scholarly journals CD73 mediates adhesion of B cells to follicular dendritic cells

Blood ◽  
1996 ◽  
Vol 88 (5) ◽  
pp. 1755-1764 ◽  
Author(s):  
L Airas ◽  
S Jalkanen
Keyword(s):  
Dendritic Cells ◽  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
Intracellular Signaling ◽  
Follicular Dendritic Cells ◽  
Adhesion Protein ◽  
Follicular Dendritic ◽  
Vascular Adhesion

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.

scholarly journals CD73 mediates adhesion of B cells to follicular dendritic cells

Blood ◽  
1996 ◽  
Vol 88 (5) ◽  
pp. 1755-1764 ◽  
Author(s):  
L Airas ◽  
S Jalkanen
Keyword(s):  
Dendritic Cells ◽  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
Intracellular Signaling ◽  
Follicular Dendritic Cells ◽  
Adhesion Protein ◽  
Follicular Dendritic ◽  
Vascular Adhesion

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.

Follicular Dendritic Cell (FDC)-Induced Microrna-Mediated up-Regulation of PRDM1 and Down-Regulation of BCL6 in Germinal Center B Lymphocytes: A Potential Mechanism for B-Cell Differentiation.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4588-4588
Author(s):  
Jianhong Lin ◽  
Tint Lwin ◽  
Jianjun Zhao ◽  
Jie Zhao ◽  
Luis Crespo ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Germinal Center ◽  
Follicular Dendritic Cells ◽  
B Cell Differentiation ◽  
Follicular Dendritic

Abstract Abstract 4588 B-cell differentiation process is tightly regulated by suppression or induction of specific transcription factors. Among various transcriptional regulators, BCL6 and PRDM-1 are master regulators for germinal center (GC) formation and terminal B-cell differentiation. Dysregulation of BCL6 and PRDM-1 have been associated with lymphomagenesis. However how these transcription factors are regulated and what determines their expression are unclear. Given that follicular dendritic cells (FDC) closely interact with B cells within the GC, provide survival signal to protect B cells from apoptosis and are essential for the differentiation of GC B cells, we used an in vitro FDC-B-cell co-culture model to explore the role of FDC-B cell interaction and FDC-induced miRNA in the regulation of BCL6 and PRDM-1 expression. In this study 1) we revealed that follicular dendritic cells (FDCs, HK) regulate expression of transcription factor (BCL6, and PRDM1) via cell-cell contact, 2) we showed that FDCs regulate expression of B-cell survival and differentiation-related microRNAs, 3) we demonstrated that microRNAs regulate expression of transcription factors BCl6 and PRDM1 and 4) we documented that follicular dendritic cells regulate expression of transcription factor (BCL6, and PRDM1) through microRNAs and plays an important role in B-differentiation. These studies establish new molecular mechanisms for regulation of BCL6 and PRDM-1. FDC-induce miRNA mediated down- and up-regulation of transcriptional factors may contribute to the phenotype maintenance of GC, and pathogenesis of non-Hodgkin's lymphoma (NHL) by interfering with normal B-cell terminal differentiation. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Follicular dendritic cells inhibit apoptosis in human B lymphocytes by a rapid and irreversible blockade of preexisting endonuclease.

1995 ◽  
Vol 181 (6) ◽  
pp. 1985-1995 ◽  
Author(s):  
E Lindhout ◽  
A Lakeman ◽  
C de Groot
Keyword(s):  
Dendritic Cells ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
Cell Cultures ◽  
Germinal Center ◽  
Follicular Dendritic Cells ◽  
Endonuclease Activity ◽  
Cd40 Ligation ◽  
Follicular Dendritic

During germinal center reactions, a minority of B lymphocytes are selected after successful binding to follicular dendritic cells (FDCs). The majority of the B cells, however, die by apoptosis. One of the characteristics of apoptosis is rapid fragmentation of DNA by an endogenous endonuclease. The regulation of apoptosis and endonuclease activity in germinal center (GC) B cells is largely unknown. In this study we have investigated the induction and inhibition of endonuclease activity in GC B cells. We also investigated the role of FDCs, surface Ig (sIg), sIgM, CD21, CD22 CD40, and intracellular Zn2+ in the regulation of endonuclease activity. We have found that DNA fragmentation in GC B cells is caused by a preexisting endonuclease very similar to NUC-18 (an 18-kD endonuclease identified in rat thymocytes). Endonuclease activity in GC B cells appears to be rapidly and irreversibly blocked after interaction with FDCs, but not after cross-linkage of sIg, sIgM, CD21, CD22, or CD40. Addition of soluble CD40-human IgM fusion protein (sCD40) to FDC-B cell cultures also did not interfere with FDC-mediated B cell rescue. Chelation of intracellular Zn2+ during FDC-B cell cultures resulted in abrogated B cell rescue. These data suggest that FDCs inhibit apoptosis in GC B cells by a rapid inactivation of preexisting endonuclease using a mechanism distinct from CD40 ligation.

scholarly journals Germinal Center Initiation, Variable Gene Region Hypermutation, and Mutant B Cell Selection without Detectable Immune Complexes on Follicular Dendritic Cells

2000 ◽  
Vol 192 (7) ◽  
pp. 931-942 ◽  
Author(s):  
Lynn G. Hannum ◽  
Ann M. Haberman ◽  
Shannon M. Anderson ◽  
Mark J. Shlomchik
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
B Cell ◽  
Immune Complexes ◽  
Germinal Center ◽  
Serum Antibody ◽  
Cell Formation ◽  
Immunoglobulin M ◽  
Follicular Dendritic Cells ◽  
Follicular Dendritic

Serum antibody (Ab) can play several roles during B cell immune responses. Among these is to promote the deposition of immune complexes (ICs) on follicular dendritic cells (FDCs). ICs on FDCs are generally thought to be critical for normal germinal center (GC) formation and the development and selection of memory B cells. However, it has been very difficult to test these ideas. To determine directly whether FDC-bound complexes do indeed function in these roles, we have developed a transgenic (Tg) mouse in which all B lymphocytes produce only the membrane-bound form of immunoglobulin M. Immune Tg mice have 10,000-fold less specific Ab than wild-type mice and lack detectable ICs on FDCs. Nonetheless, primary immune responses and the GC reaction in these mice are robust, suggesting that ICs on FDCs do not play critical roles in immune response initiation and GC formation. Moreover, as indicated by the presence and pattern of somatic mutations, memory cell formation and selection appear normal in these IC-deficient GCs.

Human follicular dendritic cells promote germinal center B cell survival by providing prostaglandins

2013 ◽  
Vol 55 (3-4) ◽  
pp. 418-423 ◽  
Author(s):  
Jini Kim ◽  
Seungkoo Lee ◽  
Young-Myeong Kim ◽  
Doo-Il Jeoung ◽  
Jongseon Choe
Keyword(s):  
Dendritic Cells ◽  
B Cell ◽  
Cell Survival ◽  
Germinal Center ◽  
Follicular Dendritic Cells ◽  
B Cell Survival ◽  
Germinal Center B Cell ◽  
Follicular Dendritic
Sign in / Sign up

Export Citation Format

Share Document