title: Hypertrophy of infected Peyer's patches arises from global, interferon-receptor, and CD69-independent shutdown of lymphocyte egress.
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.
authors.affiliation: Institute of Immunology, Hannover Medical School, Hannover, Germany.
authors.forename: O
authors.initials: O
authors.lastname: Schulz
authors.affiliation: Institute of Immunology, Hannover Medical School, Hannover, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Ugur
authors.affiliation: Institute of Immunology, Hannover Medical School, Hannover, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Friedrichsen
authors.affiliation: Department of Internal Medicine I, University of Ulm, Ulm, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Radulovic
authors.affiliation: 1] Department of Internal Medicine I, University of Ulm, Ulm, Germany [2] Current address: Department of Visceral Surgery and Medicine, Inselspital, Bern, Switzerland.
authors.forename: J-H
authors.initials: JH
authors.lastname: Niess
authors.affiliation: MediCity Research Laboratory, Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
authors.forename: S
authors.initials: S
authors.lastname: Jalkanen
authors.affiliation: Institute of Immunology, Hannover Medical School, Hannover, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Krueger
authors.affiliation: Institute of Immunology, Hannover Medical School, Hannover, Germany.
authors.forename: O
authors.initials: O
authors.lastname: Pabst
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism*; D006984:Hypertrophy; D037181:Lectins, C-Type / Q000378:metabolism*; D008024:Ligands; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D010581:Peyer's Patches / Q000276:immunology* / Q000382:microbiology / Q000473:pathology*; D017471:Receptors, Interferon / Q000378:metabolism*; D012475:Salmonella / Q000276:immunology; D012480:Salmonella Infections / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D037181:Lectins, C-Type; D008024:Ligands; D017471:Receptors, Interferon; D051193:Toll-Like Receptors; D000099192:CD69 Antigens