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Biomedical subjects

B Charpentier

Publications and source records attributed to B Charpentier.

At least 271 records · Page 15Linked to original sources
PubMed1981

[T lymphocytes functions in mercuric chloride-induced membranous glomerulonephritis in man. Evidence for a defect of presentation of the histocompatibility class II molecules at the cell surface (author's transl)].

Membranous glomerulonephritis (MGN) is one of the well documented manifestations of autoimmunity during chronic mercuric chloride (HgCl2) intoxication. We have carried out immunological investigation of the T cell functions in a patient presenting an HgC12-induced MGN. Circulating auto-antibodies and immune complexes were absent from the serum. Lymphocyte transformation with HgCl2 over a wide range of doses (10(-3) to 10(-8) M) was negative. E rosettes, mitogen reactivity, allogeneic reactivity evidenced by a one way mixed lymphocyte culture gave slightly diminished results. These findings contrasted with a severe impairment of the stimulative ability of lymphocytes. This defect might be related to the inability of D, DR products to be exposed at the cell surface and impeding the allogeneic recognition by foreign lymphocytes. This lymphocyte defect in the course of an HgC12 MGN in man would be correlated with lymphocyte abnormalities found in experimental HgC12-treated rats. The results of this study would favour the hypothesis of a direct role of HgC12 on lymphocyte rather than a direct action on glomerular basement membrane.

Adult↗
PubMed1979

[Production of O antigens and antibodies during urinary tract infections due to Escherichia coli (author's transl)].

In 138 adults with monomicrobial E. coli urinary tract infections, IgG coated bacteriuria (ACB) are found in 9/10 acute pyelonephritis, 21/24 chronic pyelonephritis, 2/5 acute prostatitis, and in only 6/99 lower UTI. These urinary antibodies are synthetised localy because IgA-S are found in 75%, in the kidney because humoral IgG antibodies are detected in only 40% of the ACB + patients. O6, O18, O22, O75, are the four most frequent O antigens (47,5%) and no difference were found in the distribution of O serotypes according to ACB production or clinical signs. But rough strains are significantly more frequent in pyelonephritis, suggesting a modification of the bacterial wall. The use of ACB test and O serotyping allows a better follow-up of patients, but relapses with ACB- and reinfection with ACB+ show the complexity of the relation host-E. coli.

Acute Disease↗
PubMed1979

Selective depression of the xenogeneic cell-mediated lympholysis in systemic lupus erythematosus.

The immunological responsiveness of a panel of 17 patients with systemic lupus erythematosus (SLE) was studied in an in vitro model of xenogeneic sensitization against mouse lymphoid cells. Generation of cytotoxic thymus-derived (T) cells evaluated by a chromium release assay against labeled target cells was found to be drastically impaired in these lupus patients. Such depression was independent of drug therapy at the time of the study, clinical status, and other immunological parameters such as antibodies against native DNA, complement levels, cryoglobulinemia, circulating immune complexes, or T- and bone marrow-derived (B)-cell numbers. In contrast to the cytotoxic response, the proliferative responses to phytohemagglutinin, to allogeneic lymphocytes, and to xenogeneic lymphocytes were not significantly different from those of normal individuals. The latter response was shown to be H-2 restricted with the primed lymphocyte test. These results suggest the presence of a selective defect in the generation or in the expression of killer cells rather than a deficiency in antigen recognition by T cells. The role of serum factor(s) was examined by educating the lymphocytes of normal subjects in the presence of serum from SLE patients. Such manipulation affected both the generation of killer cells and the proliferative response. Finally our observations indicate that depression of cell-mediated immunity in SLE patients may be associated with several mechanisms including a cellular one, specifically affecting the generation of killer T cells, and a humoral one possibly as a result of antilymphocytic antibodies and(or) immune complexes.

Adult↗