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1. Pre-treatment with IL2 gene therapy alleviates Staphylococcus aureus arthritis in mice

Author

Berglind Bergmann, Ying Fei, Pernilla Jirholt, Zhicheng Hu, Maria Bergquist, Abukar Ali, Catharina Lindholm, Olov Ekwall, Guillaume Churlaud, David Klatzmann, Tao Jin, and Inger Gjertsson

Subjects
T regulatory cells, Tregs, IL2, S. aureus, Arthritis, Mice, Infectious and parasitic diseases, RC109-216
Abstract

Abstract Background Staphylococcus aureus (S. aureus) arthritis is one of the most detrimental joint diseases known and leads to severe joint destruction within days. We hypothesized that the provision of auxiliary immunoregulation via an expanded compartment of T regulatory cells (Tregs) could dampen detrimental aspects of the host immune response whilst preserving its protective nature. Administration of low-dose interleukin 2 (IL2) preferentially expands Tregs, and is being studied as a treatment choice in several autoimmune conditions. We aimed to evaluate the role of IL2 and Tregs in septic arthritis using a well-established mouse model of haematogenously spred S. aureus arthritis. Methods C57BL/6 or NMRI mice we intravenously (iv) injected with a defined dose of S. aureus LS-1 or Newman and the role of IL2 and Tregs were assessed by the following approaches: IL2 was endogenously delivered by intraperitoneal injection of a recombinant adeno-associated virus vector (rAAV) before iv S. aureus inoculation; Tregs were depleted before and during S. aureus arthritis using antiCD25 antibodies; Tregs were adoptively transferred before induction of S. aureus arthritis and finally, recombinant IL2 was used as a treatment starting day 3 after S. aureus injection. Studied outcomes included survival, weight change, bacterial clearance, and joint damage. Results Expansion of Tregs induced by IL2 gene therapy prior to disease onset does not compromise host resistance to S. aureus infection, as the increased proportions of Tregs reduced the arthritis severity as well as the systemic inflammatory response, while simultaneously preserving the host’s ability to clear the infection. Conclusions Pre-treatment with IL2 gene therapy dampens detrimental immune responses but preserves appropriate host defense, which alleviates S. aureus septic arthritis in a mouse model.

Published
2020
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2. Pre-treatment with IL2 gene therapy alleviates Staphylococcus aureus arthritis in mice

Author

Maria Bergquist, Olov Ekwall, Ying Fei, Abukar Ali, Inger Gjertsson, Tao Jin, David Klatzmann, Pernilla Jirholt, Berglind Bergmann, Zhicheng Hu, Guillaume Churlaud, Catharina Lindholm, Sahlgrenska Academy at University of Gothenburg [Göteborg], Guizhou Medical University (贵州医科大学), Centre d’Investigation Clinique intégré en Biothérapies et immunologie [AP-HP pitié-salpêtrière, Paris] (CIC-BTi), 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), Departement Hospitalo- Universitaire - Inflammation, Immunopathologie, Biothérapie [Paris] (DHU - I2B), CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-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), 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], This work was supported by grants from Göteborg Medical Society, Swedish Science Research Council, Reumatikerförbundet (The Swedish Rheumatism Association), King Gustav V Stiftelse, IngaBritt och Arne Lundbergs Stiftelse, Lundgrens Stiftelse, Amlövs Stiftelse, Swedish Medical Society and National Natural Science Foundation of China (grant 81460334 to Y. Fei). Open access funding provided by University of Gothenburg., Biotherapy [Paris] (CIC-BTi), CHU Pitié-Salpêtrière [APHP], CHU Pitié-Salpêtrière [APHP]-Sorbonne Université (SU), Immunologie - Immunopathologie - Immunothérapie (I3), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Bodescot, Myriam, Centre d'investigation clinique Biothérapie [CHU Pitié-Salpêtrière] (CIC-BTi), Centre d'investigation clinique pluridisciplinaire [CHU Pitié Salpêtrière] (CIC-P 1421), 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)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Sorbonne Université (SU)-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)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-CHU Saint-Antoine [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-CHU Trousseau [APHP]

Subjects
Male, 0301 basic medicine, Genetic enhancement, Arthritis, medicine.disease_cause, T-Lymphocytes, Regulatory, Mice, 0302 clinical medicine, Medicine, 030212 general & internal medicine, [SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, biology, Antibodies, Monoclonal, hemic and immune systems, Dependovirus, Recombinant Proteins, 3. Good health, Infectious Diseases, [SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system, Staphylococcus aureus, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Antibody, Research Article, medicine.drug, Interleukin 2, [SDV.IMM] Life Sciences [q-bio]/Immunology, T regulatory cells, Genetic Vectors, chemical and pharmacologic phenomena, Tregs, lcsh:Infectious and parasitic diseases, 03 medical and health sciences, Immune system, Animals, lcsh:RC109-216, Arthritis, Infectious, IL2, business.industry, Weight change, Interleukin-2 Receptor alpha Subunit, Genetic Therapy, medicine.disease, S. aureus, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Immunology, biology.protein, Interleukin-2, Septic arthritis, business
Abstract

Background Staphylococcus aureus (S. aureus) arthritis is one of the most detrimental joint diseases known and leads to severe joint destruction within days. We hypothesized that the provision of auxiliary immunoregulation via an expanded compartment of T regulatory cells (Tregs) could dampen detrimental aspects of the host immune response whilst preserving its protective nature. Administration of low-dose interleukin 2 (IL2) preferentially expands Tregs, and is being studied as a treatment choice in several autoimmune conditions. We aimed to evaluate the role of IL2 and Tregs in septic arthritis using a well-established mouse model of haematogenously spred S. aureus arthritis. Methods C57BL/6 or NMRI mice we intravenously (iv) injected with a defined dose of S. aureus LS-1 or Newman and the role of IL2 and Tregs were assessed by the following approaches: IL2 was endogenously delivered by intraperitoneal injection of a recombinant adeno-associated virus vector (rAAV) before iv S. aureus inoculation; Tregs were depleted before and during S. aureus arthritis using antiCD25 antibodies; Tregs were adoptively transferred before induction of S. aureus arthritis and finally, recombinant IL2 was used as a treatment starting day 3 after S. aureus injection. Studied outcomes included survival, weight change, bacterial clearance, and joint damage. Results Expansion of Tregs induced by IL2 gene therapy prior to disease onset does not compromise host resistance to S. aureus infection, as the increased proportions of Tregs reduced the arthritis severity as well as the systemic inflammatory response, while simultaneously preserving the host’s ability to clear the infection. Conclusions Pre-treatment with IL2 gene therapy dampens detrimental immune responses but preserves appropriate host defense, which alleviates S. aureus septic arthritis in a mouse model.

Published
2020
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3. Memory B Cells in Mouse Models

Author

Inger Gjertsson, Weicheng Ren, Inga-Lill Mårtensson, Katrin Thorarinsdottir, Pernilla Jirholt, Ola Grimsholm, and Berglind Bergmann

Subjects
T-Lymphocytes, Immunology, Naive B cell, B-cell receptor, B-Lymphocyte Subsets, Gene Expression, Receptors, Antigen, B-Cell, Biology, Autoimmune Diseases, Mice, Antigen, medicine, Animals, Humans, Memory B cell, B cell, Immunity, Cellular, Cluster of differentiation, General Medicine, Germinal Center, Cell biology, Immunoglobulin Isotypes, B-1 cell, Disease Models, Animal, medicine.anatomical_structure, biology.protein, Antibody, Immunologic Memory
Abstract

One of the principles behind vaccination, as shown by Edward Jenner in 1796, and host protection is immunological memory, and one of the cells central to this is the antigen-experienced memory B cell that responds rapidly upon re-exposure to the initiating antigen. Classically, memory B cells have been defined as progenies of germinal centre (GC) B cells expressing isotype-switched and substantially mutated B cell receptors (BCRs), that is, membrane-bound antibodies. However, it has become apparent over the last decade that this is not the only pathway to B cell memory. Here, we will discuss memory B cells in mice, as defined by (1) cell surface markers; (2) multiple layers; (3) formation in a T cell-dependent and either GC-dependent or GC-independent manner; (4) formation in a T cell-independent fashion. Lastly, we will touch upon memory B cells in; (5) mouse models of autoimmune diseases.

Published
2013
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4. The Bone-Inflammation-Cartilage (BIC) Stain: A Novel Staining Method Combining Safranin O and Van Gieson's Stains

Author

Johan Mölne, Berglind Bergmann, and Inger Gjertsson

Subjects
Cartilage, Articular, Inflammation, Pathology, medicine.medical_specialty, Histology, Knee Joint, Staining and Labeling, Chemistry, Cartilage, Benzenesulfonates, Stain, Staining, chemistry.chemical_compound, Mice, medicine.anatomical_structure, Picrates, Safranin, Van Gieson's stain, medicine, Animals, Phenazines, Anatomy, Letters to the Editor
Published
2015

5. Absence of surrogate light chain results in spontaneous autoreactive germinal centres expanding V(H)81X-expressing B cells

Author

Ola Grimsholm, Anneli Strömberg, Giljun Park, Ulf Yrlid, Weicheng Ren, Haixia Chen, Susanna Cardell, Dongfeng Chen, Nina Höök, Alessandra De Riva, Angelina I. Bernardi, Inga-Lill Mårtensson, Berglind Bergmann, Sofia Andersson, Alessandro Camponeschi, and Inger Gjertsson

Subjects
physics and astronomy (all), Immunoglobulin Light Chains, Surrogate, T-Lymphocytes, General Physics and Astronomy, Receptors, Antigen, B-Cell, Biology, Plasma cell, Immunoglobulin light chain, General Biochemistry, Genetics and Molecular Biology, Mice, Antibody Repertoire, Antigen, Cell Line, Tumor, medicine, biochemistry, Animals, Humans, Mice, Knockout, B-Lymphocytes, Multidisciplinary, genetics and molecular biology (all), chemistry (all), Germinal center, Peripheral tolerance, General Chemistry, Cell biology, Anti-Bacterial Agents, Mice, Inbred C57BL, medicine.anatomical_structure, Gene Expression Regulation, Cell culture, Antibodies, Antinuclear, Immunology, biology.protein, Female, Antibody, Immunoglobulin Heavy Chains, Spleen
Abstract

Random recombination of antibody heavy- and light-chain genes results in a diverse B-cell receptor (BCR) repertoire including self-reactive BCRs. However, tolerance mechanisms that prevent the development of self-reactive B cells remain incompletely understood. The absence of the surrogate light chain, which assembles with antibody heavy chain forming a pre-BCR, leads to production of antinuclear antibodies (ANAs). Here we show that the naive follicular B-cell pool is enriched for cells expressing prototypic ANA heavy chains in these mice in a non-autoimmune background with a broad antibody repertoire. This results in the spontaneous formation of T-cell-dependent germinal centres that are enriched with B cells expressing prototypic ANA heavy chains. However, peripheral tolerance appears maintained by selection thresholds on cells entering the memory B-cell and plasma cell pools, as exemplified by the exclusion of cells expressing the intrinsically self-reactive V(H)81X from both pools.

Published
2015

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