Search PubMed⌕ Search

Biomedical subjects

C Fournier

Publications and source records attributed to C Fournier.

257 records · Page 15Linked to original sources
PubMedDate not supplied

Chemoresistance to doxorubicin and cisplatin in a murine cell line. Analysis of P-glycoprotein, topoisomerase II activity, glutathione and related enzymes.

Resistance to antineoplastic drugs has often been associated with P-glycoprotein overexpression, this certainly being not the sole mechanism. In order to characterize resistance to doxorubicin and cisplatin, we have analysed P-glycoprotein expression, topoisomerase II activity, glutathione and related enzymes in murine leukemic cells (doxorubicin or cisplatin-resistant). The doxorubicin-resistant cells contained P-glycoprotein, showed lower activities of glutathione S-transferase well as of glutathione reductase and topoisomerase II. The modifications observed in the most cisplatin-resistant cell line were a higher activity of glutathione S-transferase isoenzyme pi and topoisomerase II. These results suggest that drug uptake, glutathione metabolism as well as topoisomerase II activity are all characteristic of multidrug resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

T cell-targeted immunotherapy in murine collagen-induced arthritis.

Counteracting the effect of autoimmunity can be achieved by elimination or inactivation of autoreactive T cells. We have focused on two approaches targeting on autoaggressive T cells in the model of collagen-induced arthritis (CIA) in mice. First, type II collagen (CII) primed DBA/1 mice were treated with various monoclonal antibodies (mAb) specific for the beta chains of the T cell receptor (TCR) using a protocol resulting in a long-term elimination of the target T cells. Indeed, CIA could be suppressed by injection of anti-V beta 8.1, 2 mAb and down-regulated by that of anti-V beta 2 and/or anti-V beta 5, presumably by deleting pathogenic T cell clones. In contrast, treatment with either anti-V beta 6 or anti-V beta 11 mAb did not alter CIA. Second, we generated CII-specific T cell hybrid clones that recognize the antigenic peptides in association with Kq and IA(q) molecules respectively for CD8+ and CD4+ cells. Vaccination with the irradiated hybrid clones, 3 weeks prior to immunization, was effective in preventing the development of arthritis. Furthermore, this suppression was antigen and disease specific. Most importantly, one CD8+ clone could reverse the ongoing disease. These new therapeutic approaches derived from animal models may offer a hope of more selective interventions for the treatment of human autoimmune diseases.

Animals↗
PubMedDate not supplied

Influence of the bacterial flora on collagen-induced arthritis in susceptible and resistant strains of rats.

Collagen-induced arthritis is an experimental model for rheumatoid arthritis which can be elicited in susceptible strains of rats by intradermal injection of native type II collagen. In order to investigate whether bacterial flora may alter the pathogenic response to type II collagen, we have immunized germ-free (GF) male rats from either highly resistant Fisher (F344) or highly susceptible Dark Agouti (DA) strains. The disease was markedly enhanced in GF DA as compared to conventional (CV) DA rats. The humoral response was also stronger in GF rats of both strains. Neither GF nor CV F344 developed arthritis, although GF F344 exhibited later inflammation of the tail. These data support a suppressive influence of bacterial flora on collagen-induced arthritis.

Analysis of Variance↗