Boitard, Christian 1951-

B cells and autoantibody production in autoimmune diseases by Christian Boitard( Book )

8 editions published between 1995 and 1996 in English and held by 73 WorldCat member libraries worldwide

Diabète non insulinodépendant( Book )

3 editions published between 1997 and 1998 in French and held by 24 WorldCat member libraries worldwide

Kinetics of insulin release in health and type 2 diabetes : proceedings of the Second Servier-IGIS Symposium, St. Jean Cap Ferrat, France, 22-24 March 2001 by Servier-IGIS Symposium( Book )

1 edition published in 2002 in English and held by 11 WorldCat member libraries worldwide

Type 1 and type 2 diabetes: less apart than apparent? : proceedings of the Sixth Servier-IGIS Symposium, St. Jean Cap Ferrat, France, 10-13 March 2005( Book )

2 editions published in 2005 in English and held by 10 WorldCat member libraries worldwide

Activation et induction de tolérance des lymphocytes T dans des modèles de souris transgéniques by Nadège Bercovici( )

2 editions published in 1999 in French and held by 4 WorldCat member libraries worldwide

Antigen recognition by T cell can lead to immunity but also to antigen-specific T-cell tolerance. Immunological tolerance can be induced experimentally and may be useful for the treatment of organ-specific autoimmune diseases such as autoimmune diabetes. In this work, I have investigated the mechanisms of activation and tolerance induction in mature CD4+ and CDS+ T cells from TCR-transgenic mice. Systemic administration of soluble peptide is remarkably efficient to induce peripheral T-cell tolerance in vivo. Although one single injection induced transient T-cell tolerance, chronic intravenous (i.v.) injections of soluble peptide is able to maintain CD4+ T-cell tolerance for more than 12 weeks. I have also shown that i.v. injection of soluble peptide can tolerize naive CDS+ T cells but can also target effector CDS+ T cells thereby blocking the progression of an ongoing CDS-mediated autoimmune diabetes. Importantly, CDS+ T cell infiltrates are eliminated without bystander tissue damage. Furthermore, I have demonstrated that i.v. injection of soluble MHC class I : peptide complexes represent an alternative strategy to induce CDS+ T cell tolerance in vivo. Tolerance was achieved by deletion and anergy of antigen-specific CDS+ T cells and allow to down-regulate an ongoing CDS mediated autoimmune diabetes. In experiments conducted in vitro with naïve T cells from TCR-transgenic mice, we have shown that antigen recognition by CD4+ T cells rapidly induced cytoskeletal alterations that are crucial for calcium responses and proliferation. Under conditions in which equal numbers of specific MHC class Il :peptide complexes are presented by dendritic cells (DC) and B cells, we could demonstrate that DC are always more efficient antigen presenting cells underlying the importance of adhesion/costimulatory molecules abundantly expressed by DC. Moreover, we provide evidence for the induction of small calcium signals in CD4+ T cells interacting with DC in the absence of specific antigen that involve MHC/TCR interactions. Finally, we have shown that naive CDS+ T cells can be fully activated and differentiated after antigenic stimulation in the absence of co-stimulatory signals. Altogether, these data contribute to our understanding of the mechanisms of activation and tolerance induction of CD4+ and CDS+ T cells

Impact of treatment on islet function in type 2 diabetes: a critical appraisal : proceedings of the fifth Servier-IGIS symposium, St. Jean Cap Ferrat, France, 18-20 March 2004 by Servier-IGIS Symposium( Book )

1 edition published in 2004 in English and held by 4 WorldCat member libraries worldwide

Diabète de type 1 : les ilôts de Langerhans ne sont pas des cibles passives de l'agression autoimmune by Etienne Larger( Book )

2 editions published in 2001 in French and held by 4 WorldCat member libraries worldwide

Immunogénicité de la préproinsuline dans le diabète de type 1 humain chez un modèle murin humanisé HLA by Taghrid Hammoud Laika( Book )

2 editions published in 2008 in French and held by 3 WorldCat member libraries worldwide

Type 1 diabetes involves the activation of lymphocytes against p cell autoantigens. In animal models, the predominant role of T lymphocytes is supported by experiments in which diabetes is transferred into naive recipients by diabetogenic T cells, is prevented by antibodies that interfere with T lymphocyte activation or fails to develop in diabetes-prone mice in which key genes in T lymphocyte differentiation or activation are non functional . In man, T lymphocytes are predominant within insulitis at early stages of diabetes. Occurrence of diabetes in an immuno-deficient patient deprived of B lymphocytes further underscores the role of T lymphocytes in human diabetes. MHC class II-restricted CD4+ T cells are central in the autoimmune diabetes process but CDS* T cells play a pivotal role in its initiation in NOD mice . In the human, CD8+ T cells are predominant in the islet cell infiltrate of acutely diabetic patients in most observations. Recurrent diabetes in recipients of isografts from a discordant twin is accompanied by predominant CD8+ T cell infiltration. Among p cell autoantigens, proinsulin has been ascribed a key role in diabetes. In man, insulin and proinsulin are common targets of autoantibodies and T cells in diabetic and prediabetic individuals. Anti-insulin antibodies (IAA) are the first to be detected in children at risk for diabetes and carry a high positive predictive value for diabetes in siblings of type 1 diabetic patients. In NOD mice, injection of insulin-specific T cell clones accelerate diabetes. Protection from diabetes is obtained by injecting insulin in prediabetic mice. In addition, proinsulin 1"'" or 2"'" NOD mice show delayed or accelerated diabetes, respectively. We and others have obtained evidence that a restricted region of human proinsulin located in the B chain and adjacent C-peptide clusters proteasotne cleavage sites generating correct C-termini of putative MHC class 1 peptides and a high number of epitopes that are recognized by diabetic CDS* T cells. Other epitopes have been located within the A chain. Recognition of epitopes that are located within the C peptide and C peptide-B chain junction including residues that are excised during the insulin secretion process makes a strong case for proinsulin as an autoantigen in diabetes. However, there has been no study of epitopes located within the preproinsulin leader sequence despite strong evidence that leader sequence peptides can be presented by class I HLA molecules, especially HLA-A2.1. To characterize class I-restricted epitopes within the preproinsulin leader sequence, we selected 8- to 11-mer peptides carrying anchoring residues for class I molecules. These peptides were studied for binding to common class I molecules and for carrying C-terminal residues generated by proteasome digestion. HLA-A2-restricted peptides were further tested for immunogenicity in HLA-A*0201 transgenic mice. Peptides were studied for recognition by PBMCs from diabetic patients. To study the natural processing of preproinsulin leader peptide, mouse CD8+ T cell clones specific to HLA-A*0201 -restricted peptides were tested for cytotoxicity against PS 15 cells transfected with the HHD and preproinsulin genes

Le rôle de la voie de costimulation ICOS/ICOSL dans le développement du diabète de type 1 chez la souris NOD by Nicolas Prevot( Book )

1 edition published in 2010 in French and held by 3 WorldCat member libraries worldwide

ETUDE FONCTIONNELLE DE SUSPENSIONS DE CELLULES D'ILOTS DE LANGERHANS DE SOURIS IN VITRO : APPLICATION A L'ETUDE DE REACTIONS IMMUNITAIRES ANTIPANCREATIQUES by Christian Boitard( Book )

1 edition published in 1982 in French and held by 3 WorldCat member libraries worldwide

LES LYMPHOCYTES CIRCULANTS PROVENANT DE SUJETS DIABETIQUES INSULINO-DEPENDANTS BLOQUENT LA SECRETION D'INSULINE DE SUSPENSIONS DE CELLULES INSULAIRES DE SOURIS IN VITRO. LA SECRETION DE GLUCAGON N'EST PAS MODIFIEE. LES LYMPHOCYTES DES SUJETS DIABETIQUES NON INSULINO-DEPENDANTS N'ONT AUCUNE ACTION DANS CE MODELE. LA RESPONSABILITE DE LYMPHOCYTES T EST SUGGEREE PAR L'ETUDE DE SOUS-POPULATIONS LYMPHOCYTAIRES. LES CELLULES FORMANT DES ROSETTES E, OKT::(3)**(+), OKT::(4)**(-) (POPULATION LYMPHOCYTAIRE INCLUANT LES CELLULES T "CYTOTOXIQUES") PARAISSENT RESPONSABLES DE L'INHIBITION DE LA SECRETION D'INSULINE OBSERVEE. L'OBSERVATION IN VITRO D'UNE CYTOTOXICITE LYMPHOCYTAIRE, NON SPECIFIQUE D'ESPECE, SPECIFIQUE DES CELLULES SECRETANT L'INSULINE, RETROUVEE UNIQUEMENT AU COURS DU DIABETE INSULINO-DEPENDANT, EST COMPATIBLE AVEC LE ROLE DU SYSTEME IMMUNITAIRE DANS LE DECLENCHEMENT OU L'ENTRETIEN DES LESIONS INSULAIRES CARACTERISTIQUES. RESULTATS EN FAVEUR DE L'INDIVIDUALISATION D'AU MOINS 2 GROUPES DE DIABETIQUES INSULINO-DEPENDANTS