Antigen-dependent rescue of nose-associated lymphoid tissue (NALT) development independent of LTbetaR and CXCR5 signaling

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Antigen-dependent rescue of nose-associated lymphoid tissue (NALT) development independent of LTbetaR and CXCR5 signaling. / Krege, Janet; Seth, Sebastian; Hardtke, Svenja; Davalos-Misslitz, Ana Clara Marques; Förster, Reinhold.

In: EUR J IMMUNOL, Vol. 39, No. 10, 10.2009, p. 2765-78.

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@article{41b2e1562194465f80412a339a4ec1da,
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.",
keywords = "Adoptive Transfer, Aging/immunology, Animals, Antibodies, Monoclonal/immunology, Antigens/immunology, Antigens, Surface/metabolism, B-Lymphocytes/immunology, CD40 Ligand/immunology, Cell Adhesion Molecules/metabolism, Cell Count, Cell Movement/immunology, Germ-Free Life/immunology, Lymph Nodes/cytology, Lymphocyte Activation/drug effects, Lymphocytes/cytology, Lymphoid Tissue/blood supply, Lymphotoxin beta Receptor/physiology, Lymphotoxin-alpha/genetics, Membrane Proteins/metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Mutant Strains, Nasal Mucosa/blood supply, Propionibacterium acnes/immunology, Receptors, CXCR5/physiology, Signal Transduction/immunology, Spleen/cytology, Tumor Necrosis Factor Ligand Superfamily Member 14/antagonists & inhibitors, Venules/growth & development",
author = "Janet Krege and Sebastian Seth and Svenja Hardtke and Davalos-Misslitz, {Ana Clara Marques} and Reinhold F{\"o}rster",
year = "2009",
month = oct,
doi = "10.1002/eji.200939422",
language = "English",
volume = "39",
pages = "2765--78",
journal = "EUR J IMMUNOL",
issn = "0014-2980",
publisher = "Wiley-VCH Verlag GmbH",
number = "10",

}

RIS

TY - JOUR

T1 - Antigen-dependent rescue of nose-associated lymphoid tissue (NALT) development independent of LTbetaR and CXCR5 signaling

AU - Krege, Janet

AU - Seth, Sebastian

AU - Hardtke, Svenja

AU - Davalos-Misslitz, Ana Clara Marques

AU - Förster, Reinhold

PY - 2009/10

Y1 - 2009/10

N2 - 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.

AB - 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.

KW - Adoptive Transfer

KW - Aging/immunology

KW - Animals

KW - Antibodies, Monoclonal/immunology

KW - Antigens/immunology

KW - Antigens, Surface/metabolism

KW - B-Lymphocytes/immunology

KW - CD40 Ligand/immunology

KW - Cell Adhesion Molecules/metabolism

KW - Cell Count

KW - Cell Movement/immunology

KW - Germ-Free Life/immunology

KW - Lymph Nodes/cytology

KW - Lymphocyte Activation/drug effects

KW - Lymphocytes/cytology

KW - Lymphoid Tissue/blood supply

KW - Lymphotoxin beta Receptor/physiology

KW - Lymphotoxin-alpha/genetics

KW - Membrane Proteins/metabolism

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Mice, Mutant Strains

KW - Nasal Mucosa/blood supply

KW - Propionibacterium acnes/immunology

KW - Receptors, CXCR5/physiology

KW - Signal Transduction/immunology

KW - Spleen/cytology

KW - Tumor Necrosis Factor Ligand Superfamily Member 14/antagonists & inhibitors

KW - Venules/growth & development

U2 - 10.1002/eji.200939422

DO - 10.1002/eji.200939422

M3 - SCORING: Journal article

C2 - 19757439

VL - 39

SP - 2765

EP - 2778

JO - EUR J IMMUNOL

JF - EUR J IMMUNOL

SN - 0014-2980

IS - 10

ER -