Schulz, O. and Ugur, M. and Friedrichsen, M. and Radulovic, K. and Niess, J.-H. and Jalkanen, S. and Krueger, A. and Pabst, O.. (2014) Hypertrophy of infected Peyer's patches arises from global, interferon-receptor, and CD69-independent shutdown of lymphocyte egress. Mucosal Immunology, 7 (4). pp. 892-904.
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Official URL: https://edoc.unibas.ch/62392/
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Abstract
Lymphoid organ hypertrophy is a hallmark of localized infection. During the inflammatory response, massive changes in lymphocyte recirculation and turnover boost lymphoid organ cellularity. Intriguingly, the exact nature of these changes remains undefined to date. Here, we report that hypertrophy of Salmonella-infected Peyer's patches (PPs) ensues from a global "shutdown" of lymphocyte egress, which traps recirculating lymphocytes in PPs. Surprisingly, infection-induced lymphocyte sequestration did not require previously proposed mediators of lymphoid organ shutdown including type I interferon receptor and CD69. In contrast, following T-cell receptor-mediated priming, CD69 was essential to selectively block CD4(+) effector T-cell egress. Our findings segregate two distinct lymphocyte sequestration mechanisms, which differentially rely on intrinsic modulation of lymphocyte egress capacity and inflammation-induced changes in the lymphoid organ environment.
Faculties and Departments: | 03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Gastroenterology DBM (Niess) |
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UniBasel Contributors: | Niess, Jan Hendrik |
Item Type: | Article, refereed |
Article Subtype: | Research Article |
Publisher: | Nature Publishing Group |
ISSN: | 1933-0219 |
e-ISSN: | 1935-3456 |
Note: | Publication type according to Uni Basel Research Database: Journal article |
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Last Modified: | 15 Dec 2020 11:14 |
Deposited On: | 15 Dec 2020 11:14 |
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