期刊
MUCOSAL IMMUNOLOGY
卷 7, 期 4, 页码 892-904出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2013.105
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资金
- Hannover Biomedical Research School (HBRS)
- German Research Foundation as part of the Trilateral Chinese-Finnish-German Immunology Initiative [DFG PA921/3-1]
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.
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