WorldCat Identities

Balabanian, Karl

Overview
Works: 29 works in 35 publications in 2 languages and 132 library holdings
Genres: Laboratory manuals 
Roles: Editor, Opponent, Other, Thesis advisor, Contributor, Author, Publishing director, htt
Classifications: QP88.2, 616.0798
Publication Timeline
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Most widely held works by Karl Balabanian
Bone marrow environment : methods and protocols by Marion Espéli( )

5 editions published between 2021 and 2022 in English and held by 95 WorldCat member libraries worldwide

This volume brings together classical and cutting-edge protocols on the spatio-temporal study of the cellular subsets constituting the bone and the marrow in both mouse and human. Chapters details methods on bone marrow (BM) ecosystem, to label, sort, analyse, and culture specific cell subsets as well as techniques allowing the evaluation of the function of some of the cellular elements of the BM. Written in the highly successfulMethods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Authoritative and cutting-edge, Bone Marrow Environment: Methods and Protocols aims to help new investigators to pursue the characterization of the BM microenvironment in the coming years
Rôle de la chimiokine SDF-1 dans la compartimentalisation des lymphocytes B péritonéaux et dans le developpement de l'autoimmunité systémique by Karl Balabanian( Book )

2 editions published in 2003 in French and held by 3 WorldCat member libraries worldwide

Bone Marrow Environment : Methods and Protocols by Marion Espéli( )

2 editions published in 2021 in English and held by 3 WorldCat member libraries worldwide

This volume brings together classical and cutting-edge protocols on the spatio-temporal study of the cellular subsets constituting the bone and the marrow in both mouse and human. Chapters details methods on bone marrow (BM) ecosystem, to label, sort, analyse, and culture specific cell subsets as well as techniques allowing the evaluation of the function of some of the cellular elements of the BM. Written in the highly successfulMethods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Authoritative and cutting-edge, Bone Marrow Environment: Methods and Protocols aims to help new investigators to pursue the characterization of the BM microenvironment in the coming years
Expression of CXCL12 receptors in B cells from Mexican Mestizos patients with systemic lupus erythematosus by Vincent Biajoux( )

1 edition published in 2012 in English and held by 2 WorldCat member libraries worldwide

Nouvelles approches méthodologiques pour l'obtention d'anticorps humains monoclonaux by Mazhoura Ait Mebarek( )

1 edition published in 2012 in French and held by 2 WorldCat member libraries worldwide

The number of monoclonal antibodies used as drug or under clinical investigation increases rapidly. The first murine monoclonal antibodies (mAbs) used in therapy induces human anti-mouse antibodies (HAMAs) when administered to patients. Such HAMAs hamper the therapeutic efficacy of mAbs and induce side effects. To limit these effects, new antibodies were developed during the, last 30 years. Chimeric, humanized and fully human antibodies were engineered. The use of human monoclonal antibodies (hAbs) appears ideal to solve the problem of HAMAs. Nowadays 9 fully human antibodies are available and others are evaluated in clinical trials or currently investigated in research labs. Three methods exist to produce fully human antibodies: the phage display, the transgenic mice and the use of human B lymphocytes. The majority of fully human antibodies resulted from the phage display and the transgenic mice methods. The use of human B lymphocytes is less investigated due to a poor yield and stability problems. These last years, the immortalization process, thanks to the involvement of the Epstein-Barr virus and human myeloma, induced a rise of interest for human B lymphocytes. In this context we decided to develop fully human monoclonal antibodies using human B lymphocytes through immortalization using the Epstein-Barr virus followed or not by an immortalization with a human/mouse heteromyeloma HM. The first approach is based on hAbs production from peripheral blood memory B lymphocytes isolated from infected or vaccinated donors. The Staphylococcus aureus enterotoxine B (SEB) was used as a model. Memory B lymphocytes were purified and cultured in the presence of Epstein-Barr virus (EBV). The transformation of memory B lymphocytes by EBV allowed the generation of immortalized B lymphocytes lines producing IgGs antibodies directed against SEB. We succeeded in isolating 6 EBV-immortalized memory B lymphocytes lines secreting anti-SEB IgGs antibodies. After many attempts to immortalize EBV immortalized memory B lymphocytes lines secreting anti-SEB antibodies with myeloma, the fusion of a EBV immortalized memory B lymphocytes with the human/mouse heteromyeloma HM led to an hybridoma. Unfortunately this hybridoma has rapidly lost its capacity to secrete d'IgGs anti-SEB. In the second approach the hAbs production implies the in vitro immunization of peripheral blood naïve lymphocytes. This strategy could allow the hAbs production against antigens for which no infected or vaccinated donors may be available. The Clostridium Botulinum neurotoxin A (BoNT/A), the most powerful toxin, and its N-terminal peptide (TBA-Nter) or the fusion protein ZZTat101 were used as models. ZZTat101 is a fusion between the ZZ domain of Staphylococcus aureus and the Tat protein of the human immunodeficiency virus HIV-1. Monocytes, B lymphocytes and T lymphocytes were isolated from human PBMC depleted of Natural killer. These cells were tools to develop efficient in vitro immunization protocols. IgMs directed against TBA-Nter and also IgMs (and possibly IgGs) directed against Tat were obtained. The use of the Epstein-Barr virus induced 7 EBV immortalized lines secreting anti-TBA-Nter IgMs antibodies. Unfortunately, after fusion with the heteromyeloma HM no hybridoma was isolated against TBA-Nter and Tat. The ZZTat101 mechanism involved on humoral response was studied, showing that the 7 cysteines, the region 22-57 and the ability of Tat to bind heparane sulfate are necessary to trigger the humoral response
Description and outcome of a cohort of 8 patients with WHIM syndrome from the French Severe Chronic Neutropenia Registry by Sarah Beaussant Cohen( )

1 edition published in 2012 in English and held by 2 WorldCat member libraries worldwide

Identification of glucocorticoid-induced leucine zipper as a key regulator of tumor cell proliferation in epithelial ovarian cancer by Nassima Redjimi( )

1 edition published in 2009 in English and held by 2 WorldCat member libraries worldwide

CXCL12 expression by healthy and malignant ovarian epithelial cells by Véronique Machelon( )

1 edition published in 2011 in English and held by 2 WorldCat member libraries worldwide

Rôles de CXCL12beta dans l'hétérogénéité fibroblastique et l'immunosuppression dans les cancers de l'ovaire by Anne-Marie Givel( )

1 edition published in 2016 in French and held by 1 WorldCat member library worldwide

<> by Shulong Hu( )

1 edition published in 2015 in French and held by 1 WorldCat member library worldwide

Production et caractérisation d'anticorps polyclonaux et monoclonaux ciblant les récepteurs des endothélines en vue d'une immunothérapie des cancers by Bertrand Allard( )

1 edition published in 2012 in French and held by 1 WorldCat member library worldwide

Le développement des anticorps monoclonaux thérapeutiques est en plein essor notamment à cause de leur bénéfice important pour le traitement des cancers. Cependant, à l'heure actuelle, aucun anticorps monoclonal sur le marché ou en phase III ne cible de RCPGs, en dépit de l'implication grandissante de ces récepteurs dans la carcinogenèse. Parmi les RCPGs les plus pertinents pour l'oncologie, souvent cités dans la littérature et dont certains inhibiteurs chimiques sont en phase clinique avancée, on trouve les deux sous-types de récepteurs des endothélines ETAR et ETBR. Dans ce contexte, mon projet de thèse a consisté à produire des anticorps monoclonaux capables de lier spécifiquement les récepteurs des endothélines, puis à les caractériser dans le but d'évaluer leur potentiel antitumoral. Grâce à une stratégie d'immunisation génique, un ensemble de 27 anticorps monoclonaux, tous spécifiques de la forme native d'ETBR, a été obtenu. Un de ces anticorps, nommé rendomab-B1, a fait l'objet d'une caractérisation précise et s'est révélé être un puissant inhibiteur allostérique d'ETBR. De plus, cette propriété antagoniste a permis de bloquer l'action autocrine antiapoptotique de l'ET-1 sur des cellules endothéliales vasculaires, suggérant ainsi que le rendomab-B1 pourrait être utilisé comme agent thérapeutique afin d'inhiber les effets tumorigènes liés à la suractivation de l'axe ET1/ETBR au niveau de l'endothélium vasculaire tumoral. Par ailleurs, le rendomab-B1 a également été testé sur des lignées de mélanomes humains ; l'absence de fixation de l'anticorps malgré la présence de récepteurs ETB fonctionnels à la surface de ces cellules suggère l'existence d'une forme moléculaire atypique du récepteur, potentiellement spécifique aux mélanomes. A la lumière de ces résultats, le rendomab-B1 apparaît comme un outil prometteur, à la fois pour l'étude structurale et fonctionnelle d'ETBR, mais aussi pour une éventuelle thérapie anticancéreuse. Enfin, les 26 autres anticorps monoclonaux anti-ETBR, actuellement en cours de caractérisation, constituent également des molécules potentiellement intéressantes pour un usage fondamental ou thérapeutique impliquant ETBR. Pour conclure, ces travaux ont démontré l'intérêt de la méthode d'immunisation génique pour la production d'anticorps monoclonaux anti-RCPGs à visée thérapeutique
Rôle des récepteurs au S1P et de leur combinatoire dans la migration des lymphocytes T : chez l'homme et chez la souris by Antoinette Neyra( )

1 edition published in 2020 in French and held by 1 WorldCat member library worldwide

Le sphingosine-1-phosphate (S1P) régule la sortie des lymphocytes T des organes lymphoïdes secondaires (OLS). Sa forte concentration dans le sang et la lymphe permet d'attirer les lymphocytes T hors des OLS, où la concentration en S1P est faible. Le S1P peut se lier à cinq récepteurs membranaires (S1PR1-5) exprimés en combinatoires variables par les différentes sous-populations de lymphocytes T. On connaît actuellement assez mal le rôle du S1P dans la recirculation lymphocytaire chez l'homme, ainsi que le rôle des combinatoires des S1PR dans ce contexte. Nous souhaitons donc comprendre comment les récepteurs au S1P et leur combinatoire régulent la migration des lymphocytes T. Nous avons précédemment souligné l'existence d'un antagonisme entre S1PR1 et S1PR2 dans le contrôle de la sortie des lymphocytes T des OLS. Il a également été montré que, si S1PR1 était essentiel à la migration des lymphocytes T naïfs, les lymphocytes Natural Killer utilisaient préférentiellement S1PR5 pour sortie de la moelle osseuse et des OLS. De ce fait, ce projet de thèse se concentre sur deux axes : d'une part l'antagonisme fonctionnel entre S1PR1 et S1PR2, d'autre part la différence entre S1PR1 et S1PR5. Nous avons montré que la balance entre l'expression de S1PR1 et S1PR2 influençait fortement la réponse migratoire des Jurkat, S1PR1 réduisant la migration spontanée et augmentant la migration au S1P, et S1PR2 induisant l'effet inverse à faible dose de S1P. Nous avons également mis en évidence l'absence d'internalisation de S1PR5 par le S1P, à l'inverse de S1PR1 et S1PR2. Finalement, ces résultats soulignent des différences fonctionnelles entre les S1PR, qui permettent d'obtenir des réponses différentes à un même ligand
Etude du rôle de MYD88 et des voies NF-kB dans l'émergence des lymphomes B by Lilian Roland( )

1 edition published in 2021 in French and held by 1 WorldCat member library worldwide

Dérégulation des récepteurs de chimiokine CCR1 et CXCR4 dans le Lupus Erythémateux Disséminé et la Lymphopénie T CD4+ Idiopathique by Alexandre Bignon( )

1 edition published in 2014 in French and held by 1 WorldCat member library worldwide

My PhD works focused on the expression and function of chemokine receptors in two immune disorders, namely CCR1 in the lupus-prone NZB/W mouse model and CXCR4 in the Idiopathic CD4+ T-cell lymphopenia, a rare human immune defect.Systemic lupus erythematosus is a chronic inflammatory autoimmune disease, the development of which is characterized by a progressive loss of renal function. Such dysfunction is associated with renal leukocyte infiltration. During my PhD, I investigated the role of the CCR1 chemokine receptor in this process during the progression of nephritis in NZB/W mice. We found that peripheral T-cells, mononuclear phagocytes and neutrophils from nephritic NZB/W mice were more responsive to CCR1 ligands than the leukocytes from younger prenephritic mice. Short-term treatment of nephritic NZB/W mice with a orally available CCR1 antagonist decreased renal infiltration by T-cells and macrophages. Longer Ccr1 blockade decreased kidney accumulation of effector/memory CD4+ T-cells, Ly6C+ inflammatory monocytes, and both M1 and M2 macrophages; reduced tubulointerstitial and glomerular injuries; delayed fatal proteinuria; and prolonged animal lifespan. Altogether, these findings highlight a pivotal role for CCR1 in the recruitment of T and mononuclear phagocyte cells to inflamed kidneys of NZB/W mice, which in turn contribute to the progression of renal injury.ICL is heterogeneous immunological syndrome of unclear molecular mechanisms, characterized by a profound and persistent CD4+ T-cell defect and by opportunistic infections in particular of fungal origin. We detected using multiparametric flow-cytometry analyses, reduced levels of CXCR4 expression and chemotactic function on T-cells from 17 of 20 ICL patients. These results suggest that the impaired membrane expression and function of CXCR4 is a common biologic trait of ICL. Using a transcriptomic approach, we also identified an ICL-specific T-cell gene expression signature characteristic of low TCR sensitivity and accelerated T-cell aging. Phenotypic and functional analyses of circulating T cells confirmed these observations and extended them to include an expansion of terminally-differentiated T cells with hallmarks of aging including loss of the co-stimulatory molecules CD27 and CD28, defective in vitro TCR responses, and telomere erosion. Mechanistically, we further showed that intrinsic T-cell signaling defects were caused by higher expression of DUal-Specific Phosphatase 4 (DUSP4). These findings suggest that premature T-cell senescence occurs in ICL as a result of chronic T-cell activation. This is in part due to abnormally high DUSP4 expression in CD4+ T cells, the modulation of which may constitute a novel therapeutic avenue in ICL to improve vaccination strategies
Rôle de la désensibilisation de CXCR4 dans l'homéostasie médullaire chez la souris by Julie Nguyen( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

The CXCL12/CXCR4 signaling axis plays an essential role in the maintenance of hematopoietic stem and progenitor cell (HSPC) homeostasis and constitutes a key pathway through which the niches and HSPCs communicate in the bone marrow (BM). Heterozygous gain-of-function mutations of CXCR4, which engender a truncated receptor and affect its homologous desensitization in response to CXCL12, have been reported in the WHIM Syndrome (WS); a rare immunodeficiency notably characterized by lymphopenia. The mechanisms underpinning this remain obscure. Using a mouse model harboring a naturally occurring WS-linked Cxcr4 gain-of-function mutation, we explored the possibility that the lymphopenia in WS arise from defects at the HSPC level in the BM. We showed that Cxcr4 desensitization is required for proper quiescence/cycling balance of short-term HSCs as well as their differentiation into multipotent progenitors and downstream lymphoid-biased progenitors. Thus, our results suggest that efficient Cxcr4 desensitization is critical for lymphoid differentiation of HSPCs, and its impairment is a key mechanism underpinning the lymphopenia observed in WS mice. The role of Cxcr4 desensitization in regulating such lympho-hematopoiesis process implicated both intrinsic and extrinsic properties, thus raising the question of the impact of a gain-of-Cxcr4-function mutation on BM stroma. Therefore, the main part of my PhD project was dedicated to evaluate using this relevant knock-in model the impact of Cxcr4 desensitization on maintenance of BM mesenchymal elements. We have found unexpectedly that such regulatory mechanism is intrinsically required for regulating quiescence/cycling balance of mesenchymal stem cells (MSCs) and preserving their osteogenic potential through the control of Cxcl12 expression and availability in an autocrine manner. Therefore, these findings support autocrine and paracrine actions of the Cxcl12/Cxcr4 signaling axis within MSCs to regulate osteoblast differentiation while contributing to HSPC niches and hematopoiesis
Rôle du long ARN non-codant CRNDE dans le myélome multiple by Antoine David( )

1 edition published in 2019 in French and held by 1 WorldCat member library worldwide

Multiple myeloma (MM) is a malignancy of antibody-secreting plasma cells which remains incurable. MM is characterised by a wide clinical and prognostic spectrum, even within groups bearing the same primary cytogenetic event, for which the secondary molecular mechanisms responsible are still incompletely understood. Long non-coding RNAs (lncRNAs) are now recognised as an important class of regulatory molecules which are increasingly implicated in tumorigenesis and cancer progression. While recent studies have demonstrated prognostically relevant changes in the lncRNA expression profile in MM, the functional significance and molecular pathways downstream of these changes remain poorly characterised. In this study we have undertaken a thorough functional and molecular characterisation of the effect in MM cells of Colorectal Neoplasia Differentially Expressed (CRNDE), a known oncogenic lncRNA which has been previously implicated in diverse solid and haematological malignancies. CRNDE is overexpressed in plasma cells of MM patients, where it is a poor prognostic marker. CRISPR-mediated deletion of the CRNDE locus decreases proliferation and adhesion properties of MM cells in vitro and reduces tumour growth in an in vivo xenograft model. Transcriptomic profiling in CRNDE-deleted cells demonstrated that CRNDE activates expression of a number of genes previously implicated in the aetiology of MM, including the gene encoding the receptor of IL6 (IL6R), a cytokine critical for MM cell proliferation and survival. We further demonstrate that deletion of the CRNDE locus impacts upon IL6 signalling and proliferative responses in MM cells. Altogether this study reveals a novel mechanistic pathway by which the lncRNA CRNDE impacts upon MM growth and disease progression, by regulating the expression of IL6R and thus controlling response to IL6 signalling
Characterization of thymic hyperplasia associated with autoimmune Myasthenia Gravis : role of the chemokines CXCL12 and CXCL13 by Julia Miriam Weiss( )

1 edition published in 2011 in English and held by 1 WorldCat member library worldwide

Etude des mécanismes impliqués dans le processus métastatique dans le cancer colique humain : implication de l'axe CXCL12/CXCR4/CXCR7 by Radhia Benbrika( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

Despite early cancer detection and therapeutic advances, the mortality rate in patients diagnosed with CRC at the metastatic stage remains very high. The aim of this work was to study the role of the chemokine CXCL12 and its two receptors CXCR4 and CXCR7 in the metastatic process. I compared the expression of the chemokine CXCL12 in human colon tumors with the associated healthy tissues, then I focused on the mechanisms regulating this expression and more particularly the epigenetic regulation. I have shown that the CXCL12 promoter is methylated in 35% of the CCR and that a lack of histone acetylation of the CXCL12 promoter causes the loss of its expression. Enzymes involved in the regulation of epigenetic mechanisms, potentially related to this acetylation defect, were identified by Array PCR on tumors and among these factors, the histone acetyl transferase PCAF, whose expression is decreased in tumors, was identified. Finally, to understand the respective role of CXCR4 and CXCR7 in metastatic spread, I invalidated the expression of both receptor genes in the human colonic line SW480 by Crispr-Cas9, and then compared the migratory capacity of the cells in vitro and their metastatic potential in vivo. Inducing a loss of expression of CXCR7 receptor did not have an impact on the development of pulmonary and hepatic metastases in vivo, but resulted in a decrease in in vitro migration
Etude des conséquences de l'hypoxie dans les étapes précoces de la lymphopoïèse humaine by Sara Chabi( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

The hypoxic environment characterizes the medullary hematopoietic niche and lymphoid organs. Physiological hypoxia is fundamental for the proper functioning of hematopoietic stem cells (HSCs) by allowing its maintenance throughout the life of the individual. Hypoxia induces cell quiescence via the inactivation of mitochondrial respiration and the protection of the accumulation of reactive oxygen, toxic for HSC homeostasis. Adaptation to the hypoxic microenvironment involves sensory proteins called HIFs (hypoxia response factors). These factors are involved at several levels of the cellular machinery allowing stem cells to preserve their fundamental properties of self-renewal, quiescence and multipotency. Lymphopoiesis is the mechanism that allows the generation of lymphoid B, T and NK cells. This mechanism takes place very early in hematopoietic development from CSH and involves MPPs (multipotent progenitors), LMPPs (lymphoid-primed multipotent progenitors), Pro-TNK and Pro-B. Lymphoid development is subject to hypoxia, but very little data has been reported in the literature concerning the regulation of lymphopoiesis by low doses of oxygen. In this work we have addressed the role of hypoxia in human lymphoid development by focusing on the early stages of lymphoid differentiation. We found that hypoxia acts differently on hemato-lymphoid progenitors by specifically modulating the lymphoid potential of LMPPs and Pro-TNKs. In addition, the differential involvement of HIF factors according to LMPPs and Pro-TNK target progenitors was also highlighted. Thus, for the first time, we were able to demonstrate that hypoxia and HIF factors modulate in vitro and in vivo the early stages of human lymphoid differentiation
Impact d'un gain de fonction de CXCR4 sur la différenciation des cellules souches et des progéniteurs hématopoïétiques by Christelle Freitas( )

1 edition published in 2016 in French and held by 1 WorldCat member library worldwide

Le Syndrome WHIM (SW) est un déficit immuno-hématologique rare qui se caractérise notamment par une profonde leucopénie circulante. Le SW résulte principalement de mutations hétérozygotes autosomiques dans CXCR4 qui tronquent partiellement le domaine C-terminal de la protéine et entraînent un défaut de désensibilisation de CXCR4 en réponse à CXCL12. L'impact in vivo d'un gain de fonction de CXCR4 sur le développement et la différenciation lymphocytaires restant à définir, nous avons généré un modèle murin hétérozygote pour la mutation ponctuelle identifiée chez certains patients. L'objectif de ma thèse a été de déterminer si un défaut de différenciation des cellules souches et des progéniteurs hématopoïétiques (CSPH) était à l'origine de ces anomalies de lymphopoïèse. Nous avons observé que le nombre et la clonogénicité des CSH sont préservés dans la moelle osseuse des souris mutantes. Toutefois, les CSH porteuses de la mutation gain de fonction de Cxcr4 ont une quiescence accrue alors que leur multipotence et leur auto-renouvellement sont réduits. Ces dérégulations du compartiment des CSH entraînent, in vivo et in vitro, une altération de la production et de la spécification lymphoïde des progéniteurs multipotents (MPP). En périphérie, nous avons mis en évidence une diminution des CSPH dans le sang des souris mutantes, anomalie également retrouvée à partir de prélèvements sanguins de quatre patients atteints du SW et porteurs d'une mutation hétérozygote dans CXCR4. Ces résultats indiquent une anomalie de circulation des CSPH, hypothèse confortée par le développement d'une hématopoïèse extra-médullaire intra-splénique chez les souris mutantes. Ces données suggèrent que la désensibilisation de Cxcr4 régule la quiescence, la multipotence et l'auto-renouvellement des CSH et serait requise pour la spécification lymphoïde des MPP. Ainsi, l'absence de ce processus pourrait être à l'origine de la lymphopénie observée dans notre modèle murin et, par extrapolation, chez les patients
 
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Bone marrow environment : methods and protocols
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