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  1. Article ; Online: Human anti-smallpox long-lived memory B cells are defined by dynamic interactions in the splenic niche and long-lasting germinal center imprinting.

    Chappert, Pascal / Huetz, François / Espinasse, Marie-Alix / Chatonnet, Fabrice / Pannetier, Louise / Da Silva, Lucie / Goetz, Clara / Mégret, Jérome / Sokal, Aurélien / Crickx, Etienne / Nemazanyy, Ivan / Jung, Vincent / Guerrera, Chiara / Storck, Sébastien / Mahévas, Matthieu / Cosma, Antonio / Revy, Patrick / Fest, Thierry / Reynaud, Claude-Agnès /
    Weill, Jean-Claude

    Immunity

    2022  Volume 55, Issue 10, Page(s) 1872–1890.e9

    Abstract: Memory B cells (MBCs) can persist for a lifetime, but the mechanisms that allow their long-term survival remain poorly understood. Here, we isolated and analyzed human splenic smallpox/vaccinia protein B5-specific MBCs in individuals who were vaccinated ... ...

    Abstract Memory B cells (MBCs) can persist for a lifetime, but the mechanisms that allow their long-term survival remain poorly understood. Here, we isolated and analyzed human splenic smallpox/vaccinia protein B5-specific MBCs in individuals who were vaccinated more than 40 years ago. Only a handful of clones persisted over such an extended period, and they displayed limited intra-clonal diversity with signs of extensive affinity-based selection. These long-lived MBCs appeared enriched in a CD21
    MeSH term(s) B-Lymphocytes/metabolism ; Germinal Center ; Humans ; Immunoglobulin G/metabolism ; Immunologic Memory ; Memory B Cells
    Chemical Substances Immunoglobulin G
    Language English
    Publishing date 2022-09-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2022.08.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4227: Show issues Location:
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  2. Article ; Online: TSC-22 Promotes Interleukin-2-Deprivation Induced Apoptosis in T-Lymphocytes.

    Pépin, Aurélie / Espinasse, Marie-Alix / Latré de Laté, Perle / Szely, Natacha / Pallardy, Marc / Biola-Vidamment, Armelle

    Journal of cellular biochemistry

    2016  Volume 117, Issue 8, Page(s) 1855–1868

    Abstract: Originally described as a TGF-β-inducible gene, tsc-22 (Transforming growth factor-beta Stimulated Clone 22) encodes a transcriptional regulator affecting biological processes such as cell growth, differentiation, or apoptosis. Along with GILZ ( ... ...

    Abstract Originally described as a TGF-β-inducible gene, tsc-22 (Transforming growth factor-beta Stimulated Clone 22) encodes a transcriptional regulator affecting biological processes such as cell growth, differentiation, or apoptosis. Along with GILZ (Glucocorticoid-Induced Leucine Zipper), TSC-22 belongs to the evolutionary conserved TSC-22 Domain family. We previously showed that, in T-lymphocytes, GILZ expression was induced upon IL-2 withdrawal, delaying apoptosis through down-regulation of the pro-apoptotic protein BIM expression. The aim of this work was then to elucidate the respective roles of GILZ and TSC-22 upon IL-2 deprivation-induced apoptosis. We report here that these two highly homologous genes are concomitantly expressed in most human tissues and in primary T-lymphocytes and that expression of TSC-22 promotes T-lymphocytes apoptosis by inhibiting GILZ functions. Indeed, we demonstrated that TSC-22 expression in the murine lymphoid CTLL-2 cell line promoted IL-2 deprivation-induced apoptosis. BIM expression and caspases-9 and -3 activities were markedly increased in TSC-22 expressing clones compared to control clones. Analysis of GILZ expression revealed that TSC-22 prevented the induction of the GILZ protein upon IL-2 deprivation, by inhibiting gilz mRNA transcription. These results suggested that TSC-22 could counteract the protective effect of GILZ on IL-2-deprivation-induced apoptosis. Moreover, TSC-22-induced inhibition of GILZ expression was also found in CTLL-2 cells treated with glucocorticoids or TGF-β. In the human NKL cell line deprived of IL-2, TSC-22 showed the same effect and thus may represent a potent repressor of GILZ expression in IL-2-dependent cells, independently of the cell type, or the stimulus, leading to an increase of IL-2-deprived T-cells apoptosis. J. Cell. Biochem. 117: 1855-1868, 2016. © 2016 Wiley Periodicals, Inc.
    MeSH term(s) Animals ; Apoptosis/immunology ; Cell Line ; Gene Expression Regulation/immunology ; Humans ; Interleukin-2/genetics ; Interleukin-2/immunology ; Killer Cells, Natural/cytology ; Killer Cells, Natural/immunology ; Mice ; Repressor Proteins/genetics ; Repressor Proteins/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; Transcription Factors/genetics ; Transcription Factors/immunology
    Chemical Substances Dsip1 protein, mouse ; Interleukin-2 ; Repressor Proteins ; Tgfb1i4 protein, mouse ; Transcription Factors
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.25485
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1114: Show issues Location:
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  3. Article: Les protéines de la famille TSC-22D - De nouveaux régulateurs de l'homéostasie cellulaire ?

    Pépin, Aurélie / Biola-Vidamment, Armelle / Latré de Laté, Perle / Espinasse, Marie-Alix / Godot, Véronique / Pallardy, Marc

    Medecine sciences : M/S

    2015  Volume 31, Issue 1, Page(s) 75–83

    Abstract: The GILZ (glucocorticoid-induced leucine zipper) protein has first been identified as a glucocorticoid-responsive gene and is now presented as a major regulator of inflammation. Expanding literature documents a role for GILZ as a mediator of the immuno- ... ...

    Title translation TSC-22D proteins: new regulators of cell homeostasis?.
    Abstract The GILZ (glucocorticoid-induced leucine zipper) protein has first been identified as a glucocorticoid-responsive gene and is now presented as a major regulator of inflammation. Expanding literature documents a role for GILZ as a mediator of the immuno-modulatory and anti-inflammatory effects of glucocorticoids, mainly through interference with key signal transduction pathways such as nuclear factor-kappa B (NF-kB) or activated protein-1 (AP-1). The TSC-22 (TGF-β-stimulated clone-22) protein is described as an apoptosis modulator and as a new tumor suppressor gene. GILZ and TSC-22, characterized by the presence of a leucine zipper domain and a TSC-box, belong to the TSC-22D (TSC-22 domain) family of proteins which comprises today 18 members. Functions of these proteins suggest that this family plays a major role in cell homeostasis and in the regulation of the immune system.
    MeSH term(s) Animals ; Apoptosis/genetics ; Gene Expression Regulation ; Homeostasis/genetics ; Humans ; Inflammation/genetics ; Multigene Family/physiology ; Protein Conformation ; Repressor Proteins/chemistry ; Repressor Proteins/genetics ; Repressor Proteins/physiology
    Chemical Substances Repressor Proteins ; TSC22D1 protein, human
    Language French
    Publishing date 2015-01
    Publishing country France
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20153101016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 2872: Show issues Location:
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  4. Article ; Online: Glucocorticoid-Induced Leucine Zipper Is Expressed in Human Neutrophils and Promotes Apoptosis through Mcl-1 Down-Regulation.

    Espinasse, Marie-Alix / Pépin, Aurélie / Virault-Rocroy, Pauline / Szely, Natacha / Chollet-Martin, Sylvie / Pallardy, Marc / Biola-Vidamment, Armelle

    Journal of innate immunity

    2015  Volume 8, Issue 1, Page(s) 81–96

    Abstract: Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein, the expression of which is mainly induced by glucocorticoids (GCs) in haematopoietic cells. GILZ regulates signal transduction pathways of inflammation and plays a role ... ...

    Abstract Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein, the expression of which is mainly induced by glucocorticoids (GCs) in haematopoietic cells. GILZ regulates signal transduction pathways of inflammation and plays a role in cell survival. The objective of this study was to evaluate the expression and mechanisms of action of GILZ in the apoptosis of human neutrophils. GILZ expression was induced by GCs in human neutrophils, enhanced upon phosphatidylinositol 3-kinase inhibition and resulted in apoptosis amplification. We then stably transfected PLB-985 cells with the human gilz gene and differentiated both control and GILZ-overexpressing clones in neutrophil-like cells. GILZ overexpression in PLB-985 cells led to an exacerbated apoptosis, associated with caspase-3, caspase-9 and caspase-8 activations, and a loss of mitochondrial potential, suggesting that GILZ-induced apoptosis used the mitochondrial pathway. The expression of BH3 interacting domain death agonist, Bcl-2 interacting mediator of cell death, annexin-A1 and Bcl-2-associated X was not affected in PLB-985-GILZ clones, but phosphorylation and subsequent proteasomal degradation of myeloid cell leukemia-1 (Mcl-1) were observed. Noteworthy, Mcl-1 phosphorylation was related to a significant and sustained activation of c-Jun N-terminal kinase (JNK) in PLB-985-GILZ clones. These results reveal GILZ to be a new actor in apoptosis regulation in neutrophil-like cells involving JNK and Mcl-1.
    MeSH term(s) Apoptosis ; Caspases/metabolism ; Cell Differentiation ; Cell Line, Tumor ; Down-Regulation ; Glucocorticoids/pharmacology ; Humans ; Inflammation/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Membrane Potential, Mitochondrial ; Mitochondria/metabolism ; Myeloid Cell Leukemia Sequence 1 Protein/chemistry ; Myeloid Cell Leukemia Sequence 1 Protein/metabolism ; Neutrophils/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis ; Signal Transduction ; Transcription Factors/genetics ; Transcription Factors/immunology ; Transcription Factors/metabolism ; Transfection
    Chemical Substances Glucocorticoids ; MCL1 protein, human ; Myeloid Cell Leukemia Sequence 1 Protein ; TSC22D3 protein, human ; Transcription Factors ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Caspases (EC 3.4.22.-) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2015-09-19
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454158-8
    ISSN 1662-8128 ; 1662-811X
    ISSN (online) 1662-8128
    ISSN 1662-811X
    DOI 10.1159/000439052
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6727: Show issues Location:
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  5. Article: Neutrophil expression of glucocorticoid-induced leucine zipper (GILZ) anti-inflammatory protein is associated with acute respiratory distress syndrome severity.

    Espinasse, Marie-Alix / Hajage, David / Montravers, Philippe / Piednoir, Pascale / Dufour, Guillaume / Tubach, Florence / Granger, Vanessa / de Chaisemartin, Luc / Noël, Benoît / Pallardy, Marc / Chollet-Martin, Sylvie / Biola-Vidamment, Armelle

    Annals of intensive care

    2016  Volume 6, Issue 1, Page(s) 105

    Abstract: Background: Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein involved in neutrophil apoptosis and the resolution of inflammation. Given the numerous pathophysiologic roles of neutrophils in the acute respiratory ... ...

    Abstract Background: Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein involved in neutrophil apoptosis and the resolution of inflammation. Given the numerous pathophysiologic roles of neutrophils in the acute respiratory distress syndrome (ARDS), we postulated that neutrophil GILZ expression might be induced during ARDS, to modulate the inflammatory process and participate in lung repair.
    Methods: This single-center, prospective, observational cohort study took place in the surgical intensive care unit of Bichat Hospital (Paris, France) and involved 17 ARDS patients meeting the Berlin criteria at inclusion, and 14 ventilated controls without ARDS. Serial blood samples were obtained every 2 days until extubation or death (from 1 to 9 samples per patient). GILZ protein and gene expression was quantified in blood neutrophils, along with markers of inflammation (CRP, extracellular DNA) or its resolution (Annexin A1).
    Results: Neutrophil GILZ expression was detected at the transcriptional and/or translational level in 9/17 ARDS patients (in particular 7/10 severe ARDS) and in 2/14 ventilated controls. The highest mRNA levels were observed in the most severely ill patients (p < 0.028). GILZ was expressed in about ¾ of the corticosteroid-treated patients and its expression could also occur independently of corticosteroids, suggesting that inflammatory signals may also induce neutrophil GILZ expression in vivo.
    Conclusions: In this pilot study, we show for the first time that blood neutrophils from patients with ARDS can express GILZ, in keeping with an anti-inflammatory and regulatory endogenous role of GILZ in humans. Contrary to some markers of inflammation or its resolution, the levels of gilz gene expression were related to ARDS severity.
    Language English
    Publishing date 2016-11-02
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2617094-2
    ISSN 2110-5820
    ISSN 2110-5820
    DOI 10.1186/s13613-016-0210-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Glucocorticoid-Induced Leucine Zipper Is Expressed in Human Neutrophils and Promotes Apoptosis through Mcl-1 Down-Regulation

    Espinasse, Marie-Alix / Pépin, Aurélie / Virault-Rocroy, Pauline / Szely, Natacha / Chollet-Martin, Sylvie / Pallardy, Marc / Biola-Vidamment, Armelle

    Journal of Innate Immunity

    2015  Volume 8, Issue 1, Page(s) 81–96

    Abstract: Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein, the expression of which is mainly induced by glucocorticoids (GCs) in haematopoietic cells. GILZ regulates signal transduction pathways of inflammation and plays a role ... ...

    Institution UMR996 - Inflammation, Chemokines and Immunopathology, Inserm, Université Paris-Sud, Université Paris-Saclay, Châtenay-Malabry, and Immunology Department, Bichat Hospital, AP-HP, Paris, France
    Abstract Glucocorticoid-induced leucine zipper (GILZ) is a potent anti-inflammatory protein, the expression of which is mainly induced by glucocorticoids (GCs) in haematopoietic cells. GILZ regulates signal transduction pathways of inflammation and plays a role in cell survival. The objective of this study was to evaluate the expression and mechanisms of action of GILZ in the apoptosis of human neutrophils. GILZ expression was induced by GCs in human neutrophils, enhanced upon phosphatidylinositol 3-kinase inhibition and resulted in apoptosis amplification. We then stably transfected PLB-985 cells with the human gilz gene and differentiated both control and GILZ-overexpressing clones in neutrophil-like cells. GILZ overexpression in PLB-985 cells led to an exacerbated apoptosis, associated with caspase-3, caspase-9 and caspase-8 activations, and a loss of mitochondrial potential, suggesting that GILZ-induced apoptosis used the mitochondrial pathway. The expression of BH3 interacting domain death agonist, Bcl-2 interacting mediator of cell death, annexin-A1 and Bcl-2-associated X was not affected in PLB-985-GILZ clones, but phosphorylation and subsequent proteasomal degradation of myeloid cell leukemia-1 (Mcl-1) were observed. Noteworthy, Mcl-1 phosphorylation was related to a significant and sustained activation of c-Jun N-terminal kinase (JNK) in PLB-985-GILZ clones. These results reveal GILZ to be a new actor in apoptosis regulation in neutrophil-like cells involving JNK and Mcl-1.
    Keywords Glucocorticoid-induced leucine zipper ; Apoptosis ; Neutrophils ; Myeloid cell leukemia-1 ; Proteasome ; c-Jun N-terminal kinase
    Language English
    Publishing date 2015-09-19
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Research Article
    ZDB-ID 2454158-8
    ISSN 1662-8128 ; 1662-811X
    ISSN (online) 1662-8128
    ISSN 1662-811X
    DOI 10.1159/000439052
    Database Karger publisher's database

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