title: Antigen-dependent rescue of nose-associated lymphoid tissue (NALT) development independent of LTbetaR and CXCR5 signaling.
abstract: Nose-associated lymphoid tissue (NALT) in the rodent upper respiratory tract develops postnatally and is considered to be independent of several factors known to be involved in the organogenesis of LN and Peyer's patches (PP). In this study we demonstrate that at least two different pathways result in NALT development. Following NALT anlage formation the intrinsic pathway relies on a signaling cascade including those mediated through the chemokine receptor CXCR5 and the lymphotoxin beta receptor (LTbetaR). This allows for the formation of high endothelial venules and thereby the recruitment of lymphocytes into NALT. Alternatively, high endothelial venule formation and lymphocyte recruitment can be induced in the NALT anlage by environmental signals, which are independent of LT-betaR and chemokine receptor CXCR5 signaling but in part rely on CD40 ligand. Thus, our study identifies a novel mechanism that facilitates the rescue of NALT development at late stages in adult life independent of the canonical LTbetaR-CXCR5 signaling axis.
authors.affiliation: Institute of Immunology, Hannover Medical School, D-30625 Hannover, Germany.
authors.forename: Janet
authors.initials: J
authors.lastname: Krege
authors.forename: Sebastian
authors.initials: S
authors.lastname: Seth
authors.forename: Svenja
authors.initials: S
authors.lastname: Hardtke
authors.forename: Ana Clara Marques
authors.initials: AC
authors.lastname: Davalos-Misslitz
authors.forename: Reinhold
authors.initials: R
authors.lastname: Förster
mesh_terms: D019264:Adoptive Transfer; D000375:Aging / Q000276:immunology; D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology; D000941:Antigens / Q000276:immunology*; D000954:Antigens, Surface / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology; D023201:CD40 Ligand / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002452:Cell Count; D002465:Cell Movement / Q000276:immunology; D005856:Germ-Free Life / Q000276:immunology; D008198:Lymph Nodes / Q000166:cytology; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology; D008214:Lymphocytes / Q000166:cytology; D008221:Lymphoid Tissue / Q000098:blood supply / Q000254:growth & development* / Q000473:pathology; D053259:Lymphotoxin beta Receptor / Q000502:physiology*; D008233:Lymphotoxin-alpha / Q000235:genetics; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008817:Mice, Mutant Strains; D009088:Mucoproteins; D009297:Nasal Mucosa / Q000098:blood supply / Q000254:growth & development* / Q000473:pathology; D011425:Propionibacterium acnes / Q000276:immunology; D054380:Receptors, CXCR5 / Q000502:physiology*; D015398:Signal Transduction / Q000276:immunology*; D013154:Spleen / Q000166:cytology; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000037:antagonists & inhibitors; D014699:Venules / Q000254:growth & development / Q000378:metabolism / Q000473:pathology
chemical_list: D000911:Antibodies, Monoclonal; D000941:Antigens; D000954:Antigens, Surface; C513179:CXCR5 protein, mouse; D015815:Cell Adhesion Molecules; C069886:L-selectin counter-receptors; D053259:Lymphotoxin beta Receptor; D008233:Lymphotoxin-alpha; C489082:Madcam1 protein, mouse; D008565:Membrane Proteins; D009088:Mucoproteins; D054380:Receptors, CXCR5; C505915:Tnfsf14 protein, mouse; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14; D023201:CD40 Ligand