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  1. Article ; Online: Editorial: Dysregulation of Th17 and Treg cells in autoimmune diseases.

    Astier, Anne L / Kofler, David M

    Frontiers in immunology

    2023  Volume 14, Page(s) 1151836

    MeSH term(s) Humans ; T-Lymphocytes, Regulatory ; Autoimmune Diseases ; Th17 Cells
    Language English
    Publishing date 2023-02-14
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1151836
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Online: T Cell Regulation by the Environment

    Hafler, David A. / Astier, Anne L.

    2015  

    Abstract: Naïve T cells get activated upon encounter with their cognate antigen and differentiate into a specific subset of effector cells. These T cells are themselves plastic and are able to re-differentiate into another subset, changing both phenotype and ... ...

    Abstract Naïve T cells get activated upon encounter with their cognate antigen and differentiate into a specific subset of effector cells. These T cells are themselves plastic and are able to re-differentiate into another subset, changing both phenotype and function. Differentiation into a specific subset depends on the nature of the antigen and of the environmental milieu. Notably, certain nutrients, such as vitamins A and D, sodium chloride, have been shown to modulate T cell responses and influence T cell differentiation. Parasite infection can also skew Th differentiation. Similarly, the gut microbiota regulates the development of immune responses. Lastly, the key role of metabolism on T cells has also been demonstrated. This series of articles highlights some of the multiple links existing between environmental factors and T cell responses
    Keywords Immunologic diseases. Allergy ; Medicine (General)
    Size 1 electronic resource (115 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020091162
    ISBN 9782889197330 ; 2889197336
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  3. Article: La vaccination antigrippale à l’officine.

    Astier, A

    Annales pharmaceutiques francaises

    2017  Volume 75, Issue 1, Page(s) 1–2

    Title translation Flu vaccination by community pharmacists.
    MeSH term(s) France ; Humans ; Influenza Vaccines/administration & dosage ; Influenza, Human/prevention & control ; Pharmacies ; Pharmacists ; Vaccination
    Chemical Substances Influenza Vaccines
    Language French
    Publishing date 2017-01
    Publishing country France
    Document type Editorial
    ZDB-ID 307-4
    ISSN 0003-4509
    ISSN 0003-4509
    DOI 10.1016/j.pharma.2016.12.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Increased levels of circulating soluble CD226 in multiple sclerosis.

    Kari, Saniya / Bucciarelli, Florence / Angles, Thibault / Oster, Anne-Cecile / Cauboue, Pauline / Laviolette, Karl / Mougenot, Madeline / Morandi, Elena / Bernard, Isabelle / Pignolet, Beatrice / Bost, Chloé / Thomas, Joelle / Nogueira, Leonor / Saoudi, Abdelhadi / Liblau, Roland / Astier, Anne L

    Multiple sclerosis (Houndmills, Basingstoke, England)

    2024  , Page(s) 13524585241234489

    Abstract: Background: The glycoprotein CD226 plays a key role in regulating immune cell function. Soluble CD226 (sCD226) is increased in sera of patients with several chronic inflammatory diseases but its levels in neuroinflammatory diseases such as multiple ... ...

    Abstract Background: The glycoprotein CD226 plays a key role in regulating immune cell function. Soluble CD226 (sCD226) is increased in sera of patients with several chronic inflammatory diseases but its levels in neuroinflammatory diseases such as multiple sclerosis (MS) are unknown.
    Objective: To investigate the presence and functional implications of sCD226 in persons with multiple sclerosis (pwMS) and other neurological diseases.
    Methods: The mechanisms of sCD226 production were first investigated by analyzing CD226 surface expression levels and supernatants of CD3/CD226-coactivated T cells. The role of sCD226 on dendritic cell maturation was evaluated. The concentration of sCD226 in the sera from healthy donors (HD), pwMS, neuromyelitis optica (NMO), and Alzheimer's disease (AD) was measured.
    Results: CD3/CD226-costimulation induced CD226 shedding. Addition of sCD226 to dendritic cells during their maturation led to an increased production of the pro-inflammatory cytokine interleukin (IL)-23. We observed a significant increase in sCD226 in sera from pwMS and NMO compared to HD and AD. In MS, levels were increased in both relapsing-remitting multiple sclerosis (RRMS) and secondary-progressive multiple sclerosis (SPMS) compared to clinically isolated syndrome (CIS).
    Conclusion: Our data suggest that T-cell activation leads to release of sCD226 that could promote inflammation and raises the possibility of using sCD226 as a biomarker for neuroinflammation.
    Language English
    Publishing date 2024-02-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 1290669-4
    ISSN 1477-0970 ; 1352-4585
    ISSN (online) 1477-0970
    ISSN 1352-4585
    DOI 10.1177/13524585241234489
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Biosimilarity. Do not confuse biosimilar and biocopy. Example of tenecteplase.

    Astier, A / Abouqal, R / Abid, L / Aoudia, Y / Ahid, S

    Annales pharmaceutiques francaises

    2023  Volume 81, Issue 6, Page(s) 942–949

    Abstract: Non-innovator biological products (NIBPs) or 'biocopies' are available in several countries at lower prices than biosimilars. These drugs, sometimes so-called 'biosimilars', may not meet all of the quality criteria expected of clinically equivalent ... ...

    Abstract Non-innovator biological products (NIBPs) or 'biocopies' are available in several countries at lower prices than biosimilars. These drugs, sometimes so-called 'biosimilars', may not meet all of the quality criteria expected of clinically equivalent products. NIBPs can exhibit major differences in physicochemical and pharmacological properties compared with their reference biological but may be presented to prescribers based on clinical trial data and claimed clinical equivalence. Tenecteplase (TNK-tpA) is a recombinant derivative of tissue plasminogen activator, used as a third-generation thrombolytic agent for treatment of acute myocardial infarction. A TNK-tPA presented as biosimilar to the originator (Metalyse®, Boehringer Ingelheim; TNKase®, Roche/Genentech) is now available for use in India (Elaxim®, Gennova Pharmaceuticals). Elaxim® is not approved in Europe or the USA but has been proposed in several countries as a replacement for the originator. Based on available literature, we discuss why this biocopy cannot be considered biosimilar to the originator tenecteplase. We describe clear differences in physicochemical and pharmacological properties. For example, the biocopy demonstrates clot lysis activity that is substantially lower than the originator and contains high concentrations of foreign proteins that confer potential for immunological reactions. Clinical data on the biocopy are limited; randomized trials to demonstrate the absence of difference in efficacy and safety between the biocopy and originator have not been conducted. This example demonstrates that confirmation of similarity, by close examination of pharmaceutical quality attributes, and preclinical and clinical data, is mandatory before presenting to prescribers a biological product as clinically equivalent.
    Language English
    Publishing date 2023-07-06
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 307-4
    ISSN 0003-4509
    ISSN 0003-4509
    DOI 10.1016/j.pharma.2023.07.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Editorial: T cell regulation by the environment.

    Hafler, David A / Astier, Anne L

    Frontiers in immunology

    2015  Volume 6, Page(s) 229

    Language English
    Publishing date 2015
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2015.00229
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: T-cell regulation by CD46 and its relevance in multiple sclerosis.

    Astier, Anne L

    Immunology

    2008  Volume 124, Issue 2, Page(s) 149–154

    Abstract: CD46 is a complement regulatory molecule expressed on every cell type, except for erythrocytes. While initially described as a regulator of complement activity, it later became a 'magnet for pathogens', binding to several viruses and bacteria. More ... ...

    Abstract CD46 is a complement regulatory molecule expressed on every cell type, except for erythrocytes. While initially described as a regulator of complement activity, it later became a 'magnet for pathogens', binding to several viruses and bacteria. More recently, an alternative role for such complement molecules has emerged: they do regulate T-cell immunity, affecting T-cell proliferation and differentiation. In particular, CD46 stimulation induces Tr1 cells, regulatory T cells characterized by massive production of interleukin-10 (IL-10), a potent anti-inflammatory cytokine. Hence, CD46 is likely to control inflammation. Indeed, data from CD46 transgenic mice highlight a role for CD46 in inflammation, with antagonist roles depending on the cytoplasmic tail being expressed. Furthermore, recent data have shown that CD46 is defective in multiple sclerosis, IL-10 production being severely impaired in these patients. This lack of IL-10 production probably participates in the inflammation observed in patients with multiple sclerosis. This review will summarize the data on CD46 and T cells, and how CD46 is likely involved in multiple sclerosis.
    MeSH term(s) Animals ; Complement System Proteins/metabolism ; Humans ; Interleukin-10/biosynthesis ; Lymphocyte Activation/immunology ; Membrane Cofactor Protein/immunology ; Mice ; Multiple Sclerosis/immunology ; Protein Binding/immunology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Membrane Cofactor Protein ; Interleukin-10 (130068-27-8) ; Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2008-04-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/j.1365-2567.2008.02821.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Immune complex-induced apoptosis and concurrent immune complex clearance are anti-inflammatory neutrophil functions.

    Karmakar, Utsa / Chu, Julia Y / Sundaram, Kruthika / Astier, Anne L / Garside, Hannah / Hansen, Carsten G / Dransfield, Ian / Vermeren, Sonja

    Cell death & disease

    2021  Volume 12, Issue 4, Page(s) 296

    Abstract: Persistent neutrophilic inflammation drives host damage in autoimmune diseases that are characterized by abundant immune complexes. Insoluble immune complexes (iICs) potently activate pro-inflammatory neutrophil effector functions. We and others have ... ...

    Abstract Persistent neutrophilic inflammation drives host damage in autoimmune diseases that are characterized by abundant immune complexes. Insoluble immune complexes (iICs) potently activate pro-inflammatory neutrophil effector functions. We and others have shown that iICs also promote resolution of inflammation via stimulation of neutrophil apoptosis. We demonstrate here that iICs trigger FcγRIIa-dependent neutrophil macropinocytosis, leading to the rapid uptake, and subsequent degradation of iICs. We provide evidence that concurrent iIC-induced neutrophil apoptosis is distinct from phagocytosis-induced cell death. First, uptake of iICs occurs by FcγRII-stimulated macropinocytosis, rather than phagocytosis. Second, production of reactive oxygen species, but not iIC-internalization is a pre-requisite for iIC-induced neutrophil apoptosis. Our findings identify a previously unknown mechanism by which neutrophils can remove pro-inflammatory iICs from the circulation. Together iIC clearance and iIC-induced neutrophil apoptosis may act to prevent the potential escalation of neutrophilic inflammation in response to iICs.
    MeSH term(s) Antigen-Antibody Complex/metabolism ; Apoptosis ; Humans ; Inflammation/immunology ; Neutrophils/immunology
    Chemical Substances Antigen-Antibody Complex
    Language English
    Publishing date 2021-03-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-021-03528-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The anthelmintic drug praziquantel promotes human Tr1 differentiation.

    Eyoh, Enwono / McCallum, Patrick / Killick, Justin / Amanfo, Seth / Mutapi, Francisca / Astier, Anne L

    Immunology and cell biology

    2019  Volume 97, Issue 5, Page(s) 512–518

    Abstract: Praziquantel (PZQ) is an anthelminthic human and veterinary drug used to treat trematode and cestode worms. Changes in immune responses have been demonstrated in humans following curative PZQ treatment of schistosome infections. These changes have been ... ...

    Abstract Praziquantel (PZQ) is an anthelminthic human and veterinary drug used to treat trematode and cestode worms. Changes in immune responses have been demonstrated in humans following curative PZQ treatment of schistosome infections. These changes have been attributed to the removal of immunosupressive worms and immune responses to parasite antigens exposed from dying worms. To date, there has been no study investigating the potential direct effect of PZQ on the host immune cells. Herein, we analyzed the effect of PZQ on human CD4
    MeSH term(s) Anthelmintics/pharmacology ; Antigens, CD/immunology ; Cell Differentiation/drug effects ; Cell Differentiation/immunology ; Cell Proliferation/drug effects ; Female ; Humans ; Immunologic Factors/pharmacology ; Interleukin-10/immunology ; Male ; Praziquantel/pharmacology ; T-Lymphocytes, Regulatory/immunology
    Chemical Substances Anthelmintics ; Antigens, CD ; IL10 protein, human ; Immunologic Factors ; Interleukin-10 (130068-27-8) ; Praziquantel (6490C9U457)
    Language English
    Publishing date 2019-01-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 284057-1
    ISSN 1440-1711 ; 0818-9641
    ISSN (online) 1440-1711
    ISSN 0818-9641
    DOI 10.1111/imcb.12229
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: L’impact de la culture POP (Publish Or Perish) sur les revues pharmaceutiques.

    Guérin, A / Astier, A

    Annales pharmaceutiques francaises

    2018  Volume 76, Issue 6, Page(s) 419–420

    Title translation The impact of POP (Publish Or Perish) culture on pharmaceutical journals.
    MeSH term(s) Humans ; Periodicals as Topic ; Pharmacy ; Publishing ; Research ; Scientific Misconduct
    Language French
    Publishing date 2018-10-20
    Publishing country France
    Document type Editorial
    ZDB-ID 307-4
    ISSN 0003-4509
    ISSN 0003-4509
    DOI 10.1016/j.pharma.2018.10.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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