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C Lemoine

Publications and source records attributed to C Lemoine.

30 records · Page 2Linked to original sources

Distribution of CCK mRNA in particular regions (hippocampus, periaqueductal grey and thalamus) of the rat by in situ hybridization.

Cholecystokinin (CCK) mRNA was detected by in situ hybridization at high magnification in some rat brain regions where CCK octapeptide (CCK-8) is thought to produce its pharmacological effects. The labeling of the dentate gyrus and the sparse but intensively stained cells found in the CA1 layer, stratum radiatum and hilus could correspond to interneurons involved in hippocampal neural activity, in agreement with excitatory responses induced by local injection of CCK-8. The intense labeling of the Edinger-Westphal nucleus and more generally the presence of CCK mRNA in the periaqueductal gray and thalamus ventrobasal nuclei could account for the various effects of CCK in pain transmission.

Animals↗

Identification of genes encoding T cell defined tum- antigens.

Tum- mutants are immunogenic mutants obtained by mutagen treatment of mouse tumor cells. They express new "tum- antigens" recognized by cytolytic T cells (CTL) but not by specific antibodies. We have recently developed a method aimed at cloning the genes coding for such transplantation antigens. It is based on gene transfection and detection of transfectants by their ability to stimulate CTL. Tum- gene P91A has been isolated. It codes for a 60 kDa protein which does not carry a signal sequence at its N-terminus. The tum- allele differs from its normal counterpart by a point mutation. The sequence of this gene and that of two other tum- genes are totally unrelated with each other and with any sequence presently recorded in data banks. We will try to apply the same cloning method to isolate mouse and human tumor-specific transplantation antigens (TSTA).

Animals↗

Production of stable cytolytic T-cell clones directed against autologous human melanoma.

We have attempted to optimize the production of stable human cytolytic T lymphocyte clones directed against autologous melanoma cell lines. MLTC were restimulated every week with irradiated melanoma cells in medium containing human serum and IL-2. After 21 to 35 days, in 5 out of 6 patients, these cultures expressed a preferential cytolytic activity against the autologous melanoma cells, as compared to autologous EBV-B cells or NK target K562. Limiting dilution of MLTC responder cells was performed at times varying from days 7 to 28, in medium containing IL-2 and allogeneic EBV-B cells as feeders. Approximately 1% of these responder cells gave rise to CTL clones that lysed the autologous melanoma cells, but did not lyse K562 or autologous B cells. It was possible to maintain in culture for several months a large number of CTL clones that retained this specificity with high activity, and multiplied more than 5-fold every week. Some of these CTL clones were dependent on the presence of the autologous melanoma cells for their growth. With one melanoma, the use of autologous CTL clones made it possible to identify 3 different antigens on the tumor cells.

Antigens, Neoplasm↗

Functional properties of CD8 positive lymphocyte subsets in systemic lupus erythematosus.

CD8+ lymphocytes comprise several cell subpopulations that differ phenotypically and functionally. Although the percentage of T cytotoxic/suppressor cells (CD3+ CD8+) is usually increased in patients with active SLE, these lymphocytes are unable to suppress immunoglobulin (Ig) synthesis. However, freshly prepared lymphocytes from patients with SLE contain CD8+ DR+ cells which spontaneously suppress lymphocyte production of mitogen induced interleukin 2 (IL-2). Furthermore, CD8+ Leu 11+ non-T cells which comprise only 5% of total lymphocytes are also potent suppressors of IL-2 production. At the present time it is not known whether CD8+ suppressors of Ig synthesis and CD8+ suppressors of IL-2 production represent different maturation stages of common precursor cells or represent true heterogeneity of CD8+ lymphocytes.

Humans↗