Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma.

Autor: Boehne C; Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School, Lower Saxony, Germany., Behrendt AK; Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School, Lower Saxony, Germany., Meyer-Bahlburg A; Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School, Lower Saxony, Germany.; Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Hannover Medical School, Lower Saxony, Germany., Boettcher M; Institute of Immunology, University Hospital Jena, Jena, Thuringia, Germany., Drube S; Institute of Immunology, University Hospital Jena, Jena, Thuringia, Germany., Kamradt T; Institute of Immunology, University Hospital Jena, Jena, Thuringia, Germany., Hansen G; Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School, Lower Saxony, Germany.; Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Hannover Medical School, Lower Saxony, Germany.; Cluster of Excellence RESIST (EXC 2155), Hannover Medical School, Lower Saxony, Germany.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2021 Apr 06; Vol. 16 (4), pp. e0249605. Date of Electronic Publication: 2021 Apr 06 (Print Publication: 2021).
DOI: 10.1371/journal.pone.0249605
Abstrakt: T cell immunoglobulin and mucin domain-containing molecule-3 (Tim-3) has been described as a transmembrane protein, expressed on the surface of various T cells as well as different cells of innate immunity. It has since been associated with Th1 mediated autoimmune diseases and transplantation tolerance studies, thereby indicating a possible role of this receptor in counter-regulation of Th2 immune responses. In the present study we therefore directly examined the role of Tim-3 in allergic inflammation and respiratory tolerance. First, Tim-3-/- mice and wild type controls were immunized and challenged with the model allergen ovalbumin (OVA) to induce an asthma-like phenotype. Analysis of cell numbers and distribution in the bronchoalveolar lavage (BAL) fluid as well as lung histology in H&E stained lung sections demonstrated a comparable degree of eosinophilic inflammation in both mouse strains. Th2 cytokine production in restimulated cell culture supernatants and serum IgE and IgG levels were equally increased in both genotypes. In addition, cell proliferation and the distribution of different T cell subsets were comparable. Moreover, analysis of both mouse strains in our respiratory tolerance model, where mucosal application of the model allergen before immunization, prevents the development of an asthma-like phenotype, revealed no differences in any of the parameters mentioned above. The current study demonstrates that Tim-3 is dispensable not only for the development of allergic inflammation but also for induction of respiratory tolerance in mice in an OVA-based model.
Competing Interests: The authors have declared that no competing interests exist.
Databáze: MEDLINE
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