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Adhesion through the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) and the VLA-4 (CD49d)-VCAM-1 (CD106) pathways prevents apoptosis of germinal center B cells.

G Koopman, R M Keehnen, E Lindhout, W Newman, Y Shimizu, G A van Seventer, C de Groot and S T Pals
J Immunol April 15, 1994, 152 (8) 3760-3767;
G Koopman
Department of Pathology, University of Amsterdam, The Netherlands.
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R M Keehnen
Department of Pathology, University of Amsterdam, The Netherlands.
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E Lindhout
Department of Pathology, University of Amsterdam, The Netherlands.
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W Newman
Department of Pathology, University of Amsterdam, The Netherlands.
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Y Shimizu
Department of Pathology, University of Amsterdam, The Netherlands.
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G A van Seventer
Department of Pathology, University of Amsterdam, The Netherlands.
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C de Groot
Department of Pathology, University of Amsterdam, The Netherlands.
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S T Pals
Department of Pathology, University of Amsterdam, The Netherlands.
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Abstract

In the germinal center (GC), B cells are either selected to become memory cells or are eliminated through the process of programmed cell death. FDC which are intimately associated with the GC B cells are thought to be important in this selection process. Previously, we have shown that the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) and VLA-4 (CD49d)-VCAM-1 (CD106) adhesion pathways are involved in FDC-B cell interaction. In the present study, we have explored whether these adhesive interactions contribute to the process of B cell selection by studying the effects on apoptosis of GC B cells. Using FDC and B cells derived from human tonsils, we found that only B cells adherent to FDC remain viable: disruption of FDC-B-cell clusters with mAb against LFA-1 alpha (CD11a), VLA-4 (CD49d), ICAM-1 (CD54), or VCAM-1 (CD106) results in apoptosis of the B cells. Furthermore, we found that GC B cells, upon adhesion to plastic-coated purified ICAM-1 (CD54) or VCAM-1 (CD106), show diminished apoptosis. Importantly, we observed that, at low concentration, ICAM-1 (CD54) and VCAM-1 (CD106) act synergistically with anti-IgM, in inhibiting apoptosis. Together, our data strongly suggest that adhesion of B cells via the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) pathway and VLA-4 (CD49d)-VCAM-1 (CD106) pathway contributes to B cell selection.

  • Copyright © 1994 by American Association of Immunologists

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The Journal of Immunology
Vol. 152, Issue 8
15 Apr 1994
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Adhesion through the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) and the VLA-4 (CD49d)-VCAM-1 (CD106) pathways prevents apoptosis of germinal center B cells.
G Koopman, R M Keehnen, E Lindhout, W Newman, Y Shimizu, G A van Seventer, C de Groot, S T Pals
The Journal of Immunology April 15, 1994, 152 (8) 3760-3767;

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Adhesion through the LFA-1 (CD11a/CD18)-ICAM-1 (CD54) and the VLA-4 (CD49d)-VCAM-1 (CD106) pathways prevents apoptosis of germinal center B cells.
G Koopman, R M Keehnen, E Lindhout, W Newman, Y Shimizu, G A van Seventer, C de Groot, S T Pals
The Journal of Immunology April 15, 1994, 152 (8) 3760-3767;
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Print ISSN 0022-1767        Online ISSN 1550-6606