Journal: European Journal of Immunology

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Abbreviation

Eur. J. Immunol.

Publisher

Wiley-VCH

Journal Volumes

ISSN

0014-2980
1521-4141

Description

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Publications1 - 10 of 39
  • Zelante, Teresa; Luca, Antonella de; Bonifazi, Pierluigi; et al. (2007)
    European Journal of Immunology
  • Joller, Nicole Christine; Spörri, Roman; Hilbi, Hubert; et al. (2007)
    European Journal of Immunology
    Legionella pneumophila (Lpn) is a ubiquitous Gram-negative bacterium found in aquatic environments and is the causative agent of Legionnaires’ disease, a severe form of pneumonia. We have used Lpn-permissive A/J mice as a model to analyze the B cell response upon intravenous (i.v.) and intranasal (i.n.) infection with Lpn. A strong antibody (Ab) response was observed upon i.v. infection with wild-type (WT) Lpn and an icmT mutant strain, which is unable to replicate within permissive host cells. In contrast to i.v. infection, only WT but not icmT mutant Lpn was able to induce specific Ab responses upon i.n. infection. After primary i.n. infection with WT Lpn, a strict compartmentalization of Lpn-specific Ab isotypes was observed, as IgG was found exclusively systemically, while IgA was detectable only locally in the lung. Regardless of the infection route, isotype switching to IgG and to IgA was strictly dependent on CD4+ T cells, whereas IgM production was completely Th-independent. Finally, we analyzed the protective capacity of the Lpn-specific Ab response. Actively or passively immunized mice or mice that were infected with opsonized Lpn had 50–100-fold reduced bacterial titers compared to naive animals, clearly demonstrating the capacity of Ab to protect against infection with Lpn.
  • Neumeier, Daniel; Pedrioli, Alessandro; Genovese, Alessandro; et al. (2022)
    European Journal of Immunology
    Plasma cells and their secreted antibodies play a central role in the long-term protection against chronic viral infection. However, due to experimental limitations, a comprehensive description of linked genotypic, phenotypic, and antibody repertoire features of plasma cells (gene expression, clonal frequency, virus specificity, and affinity) has been challenging to obtain. To address this, we performed single-cell transcriptome and antibody repertoire sequencing of the murine BM plasma cell population following chronic lymphocytic choriomeningitis virus infection. Our single-cell sequencing approach recovered full-length and paired heavy- and light-chain sequence information for thousands of plasma cells and enabled us to perform recombinant antibody expression and specificity screening. Antibody repertoire analysis revealed that, relative to protein immunization, chronic infection led to increased levels of clonal expansion, class-switching, and somatic variants. Furthermore, antibodies from the highly expanded and class-switched (IgG) plasma cells were found to be specific for multiple viral antigens and a subset of clones exhibited cross-reactivity to nonviral and autoantigens. Integrating single-cell transcriptome data with antibody specificity suggested that plasma cell transcriptional phenotype was correlated to viral antigen specificity. Our findings demonstrate that chronic viral infection can induce and sustain plasma cell clonal expansion, combined with significant somatic hypermutation, and can generate cross-reactive antibodies.
  • Latorre, Daniela (2022)
    European Journal of Immunology
    According to the World Health Organization, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has already infected more than 400 million people and caused over 5 million deaths globally. The infection is associated with a wide spectrum of clinical manifestations, ranging from no signs of illness to severe pathological complications that go beyond the typical respiratory symptoms. On this note, new-onset neurological and neuropsychiatric syndromes have been increasingly reported in a large fraction of COVID-19 patients, thus potentially representing a significant public health threat. Although the underlying pathophysiological mechanisms remain elusive, a growing body of evidence suggests that SARS-CoV-2 infection may trigger an autoimmune response, which could potentially contribute to the establishment and/or exacerbation of neurological disorders in COVID-19 patients. Shedding light on this aspect is urgently needed for the development of effective therapeutic intervention. This review highlights the current knowledge of the immune responses occurring in Neuro-COVID patients and discusses potential immune-mediated mechanisms by which SARS-CoV-2 infection may trigger neurological complications.
  • Marsland, Benjamin J.; Kurrer, Michael; Reissmann, Regina; et al. (2008)
    European Journal of Immunology
  • Calvanese, Anna Laura; Cecconi, Virginia; Stäheli, Severin; et al. (2024)
    European Journal of Immunology
    Tertiary lymphoid structures (TLS) resemble follicles of secondary lymphoid organs and develop in nonlymphoid tissues during inflammation and cancer. Which cell types and signals drive the development of TLS is largely unknown. To investigate early events of TLS development in the lungs, we repeatedly instilled p(I:C) plus ovalbumin (Ova) intranasally. This induced TLS ranging from lymphocytic aggregates to organized and functional structures containing germinal centers. We found that TLS development is independent of FAP+ fibroblasts, alveolar macrophages, or CCL19 but crucially depends on type I interferon (IFN-I). Mechanistically, IFN-I initiates two synergistic pathways that culminate in the development of TLS. On the one hand, IFN-I induces lymphotoxin (LT)alpha in lymphoid cells, which stimulate stromal cells to produce the B-cell-attracting chemokine CXCL13 through LT beta R-signaling. On the other hand, IFN-I is sensed by stromal cells that produce the T-cell-attracting chemokines CXCL9, CXCL10 as well as CCL19 and CCL21 independently of LT beta R. Consequently, B-cell aggregates develop within a week, whereas follicular dendritic cells and germinal centers appear after 3 weeks. Thus, sustained production of IFN-I together with an antigen is essential for the induction of functional TLS in the lungs.
  • The osteopontin
    Item type: Journal Article
    Abel, Brian; Kurrer, Michael; Shamshiev, Abdijapar; et al. (2006)
    European Journal of Immunology
    Osteopontin (OPN) and CD44 have been implicated in the development of autoimmune diseases, including arthritis and multiple sclerosis, as well as chronic inflammatory diseases, such as atherosclerosis and colitis. To investigate their roles in autoimmune myocarditis induced by immunization with heart alpha‐myosin (MyHC‐α), a mouse model of human cardiomyopathy, we analyzed mice lacking OPN or CD44v6/v7, a CD44 isoform that binds OPN. Both, OPN–/– and CD44v6/v7–/– mice developed myocarditis with the same prevalence and severity as BALB/c wild‐type controls. Furthermore, treatment of BALB/c mice with a pan‐neutralizing anti‐CD44 antibody did not affect the disease outcome. Consistently, expansion of MyHC‐α‐specific autoimmune CD4⁺ T cells and MyHC‐α autoantibody responses from either CD44v6/v7–/– mice or OPN–/– mice was indistinguishable from their wild‐type controls. Thus, OPN and CD44v6/v7 are merely spectators rather than protagonists in autoimmune myocarditis.
  • Linder, Aline; Diab, Farah; de Pontual, Loïc; et al. (2025)
    European Journal of Immunology
  • Pochanke, Veronika; Hatak, Sarah; Hengartner, Hans; et al. (2006)
    European Journal of Immunology
  • Yegutkin, Gennady G.; Auvinen, Kaisa; Rantakari, Pia; et al. (2015)
    European Journal of Immunology
Publications1 - 10 of 39