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  1. AU="Sylvain Latour"
  2. AU="Velhal, S"
  3. AU="Lutz, Richard A"
  4. AU="Raveesh Kumar"
  5. AU="Andreas von Deimling"
  6. AU="Erik MeersauthorLaboratory of Analytical and Applied Ecochemistry, Faculty of Bioscience Engineering, University of Ghent, Coupure Links 653, 9000 Ghent, Belgium"
  7. AU="Thakkar, Nitya"
  8. AU="Hongtao Tie"
  9. AU="Bhati, Saurabh Kumar"
  10. AU="Choi, Hyunho"
  11. AU="Jayaprakash, Balamuralikrishna"
  12. AU="Lee, Brian H"
  13. AU="May, Susann"
  14. AU="Remondes-Costa, Sónia"
  15. AU="Lauren Sauer"
  16. AU="G Saiz, Paula"
  17. AU="Stoica, George"
  18. AU=Odorizzi Pamela M.
  19. AU=Pollaers Katherine
  20. AU="Stefanova, Veselina"
  21. AU="Geraldine M. O’Connor"
  22. AU="Jim E. Banta"
  23. AU="Marti-Bonmati, Luis"
  24. AU="Doris Kampner"
  25. AU="Luca Soraci"

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  1. Artikel ; Online: Inherited immunodeficiencies associated with proximal and distal defects in T cell receptor signaling and co-signaling

    Sylvain Latour

    Biomedical Journal, Vol 45, Iss 2, Pp 321-

    2022  Band 333

    Abstract: T lymphocytes are central cells of adaptive immunity. Activation of T lymphocytes by the antigen receptor of T cells (TCR) and co-stimulatory molecules involve specific signaling components and cascades. Those are essential for development, ... ...

    Abstract T lymphocytes are central cells of adaptive immunity. Activation of T lymphocytes by the antigen receptor of T cells (TCR) and co-stimulatory molecules involve specific signaling components and cascades. Those are essential for development, differentiation and effector responses of T lymphocytes. Over the last three decades, identification of primary immunodeficiencies associated with defects in development and activation of T lymphocytes provided new and unexpected insights into TCR signaling and co-signalling and their relation with protective immunity in humans. Mutations in components of the proximal and distal TCR signaling like the TCR-CD3 complex, protein tyrosine kinases and phosphatases, adaptor proteins, second messengers like Ca2+ mobilization and the MAPK kinase and nuclear factor kappa B (NFκB) pathways impede T cell development and functions, causing immunodeficiency and immune dysregulation manifestations such as autoimmunity and inflammation. Mutations that impair co-signaling delivers by co-stimulatory molecules of the tumor necrosis factor (TNF), the CD28 and the signaling lymphocytic activation molecule (SLAM) receptor families, have no effect or slight impact on T-cell development but impair T cell responses such as expansion. Interestingly, these latter are often associated with infectious susceptibility restricted to particular pathogens like Epstein-Barr virus (EBV) and human papillomavirus (HPV), highlighting the molecular “specialization” of co-stimulatory molecules to shape TCR-dependent T cell responses to specific pathogens or infected cells.
    Schlagwörter T lymphocytes ; TCR signaling ; Co-stimulatory molecule ; Primary immunodeficiency ; Infections ; Immune-dysregulation ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Loss of RASGRP1 in humans impairs T‐cell expansion leading to Epstein‐Barr virus susceptibility

    Sarah Winter / Emmanuel Martin / David Boutboul / Christelle Lenoir / Sabah Boudjemaa / Arnaud Petit / Capucine Picard / Alain Fischer / Guy Leverger / Sylvain Latour

    EMBO Molecular Medicine, Vol 10, Iss 2, Pp 188-

    2018  Band 199

    Abstract: Abstract Inherited CTPS1, CD27, and CD70 deficiencies in humans have revealed key factors of T‐lymphocyte expansion, a critical prerequisite for an efficient immunity to Epstein–Barr virus (EBV) infection. RASGRP1 is a T‐lymphocyte‐specific nucleotide ... ...

    Abstract Abstract Inherited CTPS1, CD27, and CD70 deficiencies in humans have revealed key factors of T‐lymphocyte expansion, a critical prerequisite for an efficient immunity to Epstein–Barr virus (EBV) infection. RASGRP1 is a T‐lymphocyte‐specific nucleotide exchange factor known to activate the pathway of MAP kinases (MAPK). A deleterious homozygous mutation in RASGRP1 leading to the loss RASGRP1 expression was identified in two siblings who both developed a persistent EBV infection leading to Hodgkin lymphoma. RASGRP1‐deficient T cells exhibited defective MAPK activation and impaired proliferation that was restored by expression of wild‐type RASGRP1. Similar defects were observed in T cells from healthy individuals when RASGRP1 was downregulated. RASGRP1‐deficient T cells also exhibited decreased CD27‐dependent proliferation toward CD70‐expressing EBV‐transformed B cells, a crucial pathway required for expansion of antigen‐specific T cells during anti‐EBV immunity. Furthermore, RASGRP1‐deficient T cells failed to upregulate CTPS1, an important enzyme involved in DNA synthesis. These results show that RASGRP1 deficiency leads to susceptibility to EBV infection and demonstrate the key role of RASGRP1 at the crossroad of pathways required for the expansion of activated T lymphocytes.
    Schlagwörter Hodgkin lymphoma ; immunodeficiency ; lymphocyte ; susceptibility to Epstein–Barr virus ; T‐cell proliferation ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2018-02-01T00:00:00Z
    Verlag Wiley
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: NBEAL2 deficiency in humans leads to low CTLA-4 expression in activated conventional T cells

    Laure Delage / Francesco Carbone / Quentin Riller / Jean-Luc Zachayus / Erwan Kerbellec / Armelle Buzy / Marie-Claude Stolzenberg / Marine Luka / Camille de Cevins / Georges Kalouche / Rémi Favier / Alizée Michel / Sonia Meynier / Aurélien Corneau / Caroline Evrard / Nathalie Neveux / Sébastien Roudières / Brieuc P. Pérot / Mathieu Fusaro /
    Christelle Lenoir / Olivier Pellé / Mélanie Parisot / Marc Bras / Sébastien Héritier / Guy Leverger / Anne-Sophie Korganow / Capucine Picard / Sylvain Latour / Bénédicte Collet / Alain Fischer / Bénédicte Neven / Aude Magérus / Mickaël Ménager / Benoit Pasquier / Frédéric Rieux-Laucat

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Band 12

    Abstract: Abstract Loss of NBEAL2 function leads to grey platelet syndrome (GPS), a bleeding disorder characterized by macro-thrombocytopenia and α-granule-deficient platelets. A proportion of patients with GPS develop autoimmunity through an unknown mechanism, ... ...

    Abstract Abstract Loss of NBEAL2 function leads to grey platelet syndrome (GPS), a bleeding disorder characterized by macro-thrombocytopenia and α-granule-deficient platelets. A proportion of patients with GPS develop autoimmunity through an unknown mechanism, which might be related to the proteins NBEAL2 interacts with, specifically in immune cells. Here we show a comprehensive interactome of NBEAL2 in primary T cells, based on mass spectrometry identification of altogether 74 protein association partners. These include LRBA, a member of the same BEACH domain family as NBEAL2, recessive mutations of which cause autoimmunity and lymphocytic infiltration through defective CTLA-4 trafficking. Investigating the potential association between NBEAL2 and CTLA-4 signalling suggested by the mass spectrometry results, we confirm by co-immunoprecipitation that CTLA-4 and NBEAL2 interact with each other. Interestingly, NBEAL2 deficiency leads to low CTLA-4 expression in patient-derived effector T cells, while their regulatory T cells appear unaffected. Knocking-down NBEAL2 in healthy primary T cells recapitulates the low CTLA-4 expression observed in the T cells of GPS patients. Our results thus show that NBEAL2 is involved in the regulation of CTLA-4 expression in conventional T cells and provide a rationale for considering CTLA-4-immunoglobulin therapy in patients with GPS and autoimmune disease.
    Schlagwörter Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2023-06-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Transient mTOR inhibition rescues 4-1BB CAR-Tregs from tonic signal-induced dysfunction

    Baptiste Lamarthée / Armance Marchal / Soëli Charbonnier / Tifanie Blein / Juliette Leon / Emmanuel Martin / Lucas Rabaux / Katrin Vogt / Matthias Titeux / Marianne Delville / Hélène Vinçon / Emmanuelle Six / Nicolas Pallet / David Michonneau / Dany Anglicheau / Christophe Legendre / Jean-Luc Taupin / Ivan Nemazanyy / Birgit Sawitzki /
    Sylvain Latour / Marina Cavazzana / Isabelle André / Julien Zuber

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Band 19

    Abstract: Chimeric antigen receptor engineering in T cells has been shown to be of great potential therapeutic benefit in a range of immune pathologies, although the functionality of such cell therapies can be limited due to tonic signalling and the induction of ... ...

    Abstract Chimeric antigen receptor engineering in T cells has been shown to be of great potential therapeutic benefit in a range of immune pathologies, although the functionality of such cell therapies can be limited due to tonic signalling and the induction of dysfunction. Here the authors show transient inhibition of mTOR can rescue their 41-BB-CAR-Tregs from tonic signalling-induced dysfunction.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2021-11-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Identification of SLAMF3 (CD229) as an inhibitor of hepatocellular carcinoma cell proliferation and tumour progression.

    Ingrid Marcq / Rémy Nyga / Flora Cartier / Rabbind Singh Amrathlal / Christèle Ossart / Hakim Ouled-Haddou / Hussein Ghamlouch / Antoine Galmiche / Denis Chatelain / Luciane Lamotte / Véronique Debuysscher / Vincent Fuentes / Eric Nguyen-Khac / Jean-Marc Regimbeau / Jean-Pierre Marolleau / Sylvain Latour / Hicham Bouhlal

    PLoS ONE, Vol 8, Iss 12, p e

    2013  Band 82918

    Abstract: Although hepatocellular carcinoma (HCC) is one of the most common malignancies and constitutes the third leading cause of cancer-related deaths, the underlying molecular mechanisms are not fully understood. In the present study, we demonstrate for the ... ...

    Abstract Although hepatocellular carcinoma (HCC) is one of the most common malignancies and constitutes the third leading cause of cancer-related deaths, the underlying molecular mechanisms are not fully understood. In the present study, we demonstrate for the first time that hepatocytes express signalling lymphocytic activation molecule family member 3 (SLAMF3/CD229) but not other SLAMF members. We provide evidence to show that SLAMF3 is involved in the control of hepatocyte proliferation and in hepatocellular carcinogenesis. SLAMF3 expression is significantly lower in primary human HCC samples and HCC cell lines than in human healthy primary hepatocytes. In HCC cell lines, the restoration of high levels of SLAMF3 expression inhibited cell proliferation and migration and enhanced apoptosis. Furthermore, SLAMF3 expression was associated with inhibition of HCC xenograft progression in the nude mouse model. The restoration of SLAMF3 expression levels also decreased the phosphorylation of MAPK ERK1/2, JNK and mTOR. In samples from resected HCC patients, SLAMF3 expression levels were significantly lower in tumorous tissues than in peritumoral tissues. Our results identify SLAMF3 as a specific marker of normal hepatocytes and provide evidence for its potential role in the control of proliferation of HCC cells.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2013-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: Occurrence of nodular lymphocyte-predominant hodgkin lymphoma in hermansky-pudlak type 2 syndrome is associated to natural killer and natural killer T cell defects.

    Luisa Lorenzi / Giovanna Tabellini / William Vermi / Daniele Moratto / Fulvio Porta / Lucia D Notarangelo / Ornella Patrizi / Silvano Sozzani / Genevieve de Saint Basile / Sylvain Latour / David Pace / Silvia Lonardi / Fabio Facchetti / Raffaele Badolato / Silvia Parolini

    PLoS ONE, Vol 8, Iss 11, p e

    2013  Band 80131

    Abstract: Hermansky Pudlak type 2 syndrome (HPS2) is a rare autosomal recessive primary immune deficiency caused by mutations on β3A gene (AP3B1 gene). The defect results in the impairment of the adaptor protein 3 (AP-3) complex, responsible for protein sorting to ...

    Abstract Hermansky Pudlak type 2 syndrome (HPS2) is a rare autosomal recessive primary immune deficiency caused by mutations on β3A gene (AP3B1 gene). The defect results in the impairment of the adaptor protein 3 (AP-3) complex, responsible for protein sorting to secretory lysosomes leading to oculo-cutaneous albinism, bleeding disorders and immunodeficiency. We have studied peripheral blood and lymph node biopsies from two siblings affected by HPS2. Lymph node histology showed a nodular lymphocyte predominance type Hodgkin lymphoma (NLPHL) in both HPS2 siblings. By immunohistochemistry, CD8 T-cells from HPS2 NLPHL contained an increased amount of perforin (Prf) + suggesting a defect in the release of this granules-associated protein. By analyzing peripheral blood immune cells we found a significant reduction of circulating NKT cells and of CD56(bright)CD16(-) Natural Killer (NK) cells subset. Functionally, NK cells were defective in their cytotoxic activity against tumor cell lines including Hodgkin Lymphoma as well as in IFN-γ production. This defect was associated with increased baseline level of CD107a and CD63 at the surface level of unstimulated and IL-2-activated NK cells. In summary, these results suggest that a combined and profound defect of innate and adaptive effector cells might explain the susceptibility to infections and lymphoma in these HPS2 patients.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2013-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Stepwise development of MAIT cells in mouse and human.

    Emmanuel Martin / Emmanuel Treiner / Livine Duban / Lucia Guerri / Hélène Laude / Cécile Toly / Virginie Premel / Anne Devys / Ivan C Moura / Florence Tilloy / Stéphane Cherif / Gabriella Vera / Sylvain Latour / Claire Soudais / Olivier Lantz

    PLoS Biology, Vol 7, Iss 3, p e

    2009  Band 54

    Abstract: Mucosal-associated invariant T (MAIT) cells display two evolutionarily conserved features: an invariant T cell receptor (TCR)alpha (iTCRalpha) chain and restriction by the nonpolymorphic class Ib major histocompatibility complex (MHC) molecule, MHC- ... ...

    Abstract Mucosal-associated invariant T (MAIT) cells display two evolutionarily conserved features: an invariant T cell receptor (TCR)alpha (iTCRalpha) chain and restriction by the nonpolymorphic class Ib major histocompatibility complex (MHC) molecule, MHC-related molecule 1 (MR1). MR1 expression on thymus epithelial cells is not necessary for MAIT cell development but their accumulation in the gut requires MR1 expressing B cells and commensal flora. MAIT cell development is poorly known, as these cells have not been found in the thymus so far. Herein, complementary human and mouse experiments using an anti-humanValpha7.2 antibody and MAIT cell-specific iTCRalpha and TCRbeta transgenic mice in different genetic backgrounds show that MAIT cell development is a stepwise process, with an intra-thymic selection followed by peripheral expansion. Mouse MAIT cells are selected in an MR1-dependent manner both in fetal thymic organ culture and in double iTCRalpha and TCRbeta transgenic RAG knockout mice. In the latter mice, MAIT cells do not expand in the periphery unless B cells are added back by adoptive transfer, showing that B cells are not required for the initial thymic selection step but for the peripheral accumulation. In humans, contrary to natural killer T (NKT) cells, MAIT cells display a naïve phenotype in the thymus as well as in cord blood where they are in low numbers. After birth, MAIT cells acquire a memory phenotype and expand dramatically, up to 1%-4% of blood T cells. Finally, in contrast with NKT cells, human MAIT cell development is independent of the molecular adaptor SAP. Interestingly, mouse MAIT cells display a naïve phenotype and do not express the ZBTB16 transcription factor, which, in contrast, is expressed by NKT cells and the memory human MAIT cells found in the periphery after birth. In conclusion, MAIT cells are selected by MR1 in the thymus on a non-B non-T hematopoietic cell, and acquire a memory phenotype and expand in the periphery in a process dependent both upon B cells and the bacterial flora. Thus, their development follows a unique pattern at the crossroad of NKT and gammadelta T cells.
    Schlagwörter Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2009-03-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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