9 results on '"Alicia, Bellomo"'
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2. Tracking Plasmacytoid Dendritic Cell Response to Physical Contact with Infected Cells
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Margarida Sá Ribeiro, Garima Joshi, Elodie Décembre, Célia Nuovo, Adrien Bosseboeuf, Alicia Bellomo, Manon Venet, Sonia Assil, and Marlène Dreux
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- 2023
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3. Severe COVID-19 patients have impaired plasmacytoid dendritic cell-mediated control of SARS-CoV-2-infected cells
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Remi Pescamona, Elodie Decembre, Thierry Walzer, Manon Venet, Alicia Bellomo, Alexandre Belot, Emiliano P. Ricci, Marine Villard, Magali Perret, Sophie Trouillet-Assant, Garima Joshi, Helena Paidassi, Omran Allatif, David Cluet, Margarida Sa Ribeiro, and Marlène Dreux
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Coronavirus disease 2019 (COVID-19) ,Viral replication ,Effector ,Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ,Immunology ,hemic and immune systems ,In patient ,Viral rna ,macromolecular substances ,Viral spread ,Biology ,Cell adhesion - Abstract
Type I and III interferons (IFN-I/λ) are key antiviral mediators against SARS-CoV-2 infection. Here, we demonstrate that plasmacytoid dendritic cells (pDCs) are the predominant IFN-I/λ source following their sensing of SARS-CoV-2-infected cells. Mechanistically, this short-range sensing by pDCs requires sustained integrin-mediated cell adhesion with infected cells. In turn, pDCs restrict viral spread by an IFN-I/λ response directed toward SARS-CoV-2-infected cells. This specialized function enables pDCs to efficiently turn-off viral replication, likelyviaa local response at the contact site with infected cells. By exploring the pDC response in SARS-CoV-2 patients, we further demonstrate that pDC responsiveness inversely correlates with the severity of the disease. The pDC response is particularly impaired in severe COVID-19 patients. Overall, we propose that pDC activation is essential to control SARS-CoV-2-infection. Failure to unfold this response could be key to understand severe cases of COVID-19.
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- 2021
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4. Polyclonal expansion of TCR Vb 21.3 + CD4 + and CD8 + T cells is a hallmark of multisystem inflammatory syndrome in children
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Olivier Dauwalder, David Klatzmann, Marie Duperril, Marion Moreews, Christine Lombard, Behrouz Kassai, Fanny Bajolle, Jean-Laurent Casanova, Anne-Laure Mathieu, Guillaume Monneret, Magali Perret, Rémi Pescarmona, Aurélie Portefaix, Jacqueline Marvel, Laurent Abel, Christophe Malcus, Tiphaine Louazon, Anne Moulin-Zinsch, Mehdi Mezidi, Lisa Giovannini-Chami, Omran Allatif, Hugues Patural, Thierry Walzer, Emilie Chopin, Francois Vandenesh, Encarnita Mariotti-Ferrandiz, Fabienne Venet, Céline Dupieux, Valérie Launay, Paul Bastard, Sophie Trouillet-Assant, Jean-Christophe Richard, Olivier Thaunat, Shen-Ying Zhang, Marine Villard, Samira Khaldi-Plassart, Kahina Saker, Alexandre Belot, Sophia Djebali, Marlène Dreux, Alicia Bellomo, Isabelle Rouvet, Robin Pouyau, Etienne Javouhey, Margaux Guerder, Sonia Teyssedre, Valérie Dubois, Kenz Le Gouge, Hugues Flodrops, Jean-Marie De Guillebon, Centre International de Recherche en Infectiologie - UMR (CIRI), Institut National de la Santé et de la Recherche Médicale (INSERM)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Equipe de Statistique Appliquée (UMRS 1158) (ESA), Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Neurophysiologie Respiratoire Expérimentale et Clinique, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Hospices Civils de Lyon (HCL), Centre de référence des rhumatismes inflammatoires et maladies auto-immunes systémiques rares de l’enfant / National Referee Centre for Rheumatic and AutoImmune and Systemic Diseases in Children [Lyon] (RAISE), Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hôpital Edouard Herriot [CHU - HCL], Physiopathologie de l'immunodépression associée aux réponses inflammatoires systémiques - EA 7426 (PI3), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon, Centre National de Reference des Staphylocoques, Université de Lyon, Centre hospitalier de Valence, Hôpital Louis Pradel [CHU - HCL], Centre Hospitalier Universitaire de Saint-Etienne (CHU de Saint-Etienne), INSERM U1059, SAINBIOSE - Santé, Ingénierie, Biologie, Saint-Etienne (SAINBIOSE-ENSMSE), Centre Ingénierie et Santé (CIS-ENSMSE), École des Mines de Saint-Étienne (Mines Saint-Étienne MSE), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT)-École des Mines de Saint-Étienne (Mines Saint-Étienne MSE), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT)-Université Jean Monnet [Saint-Étienne] (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpitaux Pédiatriques de Nice Lenval (CHU-Lenval), Centre Hospitalier Universitaire de Nice (CHU Nice), Université Côte d'Azur (UCA), CIC CHU Lyon (inserm), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de La Réunion (CHU La Réunion), CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Rockefeller University [New York], Etablissement français du sang - Auvergne-Rhône-Alpes (EFS), Hôpital de la Croix-Rousse [CHU - HCL], Howard Hughes Medical Institute [Boston] (HHMI), Howard Hughes Medical Institute (HHMI)-Harvard Medical School [Boston] (HMS), Departement Hospitalo- Universitaire - Inflammation, Immunopathologie, Biothérapie [Paris] (DHU - I2B), CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Université Pierre et Marie Curie - Paris 6 (UPMC), Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunologie - Immunopathologie - Immunothérapie [CHU Pitié Salpêtrière] (I3), CHU Charles Foix [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Physiopathologie de l'immunodépression associée aux réponses inflammatoires systémiques / Pathophysiology of Injury-induced Immunosuppression (PI3), Centre Hospitalier Universitaire de Saint-Etienne [CHU Saint-Etienne] (CHU ST-E), Santé Ingénierie Biologie Saint-Etienne (SAINBIOSE), Institut Mines-Télécom [Paris] (IMT)-Institut Mines-Télécom [Paris] (IMT)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Centre de Recherche en Acquisition et Traitement de l'Image pour la Santé (CREATIS), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Modeling & analysis for medical imaging and Diagnosis (MYRIAD), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Neurophysiologie Respiratoire Expérimentale et Clinique (UMRS 1158), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), ANR-16-RHUS-0001,iMAP,iMAP(2016), Référent HAL, CIRI, École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université Pierre et Marie Curie - Paris 6 (UPMC)-CHU Pitié-Salpêtrière [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)
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0301 basic medicine ,T cell ,[SDV]Life Sciences [q-bio] ,Immunology ,T-cell receptor ,Toxic shock syndrome ,General Medicine ,Human leukocyte antigen ,Biology ,medicine.disease ,3. Good health ,[SDV] Life Sciences [q-bio] ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,medicine.anatomical_structure ,Antigen ,medicine ,Cytotoxic T cell ,030212 general & internal medicine ,Cytokine storm ,CD8 - Abstract
International audience; Multisystem inflammatory syndrome in children (MIS-C) is a delayed and severe complication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that strikes previously healthy children. As MIS-C combines clinical features of Kawasaki disease (KD) and toxic shock syndrome (TSS), we aimed to compare the immunological profile of pediatric patients with these different conditions. We analyzed blood cytokine expression and the T cell repertoire and phenotype in 36 MIS-C cases, which were compared with 16 KD, 58 TSS, and 42 coronavirus disease 2019 (COVID-19) cases. We observed an increase of serum inflammatory cytokines (IL-6, IL-10, IL-18, TNF-α, IFN-γ, sCD25, MCP1, and IL-1RA) in MIS-C, TSS, and KD, contrasting with low expression of HLA-DR in monocytes. We detected a specific expansion of activated T cells expressing the Vβ21.3 T cell receptor β chain variable region in both CD4 and CD8 subsets in 75% of patients with MIS-C and not in any patient with TSS, KD, or acute COVID-19; this correlated with the cytokine storm detected. The T cell repertoire returned to baseline within weeks after MIS-C resolution. Vβ21.3 + T cells from patients with MIS-C expressed high levels of HLA-DR, CD38, and CX3CR1 but had weak responses to SARS-CoV-2 peptides in vitro. Consistently, the T cell expansion was not associated with specific classical HLA alleles. Thus, our data suggested that MIS-C is characterized by a polyclonal Vβ21.3 T cell expansion not directed against SARS-CoV-2 antigenic peptides, which is not seen in KD, TSS, and acute COVID-19.
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- 2021
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5. Macrophage‐fibroblast circuits in the spleen
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Rachel Golub, Alicia Bellomo, Marc Bajénoff, Rebecca Gentek, Trafic Vésiculaire, Réponse Innée et Virus – Vesicular trafficking, Innate response, Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), University of Edinburgh, Lymphopoïèse (Lymphopoïèse (UMR_1223 / U1223 / U-Pasteur_4)), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), This review was funded by grants from the Agence National pour la Recherche (ANR-17-CE15-0015-01), the Fondation pour la Recherche Médicale (FRM : FDT201904007871), the University of Edinburgh, the Kennedy Trust for Rheumatology Research (KENN 19 20 07) and from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program grant agreement 647257- STROMA. This work was supported by institutional grants from INSERM, CNRS, and Aix-Marseille University to the CIML., ANR-17-CE15-0015,StroMAC,Cross-talk des macrophages et du stroma au sein du ganglion lymphatique(2017), European Project: 647257,H2020,ERC-2014-CoG,STROMA(2015), Vougny, Marie-Christine, Cross-talk des macrophages et du stroma au sein du ganglion lymphatique - - StroMAC2017 - ANR-17-CE15-0015 - AAPG2017 - VALID, IMMUNOBIOLOGY OF LYMPHOID STROMAL CELLS - STROMA - - H20202015-10-01 - 2020-09-30 - 647257 - VALID, Centre International de Recherche en Infectiologie (CIRI), École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure de Lyon (ENS de Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Université Jean Monnet - Saint-Étienne (UJM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)
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0301 basic medicine ,Stromal cell ,[SDV.IMM] Life Sciences [q-bio]/Immunology ,Immunology ,Niche ,Spleen ,macrophage ,Biology ,Leukocyte Count ,03 medical and health sciences ,0302 clinical medicine ,Stroma ,Immunity ,medicine ,Homeostasis ,Humans ,Immunology and Allergy ,Macrophage ,Aged ,Macrophages ,Fibroblasts ,stromal cell ,Cell biology ,Crosstalk (biology) ,niche ,030104 developmental biology ,Lymphatic system ,medicine.anatomical_structure ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,spleen ,030215 immunology - Abstract
International audience; Macrophages are an integral part of all organs in the body, where they contribute to immune surveillance, protection, and tissue-specific homeostatic functions. This is facilitated by so-called niches composed of macrophages and their surrounding stroma. These niches structurally anchor macrophages and provide them with survival factors and tissue-specific signals that imprint their functional identity. In turn, macrophages ensure appropriate functioning of the niches they reside in. Macrophages thus form reciprocal, mutually beneficial circuits with their cellular niches. In this review, we explore how this concept applies to the spleen, a large secondary lymphoid organ whose primary functions are to filter the blood and regulate immunity. We first outline the splenic micro-anatomy, the different populations of splenic fibroblasts and macrophages and their respective contribution to protection of and key physiological processes occurring in the spleen. We then discuss firmly established and potential cellular circuits formed by splenic macrophages and fibroblasts, with an emphasis on the molecular cues underlying their crosstalk and their relevance to splenic functionality. Lastly, we conclude by considering how these macrophage-fibroblast circuits might be impaired by aging, and how understanding these changes might help identify novel therapeutic avenues with the potential of restoring splenic functions in the elderly.
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- 2021
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6. Polyclonal expansion of TCR Vbeta 21.3
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Marion, Moreews, Kenz, Le Gouge, Samira, Khaldi-Plassart, Rémi, Pescarmona, Anne-Laure, Mathieu, Christophe, Malcus, Sophia, Djebali, Alicia, Bellomo, Olivier, Dauwalder, Magali, Perret, Marine, Villard, Emilie, Chopin, Isabelle, Rouvet, Francois, Vandenesh, Céline, Dupieux, Robin, Pouyau, Sonia, Teyssedre, Margaux, Guerder, Tiphaine, Louazon, Anne, Moulin-Zinsch, Marie, Duperril, Hugues, Patural, Lisa, Giovannini-Chami, Aurélie, Portefaix, Behrouz, Kassai, Fabienne, Venet, Guillaume, Monneret, Christine, Lombard, Hugues, Flodrops, Jean-Marie, De Guillebon, Fanny, Bajolle, Valérie, Launay, Paul, Bastard, Shen-Ying, Zhang, Valérie, Dubois, Olivier, Thaunat, Jean-Christophe, Richard, Mehdi, Mezidi, Omran, Allatif, Kahina, Saker, Marlène, Dreux, Laurent, Abel, Jean-Laurent, Casanova, Jacqueline, Marvel, Sophie, Trouillet-Assant, David, Klatzmann, Thierry, Walzer, Encarnita, Mariotti-Ferrandiz, Etienne, Javouhey, and Alexandre, Belot
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Adult ,CD4-Positive T-Lymphocytes ,SARS-CoV-2 ,Child, Preschool ,Receptors, Antigen, T-Cell, alpha-beta ,COVID-19 ,Cytokines ,Humans ,HLA-DR Antigens ,CD8-Positive T-Lymphocytes ,Child ,Lymphocyte Activation ,Systemic Inflammatory Response Syndrome - Abstract
Multiple Inflammatory Syndrome in Children (MIS-C) is a delayed and severe complication of SARS-CoV-2 infection that strikes previously healthy children. As MIS-C combines clinical features of Kawasaki disease and Toxic Shock Syndrome (TSS), we aimed to compare the immunological profile of pediatric patients with these different conditions. We analyzed blood cytokine expression, and the T cell repertoire and phenotype in 36 MIS-C cases, which were compared to 16 KD, 58 TSS, and 42 COVID-19 cases. We observed an increase of serum inflammatory cytokines (IL-6, IL-10, IL-18, TNF-α, IFNγ, CD25s, MCP1, IL-1RA) in MIS-C, TSS and KD, contrasting with low expression of HLA-DR in monocytes. We detected a specific expansion of activated T cells expressing the Vβ21.3 T cell receptor β chain variable region in both CD4 and CD8 subsets in 75% of MIS-C patients and not in any patient with TSS, KD, or acute COVID-19; this correlated with the cytokine storm detected. The T cell repertoire returned to baseline within weeks after MIS-C resolution. Vβ21.3+ T cells from MIS-C patients expressed high levels of HLA-DR, CD38 and CX3CR1 but had weak responses to SARS-CoV-2 peptides in vitro
- Published
- 2021
7. Superantigenic TCR Vbeta 21.3 signature in Multisystem Inflammatory Syndrome in Children
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Encarnita Mariotti-Ferrandiz, Marlène Dreux, Kenz Le Gouge, Aurélie Portefaix, Anne-Moulin-Zinsch, Alexandre Belot, Emilie Chopin, Marie Duperril, Marion Moreews, Hugues Patural, Thierry Walzer, Jean-Christophe Richard, Anne-Laure Mathieu, Robin Pouyau, Etienne Javouhey, Olivier Thaunat, Valérie Dubois, Hugues Flodrops, Behrouz Kassai, Marine Villard, Alicia Bellomo, Laurent Abel, Fabienne Venet, Samira Khaldi-Plassart, Sophia Djebali, David Klatzmann, Jacqueline Marvel, Sonia Teyssedre, Céline Dupieux, Tiphaine Louazon, Lisa Giovannini-Chami, Sophie Trouillet-Assant, Christine Lombard, Francois Vandenesh, Mehdi Mezidi, Shen-Ying Zhang, Guillaume Monneret, Jean-Laurent Casanova, Magali Perret, Rémi Pescarmona, Margaux Guerder, Paul Bastard, Christophe Malcus, and Isabelle Rouvet
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business.industry ,medicine.medical_treatment ,T cell ,Toxic shock syndrome ,medicine.disease ,Cytokine release syndrome ,Cytokine ,medicine.anatomical_structure ,Immune system ,Immunology ,medicine ,Cytotoxic T cell ,Interferon gamma ,business ,CD8 ,medicine.drug - Abstract
ObjectivesMultiple Inflammatory Syndrome in Children (MIS-C) is the most severe pediatric form of COVID-19 and occurs in previously healthy children. MIS-C combines features of Kawasaki disease and Toxic Shock Syndrome (TSS).MethodsChildren with suspected MIS-C were included within the first week of diagnosis and a large scale immunoassay was performed to determein the immunologic signature of these patients.ResultsWe characterized the immunological profile of 27 MIS-C cases in comparison with 4 KD and 4 TSS cases. Similarly to TSS, an increase of serum inflammatory cytokines (IL-6, TNF-a, CD25s) was observed in MIS-C contrasting with low expression of HLA-DR monocytes, a feature often associated with immune paralysis. Expansions of T cells expressing the Vβ21.3 T cell receptor β chain variable region were detected in both CD4 and CD8 subsets in almost 50% of patients and Vβ21.3-positive T cells expressed high level of HLA-DR highlighting their specific activation. TCR sequencing uncovered the polyclonal nature of the Vβ 21.3+ population. SARS-CoV2 antigene-specific production of interferon gamma in T cells was not increased in MIS-C T cells compared to COVID-19 patients suggesting the antigen-specific immune response in MIS-C patients is not pivotal to the manifestation.ConclusionsOur findings argue in favor of a strong activation of the immune system related to a superantigenic immune response in MIS-C with a specific polyclonal Vβ21.3 T cell expansion.Key messagesWhat is already known about this subject ?MIS-C occurs 3-5 weeks after acute SARS-CoV2 infection and overlap features of Toxic Shock syndrome and Kawasaki disease.MIS-C appears different in term of cytokine and autoantibodies generation from KD with subtle signs of T cells activationWhat does this study add?This study demonstrates that Vβ21.3+ CD4 and CD8 T cells are highly increased in about 50% of MIS-C and distinctive of the Vβ2+ expansion observed in toxic shock syndrome in This reflects a specific T cell activation and cytokine release syndrome similar to toxic shock syndromeHow mich this impact on clinical practice or future developments?Vβ21.3+ signature can be available on a short term basis by flowcytometry and represents a signature of the MIS-C.As for TSS, immunomodulating therapies may revert the superantigenic activation and resolve this life threatening pediatric condition.
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- 2021
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8. Lymph node macrophages: Scavengers, immune sentinels and trophic effectors
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Marc Bajénoff, Myriam Baratin, Rebecca Gentek, and Alicia Bellomo
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0301 basic medicine ,Cell signaling ,Stromal cell ,Cell Survival ,T-Lymphocytes ,T cell ,Immunology ,Cell Communication ,Biology ,03 medical and health sciences ,0302 clinical medicine ,Immune system ,medicine ,Animals ,Humans ,Lymph node ,Macrophages ,Mesenchymal stem cell ,Immunity ,Cell biology ,Crosstalk (biology) ,030104 developmental biology ,medicine.anatomical_structure ,Lymph Nodes ,Lymph ,Stromal Cells ,030215 immunology - Abstract
Lymph nodes (LN) are secondary lymphoid organs dispersed throughout the body that filter lymph and assist the immune system in mounting immune responses. These functions are supported by a complex stromal microarchitecture composed of mesenchymal and vascular elements. Different subsets of macrophages (MΦ) reside in the LN and are endowed with immune and trophic functions. Here we review these different subsets with particular emphasis on the recently described T cell zone MΦ. We also address the potential crosstalk between LN stromal cells and MΦ, proposing that the former constitute niches for the latter by supplying factors required for their specification, survival and turnover. In turn, MΦ could inform their stromal partners about the immune status of the LN and orchestrate the remodelling of its microanatomy during immune responses.
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9. Reticular Fibroblasts Expressing the Transcription Factor WT1 Define a Stromal Niche that Maintains and Replenishes Splenic Red Pulp Macrophages
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Nicolas Brouilly, Marc Bajénoff, Bernard Malissen, Benjamin J. Stewart, Lionel Spinelli, Alicia Bellomo, Marine Lagueyrie, Isabelle Mondor, Menna R. Clatworthy, Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS), ANR-17-CE15-0015,StroMAC,Cross-talk des macrophages et du stroma au sein du ganglion lymphatique(2017), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU)
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0301 basic medicine ,Macrophage colony-stimulating factor ,White pulp ,Stromal cell ,Iron ,[SDV]Life Sciences [q-bio] ,Immunology ,Spleen ,Biology ,Monocytes ,Mice ,03 medical and health sciences ,0302 clinical medicine ,stomatognathic system ,medicine ,Animals ,Humans ,Immunology and Allergy ,Chemokine CCL7 ,WT1 Proteins ,Chemokine CCL2 ,ComputingMilieux_MISCELLANEOUS ,Mice, Knockout ,Macrophage Colony-Stimulating Factor ,Macrophages ,Monocyte ,Fibroblasts ,equipment and supplies ,Immunity, Innate ,Rats ,Cell biology ,Mice, Inbred C57BL ,stomatognathic diseases ,030104 developmental biology ,Infectious Diseases ,medicine.anatomical_structure ,Gene Expression Regulation ,030220 oncology & carcinogenesis ,Splenic Red Pulp ,Reticular connective tissue ,Red pulp ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,Signal Transduction - Abstract
International audience; Located within red pulp cords, splenic red pulp macrophages (RPMs) are constantly exposed to the bloodflow, clearing senescent red blood cells (RBCs) and recycling iron from hemoglobin. Here, we studied themechanisms underlying RPM homeostasis, focusing on the involvement of stromal cells as these cellsperform anchoring and nurturing macrophage niche functions in lymph nodes and liver. Microscopy revealedthat RPMs are embedded in a reticular meshwork of red pulp fibroblasts characterized by the expression ofthe transcription factor Wilms’ Tumor 1 (WT1) and colony stimulating factor 1 (CSF1). Conditional deletion ofCsf1in WT1+red pulp fibroblasts, but not white pulp fibroblasts, drastically altered the RPM network withoutaltering circulating CSF1 levels. Upon RPM depletion, red pulp fibroblasts transiently produced the mono-cyte chemoattractants CCL2 and CCL7, thereby contributing to the replenishment of the RPM network.Thus, red pulp fibroblasts anchor and nurture RPM, a function likely conserved in humans.
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