Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Chantal Denys is active.

Publication


Featured researches published by Chantal Denys.


Transplantation | 1996

Blockade of proliferation and tumor necrosis factor-alpha production occurring during mixed lymphocyte reaction by interferon-gamma-specific natural antibodies contained in intravenous immunoglobulins.

Michel Toungouz; Chantal Denys; Etienne Dupont

The mechanism of action of intravenous immunoglobulins (IVIg) for prevention of graft rejection and graft-versus-host disease (GVHD) is poorly understood. Recently, it has been shown that these preparations contain natural antibodies directed toward interferon (IFN)-gamma. During mixed lymphocyte reaction (MLR), which constitutes an in vitro model of allograft rejection and GVHD, T cell recognition of HLA differences induces IFN-gamma release. This cytokine promotes T cell proliferation and acts as a macrophage-activating factor to provoke tumor necrosis factor-alpha secretion. The aim of the present work is to investigate the influence of IVIg on IFN-gamma production occurring during MLR and its subsequent impact on T cell proliferation and tumor necrosis factor (TNF)-alpha secretion. We tested IVIg preparations for the presence of anti-IFN-gamma and anti-TNF-alpha antibodies. High amounts of anti-IFN-gamma, but not anti-TNF-alpha antibodies, were found. IVIg addition at the initiation of culture resulted in IFN-gamma secretion blockade. Likewise, lymphocyte proliferation and TNF-alpha secretion were inhibited. This inhibition was reversed by the addition of recombinant human IFN-gamma. Furthermore, the inhibitory properties of IVIg were mimicked by an IFN-gamma-specific neutralizing monoclonal antibody. We conclude that the capacity of IVIg to inhibit proliferation and TNF-alpha release during MLR is due to IFN-gamma blockade by natural antibodies. This immunosuppressive mechanism could contribute to the effect of IVIg on prophylaxis of organ graft rejection and GVHD after allogeneic bone marrow transplantation.


Transplantation | 1996

Optimal control of interferon-gamma and tumor necrosis factor-alpha by interleukin-10 produced in response to one HLA-DR mismatch during the primary mixed lymphocyte reaction.

Michel Toungouz; Chantal Denys; Donat De Groote; Marc Andrien; Etienne Dupont

Interleukin (IL)-10 is an immunosuppressive cytokine potentially involved in the control of the allogeneic response. Several studies failed to detect it in mixed lymphocyte reaction supernatants. However, experiments using IL-10-specific antibodies, revealing its inhibitory action on interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, provided indirect evidence that endogenous IL-10 was produced. The aim of the present work is to elucidate the role of IL-10 during mixed lymphocyte reaction and to investigate the influence of HLA-DR antigens on its production and on the regulatory loop involving TNF-alpha and IFN-gamma. Using a highly sensitive ELISA, a significant (P < 0.0001) but low IL-10 release could be detected (33.7 +/- 3.6 pg/ml) in response to HLA-DR disparities. However, IL-10 release was not graded as 1 DR mismatch (MM)-induced maximal secretion (32.3 +/- 5.1 pg/ml). This contrasted with TNF-alpha and IFN-gamma productions, which significantly increased in 2 DR MM pairs. Addition to IL-10-specific antibodies resulted in higher enhancement of INF-gamma (235 +/- 38% vs. 122 +/- 39%, P = 0.02) and, to a lesser extent, TNF-alpha (147 +/- 56% vs. 112 +/- 20%, NS) in 1 compared with 2 DR MM pairs. We conclude that the 1 DR MM setting is associated with optimal IL-10 secretion and more efficient inhibition of IFN-gamma and TNF-alpha compared with the 2 DR MM configuration. Although promoting enhanced IFN-gamma and TNF-alpha release, introduction of an additional DR MM does not result in increased IL-10 production. These data indicating that the IL-10 regulatory feedback loop is more effective in 1 DR rather than complete DR incompatibility could have an impact on matching policies for planned transfusion.


Vox Sanguinis | 1997

Increased in vitro Immunosuppressive Action of Anti-CMV and Anti-HBs Intravenous Immunoglobulins due to Higher Amounts of Interferon-Gamma Specific Neutralizing Antibodies

Chantal Denys; Michel Toungouz; Etienne Dupont

Background and objectives: We previously found that interferon‐γ (IFN‐γ) antibodies in intravenous immunoglobulins (IVIG) can block not only IFN‐γ production and tumor necrosis factor‐α secretion, but also T‐cell proliferation. Since the presence of IFN‐γ antibodies has been attributed to previous viral infection, we hypothesized that the viral status of the plasma donors used for IVIG pools might be a decisive factor in controlling the immunosuppressive capacity of IVIG. Materials and methods: We tested three different pooled, human IVIG preparations for the presence of IFN‐γ antibodies by ELISA. Results: Comparison of the immunomodulatory activity of polyvalent IVIG with that of specific CMV and HBs IVIG showed that the latter had higher levels of IFN‐γ antibodies and an increased capacity to block mixed lymphocyte reaction and cytokine production. Conclusion: We propose that these in vitro assays constitute a basis for the selection of plasma intended for manufacturing IVIG aimed at immunosuppression in the transplant setting.


Human Immunology | 1995

INTERLEUKIN 12 UNMASKS HLA CLASS I DIFFERENCES DURING MIXED LYMPHOCYTE REACTION INDUCED INTERFERON GAMMA PRODUCTION

Michel Toungouz; Chantal Denys; Marc Andrien; Donat De Groote; Etienne Dupont

We investigated the genetic control of IFN-gamma release during MLR and its relationship with TNF-alpha and IL-12. Blocking experiments demonstrated the IFN-gamma dependence of TNF-alpha production and the significant contribution of IL-12 to IFN-gamma secretion. We studied informative pairs allowing the evaluation of the relative importance of HLA class I and class II antigens. Maximal IFN-gamma secretion allowing discrimination between fully HLA different and identical subjects required 5 days. In class I different but DRB1 identical pairs, a moderate but discriminant IFN-gamma release was found. Exogenous IL-12 addition after 24 hours of preactivation by MLR resulted in a marked enhancement of IFN-gamma production at day 2. In pairs differing only by class I antigens, the discriminating capacity was significantly increased as compared to values obtained in absence of IL-12 at day 2 (p < 0.004) and at day 5 (p < 0.004). The crucial role of class I antigens on IFN-gamma release was further substantiated by the blocking action of the W6/32 mAb directed against a monomorphic epitope common to all HLA-A, -B, and -C antigens. We conclude that IFN-gamma production during MLR is under the control of class I antigens. Furthermore, exogenous IL-12 strongly amplifies their influence.


Human Immunology | 1993

Alloactivation induced during mixed-lymphocyte reaction provokes release of tumor necrosis factor α and interleukin 6 by macrophages and primes them to lipopolysaccharides

Michel Toungouz; Chantal Denys; Donat De Groote; Marc Andrien

We tested various factors affecting the production of the CKs IL-6 and TNF-alpha during in vitro alloactivation induced by MLR. Different MLR combinations involving familial and unrelated pairs were evaluated. In family studies, MLRs involving pairs of HLA-identical siblings (n = 6) were characterized by IL-6 and TNF-alpha secretion comparable to the one of autologous controls, in marked contrast with HLA-different combinations (n = 6). These displayed a strong and early (day 3) release of both CKs. In combinations of unrelated individuals involving HLA-A, -B, -C-different but -DR, -DQ-identical pairs (n = 3), low CK release was observed. Addition of LPS (1 micrograms/ml) considerably increased production of IL-6 and TNF-alpha. Clear discrimination of MHC class II differences required a 24-hour preculture followed by addition of LPS for 4 hours, a time relationship compatible with a priming phenomenon due to alloactivation. We conclude that MHC class II alloactivation not only provokes IL-6 and TNF-alpha secretion, but also primes macrophages to LPS so that the production of these CKs is markedly increased and occurs much earlier after LPS addition.


Hepatology | 1991

IgA triggers tumor necrosis factor α secretion by monocytes: A study in normal subjects and patients with alcoholic cirrhosis

Jacques Devière; Jean-Pierre Vaerman; Chantal Denys; Liliane Schandené; Paul Vandenbussche; Yves Sibille; Etienne Dupont


British Journal of Haematology | 2008

In vitro inhibition of tumour necrosis factor-α and interleukin-6 production by intravenous immunoglobulins

Michel Toungouz; Chantal Denys; Donat De Groote; Etienne Dupont


Transplantation | 1994

Tumor necrosis factor-alpha and interleukin-6 production induced by variations of DR4 polymorphism during the primary mixed lymphocyte reaction.

Michel Toungouz Nevessignsky; Chantal Denys; Marc Andrien; Donat De Groote; Etienne Dupont


Transplantation proceedings | 1995

HLA DR subtypes induce IL-6 and TNF-alpha production in the primary mixed lymphocyte reaction.

Michel Toungouz; Chantal Denys; Marc Andrien; Etienne Dupont


Transplantation Proceedings | 1997

Inhibition of IFN-gamma production by intravenous immunoglobulins during mixed lymphocyte reaction: consequences for proliferation and TNF-gamma production.

Michel Toungouz; Chantal Denys; Etienne Dupont

Collaboration


Dive into the Chantal Denys's collaboration.

Top Co-Authors

Avatar

Michel Toungouz

Université libre de Bruxelles

View shared research outputs
Top Co-Authors

Avatar

Etienne Dupont

Université libre de Bruxelles

View shared research outputs
Top Co-Authors

Avatar

Marc Andrien

Université libre de Bruxelles

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Jacques Devière

Université libre de Bruxelles

View shared research outputs
Top Co-Authors

Avatar

Liliane Schandené

Université libre de Bruxelles

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge