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Gilles Dietrich

Researcher at University of Toulouse

Publications -  77
Citations -  3188

Gilles Dietrich is an academic researcher from University of Toulouse. The author has contributed to research in topics: Autoantibody & Antibody. The author has an hindex of 30, co-authored 71 publications receiving 2798 citations. Previous affiliations of Gilles Dietrich include Centre national de la recherche scientifique & Université catholique de Louvain.

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Journal ArticleDOI

Intravenous immunoglobulins (IVIg) in the treatment of autoimmune diseases.

Srini V. Kaveri, +3 more
- 28 Jun 2008 - 
TL;DR: The current use of IVIg in human autoimmune diseases is discussed with a particular emphasis on the possible mechanisms by whichIVIg could suppress pathological autoimmune responses.

Anti-CD4 activity of normal human immunoglobulin G for therapeutic use. (Intravenous immunoglobulin, IVIg).

Hurez, +6 more
TL;DR: Results indicate that IVIg contains antibodies reactive with human CD4 and that these anti-CD4 antibodies exhibit biological functions, relevant to the immunoregulatory effects of normal polyspecific immunoglobulin G.
Journal ArticleDOI

Nod2: The intestinal gate keeper.

Ziad Al Nabhani, +5 more
- 02 Mar 2017 - 
TL;DR: Recent developments about the role of NOD2 in shaping the gut commensal microbiota and pathogens, including bacteria, viruses, and parasites, and the mechanisms by which Nod2 mutations participate in disease occurrence are presented.
Journal ArticleDOI

Modulation of autoimmunity by intravenous immune globulin through interaction with the function of the immune/idiotypic network.

Gilles Dietrich, +2 more
- 01 Jan 1992 - 
TL;DR: It is the view that IVIG is effective in autoimmune diseases not merely by a passive transfer of suppressive anti-idiotypes, but rather by imposing a normal function on the defective network in autoimmune patients.
Journal ArticleDOI

PGE2 inhibits natural killer and γδ T cell cytotoxicity triggered by NKR and TCR through a cAMP-mediated PKA type I-dependent signaling

Ludovic Martinet, +8 more
- 15 Sep 2010 - 
TL;DR: It is clearly demonstrated that the major NK receptors (NKR): NKG2D, CD16 and natural cytotoxicity receptors and gammadelta T cell receptors TCR Vgamma9Vdelta2, NKg2D and CD16 are inhibited by PGE(2), and how these data should impact particular approaches in the treatment of cancer is focused on.