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

ORCID
0000-0003-1879-3347
Affiliation
Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School
Boehne, Carolin;
ORCID
0000-0001-9920-6225
Affiliation
Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School
Behrendt, Ann-Kathrin;
GND
122435087
ORCID
0000-0001-8640-8282
Affiliation
Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School & Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL)
Meyer-Bahlburg, Almut;
ORCID
0000-0003-2911-8830
Affiliation
Institute of Immunology, University Hospital Jena
Boettcher, Martin;
GND
131652532
ORCID
0000-0002-4224-3962
Affiliation
Institute of Immunology, University Hospital Jena
Drube, Sebastian;
GND
123172292
ORCID
0000-0001-8443-5893
Affiliation
Institute of Immunology, University Hospital Jena
Kamradt, Thomas;
GND
123107334
ORCID
0000-0001-5185-9454
Affiliation
Department of Pediatrics and Adolescent Medicine, Pediatric Pulmonology, Allergology and Neonatology, Hannover Medical School & Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL) & Cluster of Excellence RESIST (EXC 2155), Hannover Medical School
Hansen, Gesine

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.

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