B cell-B cell interaction through intercellular adhesion molecule-1 and lymphocyte functional antigen-1 regulates immunoglobulin E synthesis by B cells stimulated with interleukin-4 and anti-CD40 antibody

1996 ◽  
Vol 26 (1) ◽  
pp. 192-200 ◽  
Author(s):  
Yoshinori Katada ◽  
Toshio Tanaka ◽  
Hiroshi Ochi ◽  
Masakazu Aitani ◽  
Akira Yokota ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Adhesion Molecule ◽  
Immunoglobulin E ◽  
Cell Interaction ◽  
Intercellular Adhesion ◽  
Interleukin 4 ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1

Splenectomy of rats selectively reduces lymphocyte function-associated antigen 1 and intercellular adhesion molecule 1 expression on B-cell subsets in blood and lymph nodes

Blood ◽  
2001 ◽  
Vol 98 (10) ◽  
pp. 3035-3041 ◽  
Author(s):  
Novica M. Milićević ◽  
Birgit Luettig ◽  
Christian Trautwein ◽  
Torsten Wüstefeld ◽  
Michael Mähler ◽  
...  
Keyword(s):  
B Cells ◽  
Lymph Nodes ◽  
B Cell ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
T Cell Subsets ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Surface Molecules

Abstract Splenectomy increases the number of B cells in the blood of humans and animals. It is unknown whether this is due to changes in migration, proliferation, or both. The numbers of naı̈ve (IgD+IgM+), memory (IgD−IgMhigh), newly formed (IgMhighCD90high), early recirculating follicular (IgMlowCD90high), recirculating follicular (IgMlowCD90−), and marginal zone (IgMhighCD90−) phenotype B cells were determined in control and splenectomized rats by flow cytometry. All subsets increased significantly in the blood after splenectomy. Because surface molecules are involved in the regulation of migration and proliferation, their expression (lymphocyte function-associated antigen 1 [LFA-1], intercellular adhesion molecule 1 (ICAM-1), L-selectin, α4-integrins, CD44, major histocompatability complex class II, interleukin 2 receptor-α chain) was determined on B- and T-cell subsets of both groups. B cells, but not T cells, showed a significantly reduced LFA-1 and ICAM-1 expression in blood and lymph nodes, whereas the expression of the other surface molecules analyzed remained unchanged. The down-regulation of these molecules did not influence the adherence of B cells to high endothelial venules in vitro. In vivo, however, ICAM-1low–expressing B cells migrated significantly faster through lymph nodes (ICAM-1low 41 ± 5 hours versus ICAM-1high58 ± 3 hours), whereas proliferation of B cells in bone marrow, lymph node, and blood remained unchanged. Thus, the presence of one organ is necessary for appropriate expression of LFA-1 and ICAM-1 on B cells in other, distant organs. The more rapid transit of ICAM-1low B cells through lymph nodes may be responsible for the increased B-cell number in the blood after splenectomy.

scholarly journals Coregulation of the APO-1 antigen with intercellular adhesion molecule- 1 (CD54) in tonsillar B cells and coordinate expression in follicular center B cells and in follicle center and mediastinal B-cell lymphomas

Blood ◽  
1993 ◽  
Vol 81 (8) ◽  
pp. 2067-2075 ◽  
Author(s):  
P Moller ◽  
C Henne ◽  
F Leithauser ◽  
A Eichelmann ◽  
A Schmidt ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Necrosis Factor ◽  
B Cell ◽  
Adhesion Molecule ◽  
Tumor Necrosis ◽  
Plasma Cells ◽  
Intercellular Adhesion Molecule ◽  
Cross Linking ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor

Abstract APO-1 is a 48-Kd transmembrane glycoprotein identical to the Fas antigen and belongs to the nerve growth factor (NGF)/tumor necrosis factor (TNF) receptor family of surface molecules. Cross-linking of APO- 1 induces apoptotic cell death in sensitive cells. We show here that APO-1 is an activation molecule on B cells. It was induced/enhanced on dense and buoyant tonsillar B cells, respectively, through surface Ig cross-linking in combination with interleukin-2 or by interferon-gamma together with tumor necrosis factor-alpha. These conditions also increased the amount of intercellular adhesion molecule-1 (CD54) on these cells. Epstein-Barr virus transformants of peripheral B cells coexpressed APO-1 and CD54 at very high levels. Immunohistologically, Apo-1 was detectable at low levels in a subpopulation of follicle center B blasts and, at higher levels, in sinusoidal B cells. APO-1 was undetectable in follicular mantle B cells and plasma cells. In isolated tonsillar B cells, APO-1 was expressed in CD10+ follicle center cells. In acute B lymphoblastic leukemia, chronic B lymphocytic leukemia, and Burkitt's lymphomas, APO-1 and CD54 molecules were immunohistochemically undetectable. Coordinate expression of these antigens was found in mediastinal B-cell lymphomas. The mode of APO-1 and CD54 expression was correlated in follicle center cell lymphomas (P < .0019), but less stringently in hairy cell leukemia. No association was found in plasmacytomas. This was in line with the differential expression of these molecules found in reactive plasma cells. Expression of APO-1 in B cells of different stages of differentiation and, correspondingly, in certain B-cell neoplasias might suggest a role of this molecule in the induction of B-cell apoptosis. This function might be influenced by CD54 and CD54-mediated signals.

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