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G Chavanel

Publications and source records attributed to G Chavanel.

8 recordsLinked to original sources
PubMed1992

Substance P enhances IL-2 expression in activated human T cells.

Jurkat and HUT 78 T cell lines, as well as peripheral blood human T cells activated with PHA plus PMA were used to investigate the capacity of substance P (SP) neuropeptide to regulate IL-2 production. By using Northern blot analysis and dosage of the IL-2 release in cell supernatants, we show that SP can act as cosignal with PHA + PMA to enhance the expression of specific IL-2 mRNA and IL-2 secretion in T cells. By using the N-terminal SP(1-4) or the C-terminal SP(4-11) fragments of the entire molecule, we show that the cosignal activity is carried by the C-terminal portion of SP. The SP and SP(4-11) optimal effects were observed at 10(-12) M and 10(-10) M when a broad range of concentrations from 10(-6) M to 10(-13) M was tested. The increase of IL-2 mRNA obtained with 10(-12) M of SP in the activated Jurkat cells was reduced by adding 10(-10) or 10(-9) M of the SP antagonist (D-Pro2,-D-Phe7,-D-Trp9)SP to the culture, indicating the specificity of SP action. The up-regulation observed when 10(-12) M of SP was applied together with the mitogens on Jurkat cells, persisted after a 16-h culture period, time at which the IL-2 mRNA signal is normally back to a minimum level when the mitogens are used alone. Furthermore, an induction of IL-2 mRNA accumulation, in a 2-h pulse, was obtained with 10(-12) M of SP on Jurkat cells previously activated with mitogens for 16 h.

Gene Expression↗
PubMed1990

Decreased lymphokine-activated killer cells in kidney transplant recipients. Correlation with a diminished number of CD3-/NKH1+ cells.

The activity of lymphokine-activated killer cells, measured either by a clonal or polyclonal technique, was assessed in 30 kidney transplant recipients (TX), in 13 hemodialyzed patients (HD-CRI), and in 18 normal (N) controls. A highly significant decrease of the LAK activity in TX in comparison with HD-CRI or N (P = 0.0001) was observed. Moreover, the percentage of CD3-/NKH1+ cells was decreased in TX in comparison with N (P = 0.01). LAK activity was strongly correlated (r = 0.72; P = 0.0001) with the percentage of CD3-/NKH1+ cells and not with that of double-positive CD3+/NKH1+ cells. Multivariate analysis showed that the sole independent variable that determined the LAK activity was the percentage of CD3-/NKH1+ cells: the pathological status (TX, HD-CRI, and N) variable was statistically not significant. On the other hand, two T cell-specific functions (IL-2 secretion and specific cytotoxic activity) were, on the whole, preserved in TX. Altogether, these results suggest that TX are LAK deficient predominantly because they have a decreased number of CD3-/NKH1+ cells. The normality of T cell functions suggests that the high rate of malignancies seen in TX is related to this LAK deficiency. Moreover, our study indicates that, in vivo, CD3+ cells do not significantly contribute to the LAK precursors.

Antigens, CD↗
PubMed1978

Leucocyte-migration-inhibition test in patients with colorectal cancer: clinicopathological correlations.

Leucocyte-migration-inhibition test was used to study the immune reactions of leucocytes from 136 colorectal cancer patients, 43 patients with non-cancerous chronic colorectal diseases and 82 controls, with saline extracts of HT29 line. A positive inhibition was found in only 43% of colorectal cancer patients. It was higher in carcinomas of limited extension than in invasive ones (64% against 39%). Furthermore, operation by itself had a depressive effect on the reaction, as the positivity in 25 patients tested twice was 64% before operation and 32% after. Leucocytes from patients with non-cancerous chronic colorectal diseases gave many positive reactions (65%). The percentage of positivity was about the same for diseases with high, low or no risk of cancerization. Hence the antigen(s) of tumour extracts that react with patient's leucocytes are, at least partially, unrelated to cancer.

Cell Migration Inhibition↗
PubMed1977

A comparative study of the localization of CEA and NCA2 in cancerous and normal gastrointestinal tissues.

The histological localization of CEA in gastrointestinal tissues was re-evaluated after absorption of anti-CEA antiserum with NCA2, another normal antigen cross-reacting with CEA. This absorbed antiserum showed clearly the presence of CEA in colonic tumors and some non-cancerous colonic mucosae, obtained even from non-cancerous patients. In contrast, some of the gastric adenocarcinomas we studied were strained very weakly by absorbed anti-CEA antiserum, although non-absorbed antiserum (or serum absorbed with NCA alone) labelled them strongly. The same difference in reactivity between both antisera was observed in intestinal metaplasia. The localization of NCA2 was studied with a specific antiserum, previously absorbed with CEA and NCA. NCA2 was found to be a noromal cytoplasmic and mucus-associated antigen of gastrointestinal tissues. It was present also in fetal stomach and colon. Sections of gastric and colonic tumors as well as intestinal metaplasia of gastric mucosae always reacted brilliantly with absorbed anti-NCA2 antiserum.

Antigens↗
PubMed1977

Use of a permanent cell line extracts to study the tumor associated immune reactions in colorectal cancer patients by leucocyte migration inhibition test.

Crude extracts of colorectal surgical tumors, either individual or pooled, and HT29 line cells were compared in leucocyte migration inhibition test. HT29 cell extract gave more positive reactions with leucocytes of colorectal cancer patients than the other ones, and less with control leucocytes. It was thus used for all the subsequent experiments. As a whole, we obtained 44% (30/68) of positive inhibitions in patients afflicted with a colorectal carcinoma, against 9% (3/31e in normal controls and 20% (8/40) in patients bearing a carcinoma from another organ. Among the latest patients, those having a gynecological carcinoma were rarely positive, contrasting with those suffering from a carcinoma from the aerodigestive organs. It seemed that the antigen(s) involved in the reaction had no organ specificity, but rather a broad tissue specificity.

Adenocarcinoma↗
PubMed1976

An optical and ultrastructural study of the localization of carcinoembryonic antigen (CEA) in normal and cancerous human rectocolonic mucosa.

An immunoenzymologic method using peroxidase-labeled antibodies has been applied for the localization of carcinoembryonic antigen (CEA) on frozen sections, on Araldite-embedded sections, and on isolated cell preparations of normal rectocolonic mucosa and of rectal and colonic cancers (adenocarcinomas and one villous tumor). CEA appears as a component intimately associated with the external coating of the striated border of the normal columnar cell and with the external coating of the apical pole of the cancerous cell. CEA is also found as an intracellular component of the normal epithelial cell of the rectocolonic mucosa, mainly the goblet cell. In tumors, it appears as an intracellular component of the mucussecreting cell. Its presence in the cell coat and interior of the cell correlates with the degree of differentiation of the cells, whether cancerous or not. Progressive accumulation of CEA in the normal colonic epithelial cell has been observed in cells undergoing maturation. Its release by the mature goblet cell has also been observed. These results confirm that CEA is a normal glycoprotein constituent of the epithelial cell of the human adult rectocolonic mucosa, synthesized and discharged by this cell. The difference in CEA content, already reported, between the cancerous and the normal rectocolonic mucosa appears quantitative and not qualitative.

Adenocarcinoma↗
PubMed1975

Study of the antigenic cross reactivity between carcinoembryonic antigen and "nonspecific cross reacting antigens" (NCA and NCA 2).

The immunochemical relationship between CEA, NCA and NCA 2 was studied in guinea-pigs. Strong cross reactions were found between these antigens, either in delayed or anaphylactic reactions. Some specific determinants for each antigen could still be demonstrated. Delayed hypersensitivity is likely to be due to the protein moiety of the molecules while anaphylactic reactivity could probably be related to their glucidic parts. Consequently, CEA and NCA have common antigenic determinants on their glucidic and peptidic moieties, perhaps more on the latter ones.

Anaphylaxis↗