Régulation de la production d'interféron-y au cours de la réaction allogénique

Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe

Régulation de la production d'interféron-y au cours de la réaction allogénique

Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe

Haematopoietic stem cell transplantation for severe autoimmune diseases: new perspectives.

Comparative StudyEditorialSCOPUS: ed.jinfo:eu-repo/semantics/publishe

Hematopoietic stem cells: therapeutic applications in autoimmune diseases and in solid organ transplantation.

Journal ArticleReviewinfo:eu-repo/semantics/publishe

Cell therapy: basis for new therapeutic strategies

(Impact factor: 0.5)info:eu-repo/semantics/publishe

Human monocyte derived dendritic cells differentiated in the presence of Interferon-β and Interleukine-3 induce production of Interleukine-17 in mixed lymphocyte reaction via the secretion of Interleukin-23 and Interleukin-6

info:eu-repo/semantics/nonPublishe

Sélection immunologique des donneurs de moelle osseuse.

SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Cell therapy: A basis for new therapeutic strategies in internal medicine

Two rapidly evolving areas of cell therapy are the use of stem cells and cancer immunotherapy. The primitive pluripotent hematopoietic stem cells (HSCs), which have the capacity to self-renew and to repopulate the different blood cell lineages, are responsible for the maintenance of the hematopoietic system. Two major sources of stem cells are bone marrow and apheresis products of peripheral blood after mobilization with G-CSF and/or chemotherapy. HSC transplantation allows for the restoration of the hematopoietic and immune systems in cancer therapy. Immunotherapy has been classified as 'active' or 'passive' depending on whether the immunotherapy is designed to activate the patient's immune system to mount an immune response towards his/her own tumor or designed to transfer immune components 'already' directed against the patient's cancer. This latter approach, also termed 'adoptive immunotherapy,' includes the use of lymphokine-activated killer cells and tumor-infiltrating lymphocytes, tumor-specific lymphokine-activated killer cells and autolymphocyte therapy, stem cell transplantation in leukemic relapse, adoptive immunotherapy of Epstein-Barr virus (EBV) lymphoma using EBV-specific cytotoxic T lymphocytes, and activated monocytes- macrophages. Another approach for cancer immunotherapy, termed 'active immunotherapy,' is based on the induction of an antitumor response in the patient by, e.g. the use of manipulated tumor cells or professional antigen- presenting cells loaded with tumor antigens. In addition to its use in cancer treatment, cell therapy is also being explored as a treatment strategy for other disorders of the hematolymphoid system, such as autoimmune diseases (AIDs). It has also been proposed that HSCs may be useful in creating tolerance in patients requiring solid organ transplantation. As cell therapy becomes more common, regulatory decisions must be made concerning whether to give cellular products the status of drugs or biological products.SCOPUS: re.jinfo:eu-repo/semantics/publishe

Increased in vitro immunosuppressive action of anti-CMV and anti-HBs intravenous immunoglobulins due to higher amounts of interferon-gamma specific neutralizing antibodies

BACKGROUND AND OBJECTIVES: We previously found that interferon-gamma (IFN-gamma) antibodies in intravenous immunoglobulins (IVIG) can block not only IFN-gamma production and tumor necrosis factor-alpha secretion, but also T-cell proliferation. Since the presence of IFN-gamma 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-gamma 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-gamma 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.Comparative StudyJournal ArticleFLWINinfo:eu-repo/semantics/publishe

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

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.In VitroJournal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe