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H Tournade

Publications and source records attributed to H Tournade.

8 recordsLinked to original sources
PubMed1992

Determination by high-performance liquid chromatography with electrochemical detection of free and conjugated N-acetyldopamine excretion in urine of children with neuroblastoma and nephroblastoma.

A simple method for the determination of N-acetyldopamine (NADA) (both free and conjugated) in children's urine by high-performance liquid chromatography with electrochemical detection has been developed. Conjugated NADA was measured as the free compound after enzymatic hydrolysis and purification on alumina. The total analysis time is 25 min. The results show a linearity of the whole assay from 0.005 to 20 mumol/l NADA; the sensitivity is 0.2 pmol per 20 microliters injected sample. Mean recoveries of 96.7 and 86.6% were obtained for free and total NADA, respectively. Modifications of the retention times (between 2 and 50 min) induced by changes in the eluent were determined. Conjugated NADA accounted for about 90% of the total excretion of NADA. These results suggest that this compound could play an important part in neuroblastoma; its concentration is thirteen times higher in children with neuroblastoma than in normal subjects.

Adolescent↗
PubMed1991

Effect of the thiol group on experimental gold-induced autoimmunity.

Brown Norway rats injected with aurothiopropanolsulfonate sodium salt develop systemic autoimmunity. The aim of this study was to assess the influence of the sulfur-containing group in this experimental model of gold-induced autoimmunity. It was shown that the sulfur-containing group does not induce autoimmunity of itself, but potentiates the immunotoxic effects of gold.

Animals↗
PubMed1991

Experimental gold-induced autoimmunity.

The pathogenesis of gold-induced autoimmunity and membranous glomerulopathy is not well understood. HgCl2 and D-penicillamine, other chemicals known to trigger membranous glomerulopathy in humans, induce autoimmune manifestations in Brown-Norway (BN) rats but not in Lewis (LEW) rats. These chemicals trigger T-cell clones which are specific for self class II molecules from the major histocompatibility complex and are probably responsible for the polyclonal B-cell activation observed. The aim of this work was to test the effects of aurothiopropanolsulphonate (ATPS) in BN and LEW rats. In BN rats, ATPS induced a polyclonal B-cell activation marked by lymphoproliferation, hyperimmunoglobulinaemia affecting mainly IgE, and by the production of numerous autoantibodies. A glomerulonephritis occurred, initially due to anti-glomerular basement membrane antibody deposition, and later to the formation of granular deposits, occasionally resulting in a typical membranous glomerulopathy. Self class-II-specific T-cells were found that might be responsible for the polyclonal B-cell activation. Lewis rats were free of glomerulopathy but, like BN rats, exhibited an interstitial nephritis and some degree of polyclonal B-cell activation. These findings demonstrate that, depending on the strain, ATPS triggers different B-cell clones inducing different degrees of autoimmunity.

Animals↗
PubMed1990

D-penicillamine-induced autoimmunity in Brown-Norway rats. Similarities with HgCl2-induced autoimmunity.

D-penicillamine (DP) has been previously shown to induce an autoimmune disease in Brown-Norway (BN) rats, characterized by a dermatitis, by the production of antinuclear antibodies, by the formation fo circulating immune complexes, and by linear IgG deposits along the glomerular basement membrane. These manifestations are quite similar to those observed in mercuric chloride (HgCl2)-induced autoimmunity. The mechanism of the latter disease has been recently partly elucidated. The aim of this study was to compare DP and HgCl2-induced autoimmunity in BN rats and to compare the mechanisms involved in both situations. A transient increase in the number of spleen cells, affecting B cells and CD4+ T cells, and an increase in serum IgE concentration, previously reported in HgCl2-induced autoimmunity, were observed during DP treatment. Autoreactive anti-class II T cells able to proliferate not only in the presence of autologous B cells but also in the presence of syngeneic normal B cells were found in DP-treated BN rats. Spontaneous regulation occurred, associated with the disappearance of autoreactive T cells. Suppressor CD8+ T cells were not involved in this phenomenon. Mechanisms involved in both the induction and the regulation of DP-induced autoimmunity seem to be quite similar to those reported in HgCl2-induced autoimmunity.

Animals↗
PubMed1990

Rat anti-glomerular basement membrane antibodies in toxin-induced autoimmunity and in chronic graft-vs.-host reaction share recurrent idiotypes.

Cross-reactive idiotypes (CRId) borne on autoanti-glomerular basement membrane antibodies of Brown-Norway (BN) rats with mercury-induced glomerulonephritis have been described in the preceding study (Guéry, J.-C. et al., Eur. J. Immunol. 1990. 20:93). BN rats treated with sodium aurothiopropanol sulfonate or D-penicillamine, as well as (LEW X BN)F1 hybrids transferred with BN rat spleen cells, developed quite similar autoimmune abnormalities. In the present study, it is shown that immunoglobulins bearing such "public" idiotypes are also produced and deposited in the kidney in these three models. The CRId here described may, therefore, be considered as a marker of sets of recurrently expressed V region genes during the course of these autoimmune disorders. Anti-self class II T cells are present in the three models of toxin-induced autoimmunity and anti-allo class II T cells are responsible for the chronic graft-vs.-host reaction. The same B cell clones are probably triggered during these processes as a consequence of a polyclonal B cell activation mediated by anti-class II T cells.

Animals↗
PubMed1990

Graft-versus-host reactions in the rat mimic toxin-induced autoimmunity.

Gold salts, D-penicillamine or mercurials induce autoimmunity in Brown Norway (BN) rats and provoke an immunosuppression in Lewis (LEW) rats. It has been suggested that immunologically mediated manifestations induced by drugs could result from graft-versus-host (GVH) like reactions. We show that BN spleen cells transferred into (LEW x BN)F1 hybrids induce a chronic GVH reaction (GVHR). This reaction led to an autoimmune disease quite similar to that induced by drugs in BN rats. In both situations, a common part of the B cell repertoire is triggered. In contrast, LEW spleen cells transferred into (LEW x BN)F1 hybrids provoke a lethal GVHR. This is to be compared with the CD8-mediated immunosuppression observed in LEW rats injected with HgCl2. These findings are in agreement with the prediction that immune dysregulation induced by drugs leads to GVH-like reactions either stimulatory or suppressive depending upon the strain tested.

Animals↗
PubMed1989

[Immune glomerulopathies of toxic origin. Possible mechanisms of induction].

Mechanisms of toxic-induced autoimmunity including drug-induced autoimmune glomerulonephritis are unknown. In the mercury-induced autoimmune disease in Brown-Norway (BN) rats it has been shown that B cells are polyclonally activated provided that T cells are present. Autoreactive T cells that recognized self-Ia on normal B cells have been found to be highly frequent in HgCl2-injected BN rats. It has been possible to transfer all the autoimmune abnormalities by injecting T cells from HgCl2-exposed BN rats into normal syngeneic animals. However the recipient had to be depleted in suppressor/cytotoxic T cells by treatment with an anti-CD8 antibody for a full-blown disease to appear. These experiments show that a toxic agent may induce an autoimmune glomerulonephritis in the context of an autoimmune disease by generating or expanding anti-self Ia autoreactive T cells provided that suppressor/cytotoxic T cells have been inhibited. Autoreactive T cells are probably responsible for the polyclonal activation of B cells in this model. This mechanism does not rule out that other mechanisms could play a role.

Animals↗