Human follicular dendritic cells in vitro and follicular dendritic-cell-like cells

1997 ◽  
Vol 288 (2) ◽  
pp. 381-389 ◽  
Author(s):  
Rikiya Tsunoda ◽  
Alain Bosseloir ◽  
Kikuo Onozaki ◽  
Ernst Heinen ◽  
Katsuya Miyake ◽  
...  
2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Hyo-Kyung Pak ◽  
Yong-Woo Kim ◽  
Bora Nam ◽  
A-Neum Lee ◽  
Jin Roh ◽  
...  

Follicular dendritic cells are important stromal components of the germinal center (GC) and have pivotal roles in maintaining the GC microenvironment for high-affinity antibody production. Tumor necrosis factor-α (TNFα) is essential for the development and functions of follicular dendritic cells. Despite the importance of follicular dendritic cells in humoral immunity, their molecular control mechanisms have yet to be fully elucidated due to the lack of an adequate investigation system. Here, we have used a unique human primary follicular dendritic cell-like cell (FDCLC) to demonstrate that the migration of these cells is enhanced by TNFα-mediated metalloproteinase 3 (MMP3) expression. MMP3 was found to be highly expressed in normal human GCs and markedly upregulated in human primary FDCLCs by TNFα. TNFα induced ERK1/2 phosphorylation and the transcription of MMP3 through AP1. TNFα treatment increased FDCLC migration, and a knockdown of MMP3 significantly reduced the TNFα-induced migration of FDCLCs. Overall, we have newly identified a control mechanism for the expression of MMP3 in FDCLCs that modulates their migration and may indicate an important role in GC biology. Since GCs are observed in the lesions of autoimmune diseases and lymphomas, targeting the MMP3/TNFα-mediated migration of stromal cells in the B cell follicle may have great potential as a future therapeutic modality against aberrant GC-associated disorders.


2011 ◽  
Vol 141 (1-2) ◽  
pp. 26-32 ◽  
Author(s):  
Vinciane Toppets ◽  
Valerie Defaweux ◽  
Joelle Piret ◽  
Nathalie Kirschvink ◽  
Luc Grobet ◽  
...  

2020 ◽  
Author(s):  
Theinmozhi Arulraj ◽  
Sebastian C. Binder ◽  
Michael Meyer-Hermann

AbstractFollicular Dendritic Cells (FDCs) retain immune complexes (ICs) for prolonged time periods and are important for germinal center (GC) reactions. ICs undergo periodic cycling in FDCs, a mechanism supporting an extended half-life of antigen. Based on experimental data we estimated that the average residence time of Phycoerythrin-ICs (PE-ICs) on FDC surface and interior were 21 and 36 minutes, respectively. GC simulations show that antigen cycling might impact GC dynamics due to redistribution of antigen on the FDC surface and by protecting antigen from degradation. Antigen protection and influence on GC dynamics varied with antigen cycling time and total antigen concentration. Simulations predict that blocking antigen cycling terminates the GC reaction and decreases plasma cell production. Considering that cycling of antigen could be a target for the modulation of GC reactions, our findings highlight the importance of understanding the mechanism and regulation of IC cycling in FDCs.


Blood ◽  
1996 ◽  
Vol 88 (5) ◽  
pp. 1755-1764 ◽  
Author(s):  
L Airas ◽  
S Jalkanen

Abstract Lymphocyte-vascular adhesion protein-2 was recently identified as CD73. The CD73 molecule, otherwise known as ecto-5′-nucleotidase, is a lymphocyte maturation marker that is involved in intracellular signaling, and lymphocyte proliferation and activation. We now show that CD73, in addition to mediating lymphocyte binding to endothelial cells, also mediates adhesion between B cells and follicular dendritic cells (FDC), as a monoclonal antibody (MoAb) against CD73 inhibited the aggregation of isolated germinal center B cells and FDC in vitro. Cytocentrifuge preparations of isolated germinal center cells and two- color immunofluorescence stainings of different tonsillar B-cell populations show that CD73 is expressed on FDC and on small, recirculating IgD+ B cells, but only on a few B cells inside the germinal center. Thus, we propose that CD73 on FDC has an important role in controlling B cell-FDC interactions and B-cell maturation in germinal centers.


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