Tarfa Altorki1,2, Werner Muller1, Andrew Brass3, Sheena Cruickshank4. 1. Faculty of Biology, Medicine and Health, Lydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, A.V. Hill Building, The University of Manchester, Oxford Road, Manchester, M13 9PT, UK. 2. Present address: Faculty of Medical Applied Sciences, Department of Medical Laboratory Sciences, King Abdul-Aziz University, Jeddah, Saudi Arabia. 3. Faculty of Biology, Medicine and Health, Division of Informatics, Imaging and Data Sciences, Stopford Building, The University of Manchester, Oxford Road, Manchester, M13 9PT, UK. 4. Faculty of Biology, Medicine and Health, Lydia Becker Institute of Immunology and Inflammation, Manchester Academic Health Science Centre, A.V. Hill Building, The University of Manchester, Oxford Road, Manchester, M13 9PT, UK. Sheena.Cruickshank@manchester.ac.uk.
Abstract
BACKGROUND: Dendritic cells (DCs) play a key role in shaping T cell responses. To do this, DCs must be able to migrate to the site of the infection and the lymph nodes to prime T cells and initiate the appropriate immune response. Integrins such as β2 integrin play a key role in leukocyte adhesion, migration, and cell activation. However, the role of β2 integrin in DC migration and function in the context of infection-induced inflammation in the gut is not well understood. This study looked at the role of β2 integrin in DC migration and function during infection with the nematode worm Trichuris muris. Itgb2tm1Bay mice lacking functional β2 integrin and WT littermate controls were infected with T. muris and the response to infection and kinetics of the DC response was assessed. RESULTS: In infection, the lack of functional β2 integrin significantly reduced DC migration to the site of infection but not the lymph nodes. The lack of functional β2 integrin did not negatively impact T cell activation in response to T. muris infection. CONCLUSIONS: This data suggests that β2 integrins are important in DC recruitment to the infection site potentially impacting the initiation of innate immunity but is dispensible for DC migration to lymph nodes and T cell priming in the context of T. muris infection.
BACKGROUND: Dendritic cells (DCs) play a key role in shaping T cell responses. To do this, DCs must be able to migrate to the site of the infection and the lymph nodes to prime T cells and initiate the appropriate immune response. Integrins such as β2 integrin play a key role in leukocyte adhesion, migration, and cell activation. However, the role of β2 integrin in DC migration and function in the context of infection-induced inflammation in the gut is not well understood. This study looked at the role of β2 integrin in DC migration and function during infection with the nematode worm Trichuris muris. Itgb2tm1Bay mice lacking functional β2 integrin and WT littermate controls were infected with T. muris and the response to infection and kinetics of the DC response was assessed. RESULTS: In infection, the lack of functional β2 integrin significantly reduced DC migration to the site of infection but not the lymph nodes. The lack of functional β2 integrin did not negatively impact T cell activation in response to T. muris infection. CONCLUSIONS: This data suggests that β2 integrins are important in DC recruitment to the infection site potentially impacting the initiation of innate immunity but is dispensible for DC migration to lymph nodes and T cell priming in the context of T. muris infection.
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