Julie Tabiasco

Inserm

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Philippe Le Bouteiller

Inserm

Hicham El Costa

Inserm

Daniel Rukavina

University of Rijeka

Armand Bensussan

Inserm

Maryse Aguerre‐Girr

Centre de Physiopathologie de Toulouse-Purpan

Yves Delneste

Université d'Angers

Nabila Jabrane‐Ferrat

Inserm

Gordana Laškarin

University of Rijeka

Sènan Mickael D'Almeida

École Polytechnique Fédérale de Lausanne

NŠ

Nataša Štrbo

University of Miami

Cooperative Institutions

Inserm

124

Centre National de la Recherche Scientifique

Université d'Angers

Université Toulouse III - Paul Sabatier

Nantes Université

Centre Hospitalier Universitaire d'Angers

Université Paris Cité

Université de Toulouse

Centre de Recherche en Cancérologie et Immunologie Intégrée Nantes Angers

Centre de Physiopathologie de Toulouse-Purpan

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Critical and Differential Roles of NKp46- and NKp30-Activating Receptors Expressed by Uterine NK Cells in Early Pregnancy

The Journal of Immunology (2008)

Hicham El Costa Audrey Casemayou Maryse Aguerre‐Girr Magali Rabot Alain Berrébi

In early human pregnancy, uterine decidual NK cells (dNK) are abundant and considered as cytokine producers but poorly cytotoxic despite their cytolytic granule content, suggesting a negative control of this latter effector function. To investigate the basis of this control, we examined the relative contribution to the cytotoxic function of different activating receptors expressed by dNK. Using a multicolor flow cytometry analysis, we found that freshly isolated dNK exhibit a unique repertoire of activating and inhibitory receptors, identical among all the donors tested. We then demonstrated that in fresh dNK, mAb-specific engagement of NKp46-, and to a lesser extent NKG2C-, but not NKp30-activating receptors induced intracellular calcium mobilization, perforin polarization, granule exocytosis and efficient target cell lysis. NKp46-mediated cytotoxicity is coactivated by CD2 but dramatically blocked by NKG2A coengagement, indicating that the dNK cytotoxic potential could be tightly controlled in vivo. We finally found that in dNK, mAb-specific engagement of NKp30, but not NKp46, triggered the production of IFN-gamma, TNF-alpha, MIP-1alpha, MIP-1beta, and GM-CSF proinflammatory molecules. These data demonstrate a differential, controlled role of NKp46- and NKp30-activating receptors expressed by dNK that could be critical for the outcome of pregnancy and the killing of uterine cells infected by pathogens.

Thymic stromal lymphopoietin

Decidua

CD16

10.4049/jimmunol.181.5.3009

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Citations (135)

Engagement of CD160 receptor by HLA-C is a triggering mechanism used by circulating natural killer (NK) cells to mediate cytotoxicity

Proceedings of the National Academy of Sciences (2002)

Philippe Le Bouteiller Alíz Barakonyi Jérôme Giustiniani Françoise Lenfant Anne Marie‐Cardine

Circulating human natural killer (NK) lymphocytes have been functionally defined by their ability to exert cytotoxic activity against MHC class I-negative target cell lines, including K562. Therefore, it was proposed that NK cells recognized the “missing self.” We show here that the Ig-like CD160 receptor expressed by circulating CD56 dim+ NK cells or IL-2-deprived NK cell lines is mainly involved in their cytotoxic activity against K562 target cells. Further, we report that HLA-C molecules that are constitutively expressed by K562 trigger NK cell lysis through CD160 receptor engagement. In addition, we demonstrate, with recombinant soluble HLA-Cw3 and CD160 proteins, direct interaction of these molecules. We also find that CD158b inhibitory receptors partially interfere with CD160-mediated cytotoxicity, whereas CD94/CD159a and CD85j have no effect on engagement with their respective ligands. Thus, CD160/HLA-C interaction constitutes a unique pathway to trigger NK cell cytotoxic activity.

K562 cells

Lymphokine-activated killer cell

10.1073/pnas.012681099

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Citations (134)

Faecalibacterium prausnitzii Skews Human DC to Prime IL10-Producing T Cells Through TLR2/6/JNK Signaling and IL-10, IL-27, CD39, and IDO-1 Induction

Frontiers in Immunology (2019)

Joudy Alameddine Emmanuelle Godefroy Loukas Papargyris Guillaume Sarrabayrouse Julie Tabiasco

The human colonic mucosa contains regulatory type 1-like (Tr1-like, i.e. IL-10-secreting and Foxp3-negative) T cells specific for the gut Clostridium Faecalibacterium prausnitzii (F. prausnitzii), which are both decreased in Crohn's disease patients. These data, together with the demonstration, in mice, that colonic regulatory T cells (Treg) induced by Clostridium bacteria are key players in colon homeostasis, support a similar role for F. prausnitzii-specific Treg in the human colon. Here we assessed the mechanisms whereby F. prausnitzii induces human colonic Treg. We demonstrated that F. prausnitzii, but not related clostridia, skewed human dendritic cells to prime IL-10-secreting T cells. Accordingly, F. prausnitzii induced dendritic cells to express a unique array of potent Tr1/Treg polarizing molecules: IL-10, IL-27, CD39, IDO-1 and PDL-1 and, following TLR4 stimulation, inhibited their up-regulation of costimulation molecules as well as their production of pro-inflammatory cytokines IL-12 (p35 and p40) and TNFα. We further showed that these potent tolerogenic effects relied on F. prausnitzii-induced TLR2/6 triggering, JNK signaling and CD39 ectonucleotidase activity, which was induced by IDO-1 and IL-27. These data, together with the presence of F. prausnitzii-specific Tr1-like Treg in the human colon, point out to dendritic cells polarization by F. prausnitzii as the first described cellular mechanism whereby the microbiota composition may affect human colon homeostasis. Identification of F. prausnitzii-induced mediators involved in Tr1-like Treg induction by dendritic cells opens therapeutic avenues for the treatment of inflammatory bowel diseases.

Faecalibacterium prausnitzii

10.3389/fimmu.2019.00143

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Citations (87)

Perforin and Fas/FasL Cytolytic Pathways at the Maternal–Fetal Interface

American Journal of Reproductive Immunology (2005)

Tatjana Bogović Crnčić Gordana Laškarin Koraljka Juretić Nataša Štrbo Jana Dupor

The immunogenetic enigma of maternal acceptance of the fetal semiallograft has been termed an immunological paradox. The first trimester decidua is heavily infiltrated with CD56 bright CD16 − uterine natural killer (uNK) cells which must be prepared to respond to potential pathogen challenges and still be able to control immune responses that allow the development of the fetus. The significant presence of cytolytic mediators, perforin and Fas/Fas ligand (FasL), at the maternal–fetal interface raises a question of their role(s) in the immunological interrelations between maternal tissues and trophoblast cells. As uNK cells in vitro lyse target cell lines (K562, P815 and P815Fas) using these effector molecules, it seems that, although immunocompetent, their cytotoxicity is not directed against trophoblast during normal pregnancy. Therefore, it is generally believed that the hormonal and Th1/Th2 cytokine balance plays an important role in the tolerance and maintenance of pregnancy. This paper gives an overview of the recent findings on the complex immunological events that occur at the maternal–fetal interface.

Fas ligand

Trophoblast

Decidua

Granzyme

10.1111/j.1600-0897.2005.00320.x

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Citations (37)

Active trans-synaptic capture of membrane fragments by natural killer cells

European Journal of Immunology (2002)

Julie Tabiasco Éric Espinosa Denis Hudrisier Etienne Joly Jean‐Jacques Fournié

Prior to delivery of a lethal hit, NK cells form an immunological synapse to scan the target cells and engage their activatory and inhibitory receptors. Using freshly isolated NK cells, IL-2-activated polyclonal NK bulk or the NKL cell line, we report here that early during this recognition process, human NK cells actively capture target cell membrane fragments. This novel NK cell function occurs via the immunological synapse, is controlled by Src kinase, ATP, Ca2+ and PKC and involves rearrangements of the actin cytoskeleton. Furthermore, this process is down-regulated bysignals emanating from inhibitory NK receptors recognizing protective MHC class I alleles.

Immunological synapse

Polyclonal antibodies

10.1002/1521-4141(200205)32:5<1502::aid-immu1502>3.0.co;2-y

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Citations (104)

IL-27 neutralization to modulate the tumor microenvironment and increase immune checkpoint immunotherapy efficacy

bioRxiv (Cold Spring Harbor Laboratory) (2024)

Loukas Papargyris Quentin Glaziou Laëtitia Basset Sènan Mickael D'Almeida Pascale Pignon

Objectives Tumor-associated macrophages (TAMs) accumulate in the majority of solid tumors, producing inflammatory cytokines and growth factors involved in tumor maintenance. They have recently emerged as targets for restoring an effective antitumor response and limiting tumor growth. In the present study, we investigated the potential of IL-27 neutralization to modify macrophage polarization and thus the tumor immune microenvironment. Methods and Analysis We monitored the effect of IL-27 neutralization on human macrophages. Flow cytometry, quantitative reverse transcription-PCR, ELISA and western blot were performed to validate, in vitro, the role of IL-27 on the acquisition of macrophage immunoregulatory functions. A murine Colon Adenocarcinoma model (MC38) was used to assess IL-27 neutralization in the microenvironment in vivo. Results In this study, we demonstrated the importance of IL-27 in the generation of human immunoregulatory macrophages. Mechanistically, IL-27 neutralization reduced the immunosuppressive properties of macrophages, such as cytokine secretion and membrane expression of immunosuppressive molecules. These modifications led to a reduction in the ability of macrophages to inhibit the function of CD4+ and CD8+ T cells. Furthermore, in vivo neutralization of IL-27 reduced MC38 tumor growth and could improve immune checkpoint inhibitor efficacy. Conclusions Collectively, we uncovered the role of IL-27 in the immunosuppressive tumor microenvironment (TME). We showed that IL-27 could be a target for macrophage repolarization and boosting of CD4+ and CD8+ T cell responses. IL-27 neutralization thus appears as a promising strategy to target macrophages in immunosuppressive TME and improve the clinical efficacy of immunotherapy protocols.

Immune checkpoint

Cancer Immunotherapy

Immune escape

10.1101/2024.09.13.612803

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Rupture de tolérance et dysrégulation lymphocytaire T chez les travailleurs exposés à la silice sans atteinte pulmonaire

Néphrologie & Thérapeutique (2019)

Benoît Brilland Céline Beauvillain Gery Mazurkiewicz P. Rucay Julie Tabiasco

10.1016/j.nephro.2019.07.299

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