-A/J combination (anti-IA'K,IBk,IJk,IEk).

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The possibility of antiidiotypic activity in multipareous mice.

CBA females pregnant of A/J males were tested for the presence in their sera of antiidiotypic antibodies, capable of combining with antipaternal Ig determinants. Radioimmunoassay tests have shown that in comparison to females pregnant of isogeneic males, allopregnant sera presented values indicating the presence of an antiidiotypic reaction in five out of seven trials. The possible role of antiidiotypic reactions in the control of maternofoetal relationship is discussed.

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[Responsible agents and mechanisms of direct allogeneic anaphylactic degranulation].

Because mast cells from inbred mice possess both H-2 Ag and Fe receptors they can be degranulated by anaphylactic allo-Ab (DAAD). Beside IgG1, IgE allo-Ab were shown to exist and to be able to achieve DAAD. So far, to be the target of DAAD, an Ag must be present on the mast cell membrane and presumably not linked to the Fe receptor. The mechanism of DAAD involves very likely a double interaction of the Ab (by its two reactive ends) with the mast cell membrane.

Anaphylaxis↗
PubMedDate not supplied

Antisense insulin-like growth factor I transferred into a rat hepatoma cell line inhibits tumorigenesis by modulating major histocompatibility complex I cell surface expression.

We have established a hepatocarcinoma cell line (LFCI2 A) that produces voluminous tumors when injected subcutaneously into syngeneic Commentry rats. These neoplastic cells express both insulin-like growth factors (IGF) I and II. When transfected with an episomal cassette-expressing IGF-I antisense RNA, the modified LFCI2 A cell lines become poorly tumorigenic and, when injected subcutaneously, are associated with inhibition of the growth of the parental tumoral cells and/or induction of regression of established tumors. By contrast, cell lines isolated after transfection with the IGF-II antisense-expressing vector were as tumorigenic as the parental cell lines. The results are discussed in terms of protective immunity induced by the tumoral cells transfected by the IGF-I antisense vector. In the transfected hepatocarcinoma cells that do not produce IGF-I, the expression of major histocompatibility complex class I antigen was increased at least 4-fold compared with parental cells. The introduction of these cells in vivo induced a tumor-specific immunity that was associated with CD8 T cells.

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