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C Lemercier

Publications and source records attributed to C Lemercier.

21 records · Page 2Linked to original sources

Evidence for an active hydrophobic form of factor H that is able to induce secretion of interleukin 1-beta or by human monocytes.

We studied the capacity of human factor H to promote the secretion of a lymphocyte-activating factor (LAF) by human monocytes cultured under serum-free conditions. Presence of LAF in the culture supernatants was assessed with the mouse thymocyte assay. Highly purified factor H alone had no effect on thymocyte proliferation. When monocytes were cultured with factor H for 24 h, a significant secretion of LAF was observed. The effect was dose dependent over a range of factor H concentrations from 1 to 15 micrograms/ml. Polymyxin B did not abrogate the capacity of factor H to induce LAF secretion. Adsorption of factor H preparations onto anti-factor H-Sepharose completely suppressed the phenomenon. Conversely, the activity was recovered in the acidic eluate. Furthermore, factor H subpopulation phi 2, that was able to bind to phenyl-Sepharose, was a stronger inducer of LAF secretion by monocytes than the subpopulation phi 1 (which did not bind to phenyl-Sepharose). Using a specific radioimmunoassay for interleukin 1-beta (IL 1 beta), we observed a good correlation between the LAF activity and the amount of IL 1 beta secreted by human monocytes stimulated with factor H. We have shown previously that factor H (phi 2) bound specifically on Raji cells whereas factor H (phi 1) did not. These results argue for the participation of the interaction of factor H with its receptor to stimulate the secretion of IL 1 by monocytes and that the phi 2 form of factor H is a ligand for the human factor H receptor.

Cells, Cultured↗

Expression of complement alternative pathway proteins by endothelial cells. Differential regulation by interleukin 1 and glucocorticoids.

We have studied the secretion of proteins of the alternative pathway of complement C3, factor B and factor H by human umbilical vein endothelial cells (HUVEC). Results showed that factor H and factor B are quantitatively secreted in abundance whereas C3 could only be detected when the cells are maintained in culture during long periods of time. Interferon-gamma stimulated factor H, factor B and, to a lesser extent, C3 secretions. Interleukin (IL) 1 had a differential effect on spontaneous C3, factor B and factor H secretions. In the presence of IL 1, there was a significant secretion of C3 occurring within a short period of culture. IL 1 also stimulated factor B secretion. There was a synergistic stimulating effect between IL 1 and interferon-gamma to bring C3 and factor B productions by HUVEC to very high levels. In contrast, factor H secretion was consistently inhibited by IL 1. Local increase in C3 and factor B secretions by endothelial cells in the presence of IL 1 may have important implications in the inflammatory reaction. In striking contrast, the glucocorticoid dexamethasone (DXM) had modulatory effects which are consistent with its anti-inflammatory properties. DXM, at therapeutic concentrations, decreased C3 and factor B secretions and increased factor H secretion. Local modulation of complement protein secretion by DXM appears to be a new mechanism by which this glucocorticoid may control inflammation.

Complement C3b Inactivator Proteins↗

[Study of the complement system. General principles and perspectives].

Measurement of complement in clinical medicine is traditionally based on the determination of CH50 and immunochemical and/or functional measurement of complement proteins C1q, factor B, C3 and C4. The interpretation of these measurements, as far as complement activation is concerned, can however be difficult as these tests do not allow to discriminate between consumption due to activation, hereditary deficiency, increased rate of synthesis or even hyposynthesis. This explains why their use as markers of evolutivity in diseases where complement activation is occurring has given variable results. New tests for complement activation have been more recently introduced. These are mainly the measurements of the anaphytotoxins, the degradation products of C3 and the membrane attack complex. As these tests reflect more directly complement activation, they may be more reliable markers. The immunochemical and functional measurements of C1-inhibitor are of special interest as they are the tests which allow definitive diagnosis of the hereditary angio-oedema. General principles for the interpretation of the different tests used to evaluate the complement system are presented and discussed.

Anaphylatoxins↗