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Search Results: 1 - 10 of 2176 matches for " Laurence Morel "
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Mouse Models of Human Autoimmune Diseases: Essential Tools That Require the Proper Controls
Laurence Morel
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.0020241
Abstract:
Mouse Models of Human Autoimmune Diseases: Essential Tools That Require the Proper Controls
Laurence Morel
PLOS Biology , 2004, DOI: 10.1371/journal.pbio.0020241
Abstract:
Autoreactive marginal zone B cells enter the follicles and interact with CD4+ T cells in lupus-prone mice
Zhenhai Zhou, Haitao Niu, Ying-Yi Zheng, Laurence Morel
BMC Immunology , 2011, DOI: 10.1186/1471-2172-12-7
Abstract: The intrafollicular location of B6.TC MZB cells starts before disease manifestations and puts MZB cells in direct contact with CD4+ T cells. Two different autoreactive B cell receptor (BCR) transgenic models showed that the expression of the Sle susceptibility loci enhances the presence of MZB cells inside the follicles. In vitro, B6.TC MZB cells were better effectors than B6 MZB cells with enhanced proliferation and antibody (Ab) production, including anti-DNA Ab, in response to stimulation with TLR ligands, immune complexes or anti-CD40. Furthermore, B6.TC MZB and CD4+ T cells showed a reciprocally enhanced activation, which indicated that their contacts inside B6.TC follicles have functional consequences that suggest an amplification loop between these two cell types.These results showed that the NZM2410 susceptibility loci induce MZB cells to locate into the follicles, and that this breach of follicular exclusion occurs early in the development of the autoimmune pathogenesis. The enhanced responses to stimulation and increased effector functions of MZB cells from lupus-prone mice as compare to non-autoimmune MZB cells provide a mechanism by which the failure of MZB cell follicular exclusion contributes to the autoimmune process.Systemic lupus erythematosus (SLE) is an autoimmune disease in which defects in multiple B cell subsets have long been recognized [1]. Marginal zone (MZ) B cells are enriched for autoreactive specificities through the expression of self-reactive germline-encoded BCRs [2]. MZB cells transport antigen inside the follicles [3] and are potent T-cell activators that respond more rapidly than follicular (FO) B cells to T-dependent antigen [4]. MZB cells also differentiate rapidly into plasma cells [5-9]. Finally, MZB cells respond better to T cells than FOB cells in vitro but not in vivo [10], showing that physiological barriers prevent in vivo activation of MZB cells [11]. These observations have led to hypothesize the existence of a tolerance
The Current Concept of T H 17 Cells and Their Expanding Role in Systemic Lupus Erythematosus
Daniel Perry,Ammon B. Peck,Wendy C. Carcamo,Laurence Morel,Cuong Q. Nguyen
Arthritis , 2011, DOI: 10.1155/2011/810649
Abstract: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a multifaceted range of symptoms affecting almost every organ system. The prototypical pathology of SLE involves the production of antinuclear antibodies and the deposition of immune complexes in basement membranes throughout the body where they induce inflammatory responses. The genetic and environmental etiologies of this process are being intensively sought, and recently, TH17 cells have been implicated in the pathogenesis of SLE. TH17 cells are CD4
Murine Models of Systemic Lupus Erythematosus
Daniel Perry,Allison Sang,Yiming Yin,Ying-Yi Zheng,Laurence Morel
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/271694
Abstract: Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disorder. The study of diverse mouse models of lupus has provided clues to the etiology of SLE. Spontaneous mouse models of lupus have led to identification of numerous susceptibility loci from which several candidate genes have emerged. Meanwhile, induced models of lupus have provided insight into the role of environmental factors in lupus pathogenesis as well as provided a better understanding of cellular mechanisms involved in the onset and progression of disease. The SLE-like phenotypes present in these models have also served to screen numerous potential SLE therapies. Due to the complex nature of SLE, it is necessary to understand the effect specific targeted therapies have on immune homeostasis. Furthermore, knowledge gained from mouse models will provide novel therapy targets for the treatment of SLE.
The Current Concept of T H 17 Cells and Their Expanding Role in Systemic Lupus Erythematosus
Daniel Perry,Ammon B. Peck,Wendy C. Carcamo,Laurence Morel,Cuong Q. Nguyen
Arthritis , 2011, DOI: 10.1155/2011/810649
Abstract: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a multifaceted range of symptoms affecting almost every organ system. The prototypical pathology of SLE involves the production of antinuclear antibodies and the deposition of immune complexes in basement membranes throughout the body where they induce inflammatory responses. The genetic and environmental etiologies of this process are being intensively sought, and recently, TH17 cells have been implicated in the pathogenesis of SLE. TH17 cells are CD4+ memory T cells that behave as both helper and effector cell populations functioning through their signature IL-17 cytokines. Their differentiation is distinct to either the TH1 or TH2 cell lineage, but strongly influences development of adaptive responses, including autoimmunity. This paper details the biological functions and regulation of TH17 cells, followed by an update of their expanding role in SLE. 1. Introduction The vertebrate immune system has evolved to protect its host against invading pathogens and other environmental antigens. It is strategically organized to optimally guard against foreign or “nonself” antigens through intricate interactions between innate and adaptive immunity, allowing for the survival of the host. The adaptability and resiliency of the immune system rely on complex physiological and immunological mechanisms, many of which remain to be unraveled. Since the initial classification of TH1 and TH2 cells by Coffman, Mosmann, and colleagues in 1986, much focus has attempted to elucidate the role of helper T cell populations. These efforts have led to the identification of a distinct T helper population, called TH17 cells [1–3], which challenges the long-standing TH1/ TH2 paradigm and has advanced our overall understanding of T helper cells in health and disease. Paradoxically, the same mechanisms that prevent disease quite commonly induce hypersensitivity and autoimmunity. In fact, it was in the study autoimmunity in which the key observations that led to the discovery of TH17 cells were made. These studies found that TH1 cells were not required for induction of experimental autoimmune encephalomyelitis (EAE) in mice, as had been thought [4, 5]. EAE induction instead required an IL-23-dependent set of T cells that were later identified as the unique TH17 cell subset. Since then, numerous reports have shown TH17 cells to be relevant, and sometimes central, to autoimmune pathogenesis, highlighting them as therapeutic targets. Recently, TH17 cells have been implicated in SLE pathogenesis. SLE is a chronic
Spontaneous gelation of wheat gluten proteins in a food grade solvent
Mohsen Dahesh,Amélie Banc,Agnès Duri,Marie-Hélène Morel,Laurence Ramos
Physics , 2015, DOI: 10.1016/j.foodhyd.2015.06.014
Abstract: Structuring wheat gluten proteins into gels with tunable mechanical properties would provide more versatility for the production of plant protein-rich food products. Gluten, a strongly elastic protein material insoluble in water, is hardly processable. We use a novel fractionation procedure allowing the isolation from gluten of a water/ethanol soluble protein blend, enriched in glutenin polymers at an unprecedented high ratio (50%). We investigate here the viscoelasticity of suspensions of the protein blend in a water/ethanol (50/50 v/v) solvent, and show that, over a wide range of concentrations, they undergo a spontaneous gelation driven by hydrogen bonding. We successfully rationalize our data using percolation models and relate the viscoelasticity of the gels to their fractal dimension measured by scattering techniques. The gluten gels display self-healing properties and their elastic plateaus cover several decades, from 0.01 to 10000 Pa. In particular very soft gels as compared to standard hydrated gluten can be produced.
Polymeric Assembly of Gluten Proteins in an Aqueous Ethanol Solvent
Mohsen Dahesh,Amélie Banc,Agnès Duri,Marie-Hélène Morel,Laurence Ramos
Physics , 2014, DOI: 10.1021/jp5047134
Abstract: The supramolecular organization of wheat gluten proteins is largely unknown due to the intrinsic complexity of this family of proteins and their insolubility in water. We fractionate gluten in a water/ethanol (50/50 v/v) and obtain a protein extract which is depleted in gliadin, the monomeric part of wheat gluten proteins, and enriched in glutenin, the polymeric part of wheat gluten proteins. We investigate the structure of the proteins in the solvent used for extraction over a wide range of concentration, by combining X-ray scattering and multi-angle static and dynamic light scattering. Our data show that, in the ethanol/water mixture, the proteins display features characteristic of flexible polymer chains in a good solvent. In the dilute regime, the protein form very loose structures of characteristic size 150 nm, with an internal dynamics which is quantitatively similar to that of branched polymer coils. In more concentrated regimes, data highlight a hierarchical structure with one characteristic length scale of the order of a few nm, which displays the scaling with concentration expected for a semi-dilute polymer in good solvent, and a fractal arrangement at much larger length scale. This structure is strikingly similar to that of polymeric gels, thus providing some factual knowledge to rationalize the viscoelastic properties of wheat gluten proteins and their assemblies.
Alterations of renal phenotype and gene expression profiles due to protein overload in NOD-related mouse strains
Karen HS Wilson, Richard A McIndoe, Sarah Eckenrode, Laurence Morel, Anupam Agarwal, Byron P Croker, Jin-Xiong She
BMC Nephrology , 2005, DOI: 10.1186/1471-2369-6-17
Abstract: Proteinuria was induced by protein overload on NON and NOD.B10 mouse strains and histology and microarray technology were used to follow the kidney response. The effects of proteinuria were assessed and subsequently compared to changes that were observed in a prior study on NOD diabetic nephropathy.Overload treatment significantly modified the renal phenotype and out of 5760 clones screened, 21 and 7 kidney transcripts were respectively altered in the NON and NOD.B10. Upregulated transcripts encoded signal transduction genes, as well as markers for inflammation (Calmodulin kinase beta). Down-regulated transcripts included FKBP52 which was also down-regulated in diabetic NOD kidney. Comparison of transcripts altered by proteinuria to those altered by diabetes identified mannosidase 2 alpha 1 as being more specifically induced by proteinuria.By simulating a component of diabetes, and looking at the global response on mice resistant to the disease, by virtue of a small genetic difference, we were able to identify key factors in disease progression. This suggests the power of this approach in unraveling multifactorial disease processes.The cause of the relentless progression of chronic kidney disease (CKD) to chronic renal failure is likely to be multifactorial. CKD itself has a variety of inciting etiologies [1]. Accumulating clinical evidence indicates that proteinuria is associated with CKD [2] and predictive of progression in CKD regardless of diverse etiologies [3]. Subsequent animal studies and in vitro experiments provided additional evidence for proteinuria in progressive CKD. Because kidney complications occur frequently in diabetic patients, we recently conducted a microarray study on gene transcripts altered by diabetes in non-obese diabetic (NOD) mice kidneys [4]. As NOD spontaneously develops both diabetes and proteinuria, our previous studies could not distinguish gene expression changes due to diabetes versus proteinuria. To identify gene expression chang
Irinotecan induces steroid and xenobiotic receptor (SXR) signaling to detoxification pathway in colon cancer cells
Agnes Basseville, Laurence Preisser, Sophie de Carné Trécesson, Michèle Boisdron-Celle, Erick Gamelin, Olivier Coqueret, Alain Morel
Molecular Cancer , 2011, DOI: 10.1186/1476-4598-10-80
Abstract: In this study, we have shown that endogenous SXR is activated in response to SN-38, the active metabolite of the anticancer drug irinotecan, in human colon cancer cell lines. We have found that endogenous SXR translocates into the nucleus and associates with RXR upon SN-38 treatment. Using ChIP, we have demonstrated that endogenous SXR, following its activation, binds to the native promoter of the CYP3A4 gene to induce its expression. RNA interference experiments confirmed SXR involvement in CYP3A4 overexpression and permitted us to identify CYP3A5 and MRP2 transporter as SXR target genes. As a consequence, cells overexpressing SXR were found to be less sensitive to irinotecan treatment.Altogether, these results suggest that the SXR pathway is involved in colon cancer irinotecan resistance in colon cancer cell line via the upregulation of select detoxification genes.One of the challenges in cancer treatment is to understand why some tumors fail to respond to chemotherapy. Delineating in advance the subsets of tumors presenting treatment failure and identifying which pathways are involved in drug resistance would thus represent a significant advance. Several factors contribute to the development of drug resistance. Inadequate drug access to the tumor, drug metabolism and excretion, activation of DNA repair mechanisms, and inactivation of cell death pathways have all been proposed as potential mechanisms used by tumor cells to escape treatment [1,2].Drug metabolism reactions are divided into three phases: functionalization (phase I enzyme), conjugation (phase II enzymes), and transport (phase III proteins), but it is essentially carried out by cytochrome p450 3A4 (CYP3A4), which metabolizes more than 50% of all administered drug [3]. CYP3A4 is the predominant isoform of monooxygenases present in the liver but there is also evidence that metabolism occurs within the tumors that express this isoform, and thereby reduces the efficacy of chemotherapeutic agents [4,5]. It
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