Biomedical subjects

G Bordenave

Publications and source records attributed to G Bordenave.

At least 37 records · Page 2Linked to original sources

PubMed1992

Plasmodium chabaudi and Trypanosoma cruzi infections can reverse IgG2ab chronic suppression in mice.

The effects of infections with Plasmodium chabaudi or Trypanosoma cruzi on chronic CD8+ T cell dependent IgG2ab suppression were analyzed in homozygous Ighb/b adult mice. These parasites are known to induce a CD4+ T cell dependent polyclonal activation characterized in particular by a considerable increase in IgG2a expression. We report here that infection with either parasite reversed the IgG2ab suppression in 18 out of 32 mice. However, in mice treated with anti-CD4 mAb in parallel to the parasite infection, the polyclonal activation was largely reduced and the suppression of IgG2ab expression was always maintained. The parasite induced escape from suppression could result from increased helper T cell activation stimulating some of the Ig production. A weakening of the CD8+ T cell activity which is specific of IgG2ab could also contribute to the IgG2ab production. Both effects would shift the previous equilibrium which was in favour of suppression to a new balance allowing expression of the IgG2ab allotype.

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PubMed1989

T cell-induced Ig allotypic suppression in mice. II. Both CD4+ CD8- and CD4- CD8+ T cell subsets from sensitized Igha mice are required to induce suppression of Igh-1b allotype expression.

We established the phenotype of T splenocytes (Ts) from Igha/a BALB/c mice sensitized against B splenocytes from the Ighb/b CB20 congenic mice that induce Igh-1b (IgG2a of the Ighb haplotype) suppression. This was achieved by studying the action of anti-T cell subset mAb on the capacity of Ts to induce this chronic allotypic suppression in Igha/b (BALB/c x CB20)F1 mice. The Ts were treated with cytotoxic anti-mouse CD4 or anti-mouse CD8 rat mAb in vitro before their injection into the Igha/b newborns or in vivo after their injection into the Igha/b newborns. Exposure to either anti-CD8 or anti-CD4 mAb in vitro or in vivo leads to loss of the capacity of Ts to induce Igh-1b allotypic suppression. Mixing CD4+-cell-depleted Ts and CD8+-cell-depleted Ts preparations restored the capacity of the cells to induce Igh-1b suppression. Thus, both CD4+ CD8- Ts and CD4- CD8+ Ts are required for the induction of this allotypic suppression. Bone marrow cells and B splenocytes from Igh-1b-suppressed adult Igha/b mice were shown to be able to durably express Igh-1b when transferred into irradiated Igha/a BALB/c hosts whereas whole spleen cells from such donors failed to do it. Abrogation of Igh-1b suppression by in vivo anti-CD8 mAb treatment was achieved in adult Igha/b heterozygotes but with a lower efficiency than in adult Ighb/b homozygotes, all being chronically Igh-1b suppressed. The CD4- CD8+ cell population essential for maintaining this suppression is resistant to in vivo 600 rad irradiation and seems to be slightly inhibited by in vivo administration of free Igh-1b.

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PubMed1988

Cellular induction of chronic allotype suppression of IgG2a in Ighb/b homozygous mice and its abrogation by in vivo treatment with anti-CD8 monoclonal antibody.

We report here the successful induction of allotype suppression in homozygous Ighb/b mice (CB20 or C57BL/6) by neonatal injection of T splenocytes from Igha congenic sensitized mice (BALB/c or BC8, respectively). The sensitization of the T cell donors was achieved by two intravenous injections of B splenocytes from Ighb congenic mice. Treated homozygous Ighb/b mice developed, as of 16-24 wk of age, a chronic suppression of Igh-1b expression (IgG2a of Ighb haplotype). The other productions tested (IgM, IgD, and IgA) of Ighb haplotype were unaffected. In vivo treatment with cytotoxic anti-CD4 or anti-CD8 mAb of mice subjected to chronic Igh-1b suppression clearly showed that CD8+ lymphocytes (suppressor or cytotoxic cell) were essential for the maintenance of the suppression. The suppression was indeed abrogated after a 1-wk treatment with anti-CD8 mAb containing culture supernatant, whereas, the anti-CD4-treated mice continued to be subjected to suppression. This anti-CD8 in vivo treatment was shown to have no effect on thymus but to severely reduce the percentages of CD8+ cells in spleen and in peripheral blood without affecting the percentages of CD4+ cells, leading to a large and rapid Igh-1b expression (up to 0.5 mg per ml of serum, the day after the end of the treatment). This suppression abrogation, and thus the Igh-1b expression, was either transient or permanent. When it was transient, a second 1-wk treatment with anti-CD8 mAb containing culture supernatant induced once again a rapid and significant production of Igh-1b (up to 0.3 mg of Igh-1b per ml of serum).

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PubMed1988

Enhancement in Igha mouse strains of the "natural" suppressive activity of normal T splenocytes against the expression of Igh-1b allotype. I. Molecular aspects of the chronic suppression obtained.

Several approaches have been used in our attempts to increase the "natural" ability of normal T splenocytes (Tn) from BALB/c or BC8 mice (both Igha) to induce, in F1 hybrids, a suppression of Igh-1b expression (IgG2a of b haplotype). These heterozygous F1 were produced by mating these Igha mice and their Ighb-congenic partners (CB20 and C57BL/6, respectively). The most powerful approaches were to sensitize the Igha mice by either autologous splenocytes coated with Igh-1b or B splenocytes from Ighb-congenic mice. In F1 having paternally inherited the b haplotype the sensitized T splenocytes (Ts) prepared from such mice are able to induce, like Tn, when injected at birth, a chronic suppression of Igh-1b expression. However, the suppression was established with a much higher efficiency: already at 6 weeks of age in 100% of the F1 treated with 1 x 10(7) Ts, vs. a final rate of 70% progressively reached only at 42 weeks of age in the F1 treated with 4 x 10(7) Tn. In F1 having maternally inherited Ighb the differences were even more pronounced than with 4 x 10(7) Tn, i.e. the suppression induction was almost totally ineffective, whereas with 2 x 10(7)-4 x 10(7) Ts, a rate of 100% treated F1 subjected to suppression was reached at 19 weeks of age. As the productions of IgM, IgD and IgA of the b haplotype were not affected by the suppression, the Ts are believed to act on the Igh-1b+ cells. Attempts were also made to induce allotypic suppression of other b allotypes by the use, as sensitizing cells, of myeloma cells carrying Igh-6b (IgM of b haplotype). We failed in revealing any sign of a T cell reactivity against Igh-6b similar to the reactivity against Igh-1b. The use of Igh-6b+ myeloma cells grown in an Ighb or in an Igha background allowed us to assume that the cells responsible for the sensitization are, in the Ighb B lymphocyte population, either the Igh-1b+ lymphocytes or the lymphocytes having passively adsorbed this allotype, or both.

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PubMed1987

Normal T splenocytes are able to induce immunoglobulin allotypic suppression in F1 hybrid mice.

A chronic suppression of Igh-1b and Igh-3b (IgG2a and IgG2b of b haplotype) allotype expression has been induced by injecting T splenocytes from normal BALB/c or BC8 mice into newborn F1 hybrids of appropriate Igh congenic strains: BALB/c into (BALB/c Igha X CB20 Ighb)F1 and BC8 into (BC8 Igha X C57BL/6 Ighb)F1 or (C57BL/6 X BC8)F1. This suppression does not affect IgM (IgH-6b) or IgA (Igh-2b) expression. When the Ighb haplotype is paternally transmitted, the proportion of T splenocyte recipients showing allotypic suppression increases with time reaching 70% 40 weeks after birth. We also succeeded in inducing this pattern of suppression in 2 out of 13 cases when the Ighb was inherited from the mother. These normal T splenocytes are therefore clearly allotype specific. As Igh-6b production is not affected by the suppression, these T splenocytes are believed to influence B cells more or less committed to Igh-1b or Igh-3b production rather than more precocious Igh-6b (IgM of b haplotype) carrying precursors in the classical IgM-IgG filiation pathway.

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PubMed1987

Idiotypic relationships between allotypically different rabbit antibodies.

Homozygous rabbits genotypically different for the allotypy of the VH region and the C kappa region of their immunoglobulins (al/al, b4/b4 and a3/a3, b5/b5, respectively) were transferred together at the blastocyst stage to be born from the same foster mother. At the time of transfer the foster mothers were active anti-anti-idiotypic (Ab3) antibody producers and, according to their own genotype, the idiotypes (Ab1) which initiated the immunization cascade ending with their Ab3 were allotypically either a1,b4 or a3,b5. This experimental scheme was carried out, at the level of the Ab1 and of the Ab'1 (antibodies produced by the transferred rabbits subjected to the Ab3 action), with three different exogenous antigens, namely a protein, a polysaccharide and a hapten which elicited in normal rabbits the production of antibodies with private idiotypic specificities. Two of them, the protein and the polysaccharide enabled us to find idiotypic relationships between antibodies totally different for their allotypy and particularly for the allotypy of the variable region of their heavy chains. In these examples, the structural coercions implied by the different allotypic markers of the VH did not seem to prevent the association of at least related genetic elements responsible for the observed idiotypic community. In these idiotypic relationships, only subpopulations of the Ab1 and of the Ab'1 were implicated and they could be different for the diverse littermates.

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PubMed1984

Induction of immunoglobulin allotypic suppression in the rabbit: a cellular approach.

Adult rabbits were sensitized against rabbit immunoglobulin allotypic specificities of the a and b series by means of two injections of their own lymphocytes coated with the appropriate IgG. The splenic lymphocytes from these sensitized rabbits were injected, 24 hr after birth, into newborns that had inherited from their father the allotypic specificities susceptible to recognition by the sensitized lymphocytes. A significant percentage (40%) of the young rabbits subjected to this treatment developed a total suppression of expression of these specificities with the well-known compensatory effect due to an increased expression of the corresponding allele. We have observed that the T Julius subset of the sensitized splenic lymphocytes was responsible for the induction of this suppression that was established without discernible intervention of anti-allotype antibodies. In one instance we observed that the expression of the allotypic specificities transmitted by the father, although established at 5 weeks of age, gradually declined and totally disappeared at 13 weeks of age.

Animals↗

PubMed1982

Preparation of peroxidase: antiperoxidase (PAP) complexes for immunohistological labeling of monoclonal antibodies.

The production of mouse peroxidase:antiperoxidase (PAP) complexes suitable for immunohistological use in conjunction with monoclonal antibodies is described. Three approaches were explored: 1) production of conventional polyclonal PAP complexes; 2) conversion of rabbit PAP to "pseudo-mouse PAP" by incubation with monoclonal mouse anti-rabbit immunoglobulin; 3) formation of PAP complexes from monoclonal mouse antiperoxidase. PAP complexes prepared by the latter technique gave the best immunohistological labeling reactions, being stable on storage and compatible with a wide range of human monoclonal antibodies. Gel filtration revealed that monoclonal PAP is of lower molecular weight than conventional PAP complexes (fulfilling theoretical predictions based on the monospecificity of monoclonal antibodies).

Animals↗

PubMed1981

Mitogenic response of C3H/HeJ mouse lymphocytes to polyanionic polysaccharides obtained from Bordetella pertussis endotoxin and from other bacterial species.

Lipopolysaccharide extracted from Bordetella pertussis was mitogenic for spleen cells of endotoxin-resistant C3H/HeJ mice. Although endotoxic lipid A was inactive, mitogenic activity of lipopolysaccharide was exhibited by purified preparations of polysaccharides I and II, which constitute the carbohydrate moiety of the macromolecule. These low-molecular-weight (2,800 and 3,600) polysaccharides, containing carboxyl groups, were not mitogenic for thymocytes and splenic T-cells of C3H/HeJ mice, but did show mitogenic activity for splenic B-cells of C3H/HeJ mice and for spleen cells of C57BL/6 athymic nude mice. The mitogenic activities of polysaccharides I and II were also compared with those of other polyanionic polysaccharides, and the results indicate that high molecular weight is not necessary, and negative charges are not sufficient, for mitogenicity.

Animals↗

PubMed1974