Header

UZH-Logo

Maintenance Infos

Lymphotoxin-beta receptor-dependent genes in lymph node and follicular dendritic cell transcriptomes.


Huber, C; Thielen, C; Seeger, H; Schwarz, Petra; Montrasio, F; Wilson, M R; Heinen, E; Fu, Yang-Xin; Miele, G; Aguzzi, A (2005). Lymphotoxin-beta receptor-dependent genes in lymph node and follicular dendritic cell transcriptomes. Journal of Immunology, 174(9):5526-5536.

Abstract

Affinity maturation and Ab class switches occur in lymphoid germinal centers (GCs), in which differentiation and maintenance depend on lymphotoxin (LT) signaling and include differentiation of follicular dendritic cells (FDCs). The events leading to FDC and GC maturation are poorly defined. Using several approaches of functional genomics, we enumerated transcripts affected in mice by suppressing LT beta receptor (LTbetaR) signaling and/or overrepresented in FDC-enriched GC isolates. Protein expression analysis of 3 of 12 genes both enriched in FDCs and down-regulated by LTbetaR signaling suppression validated them as FDC markers. Functional analysis of one of these three, clusterin, suggests a role as an FDC-derived trophic factor for GC B cells. Hence, the set of genes presented in this study includes markers emanating from LTbetaR signaling and transcripts relevant to GC and FDC function.

Abstract

Affinity maturation and Ab class switches occur in lymphoid germinal centers (GCs), in which differentiation and maintenance depend on lymphotoxin (LT) signaling and include differentiation of follicular dendritic cells (FDCs). The events leading to FDC and GC maturation are poorly defined. Using several approaches of functional genomics, we enumerated transcripts affected in mice by suppressing LT beta receptor (LTbetaR) signaling and/or overrepresented in FDC-enriched GC isolates. Protein expression analysis of 3 of 12 genes both enriched in FDCs and down-regulated by LTbetaR signaling suppression validated them as FDC markers. Functional analysis of one of these three, clusterin, suggests a role as an FDC-derived trophic factor for GC B cells. Hence, the set of genes presented in this study includes markers emanating from LTbetaR signaling and transcripts relevant to GC and FDC function.

Statistics

Citations

42 citations in Web of Science®
40 citations in Scopus®
Google Scholar™

Altmetrics

Additional indexing

Item Type:Journal Article, refereed
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:1 May 2005
Deposited On:11 Feb 2008 12:25
Last Modified:06 Dec 2017 13:30
Publisher:American Association of Immunologists
ISSN:0022-1767
Publisher DOI:https://doi.org/10.4049/jimmunol.174.9.5526
Related URLs:http://www.jimmunol.org/cgi/content/full/174/9/5526
PubMed ID:15843551

Download

Full text not available from this repository.
View at publisher