PeproTech Inc.
Originally published online as doi:10.1189/jlb.0303095 on September 12, 2003

Published online before print September 12, 2003
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.0303095v1
74/6/1083    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Layseca-Espinosa, E.
Right arrow Articles by Rosenstein, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Layseca-Espinosa, E.
Right arrow Articles by Rosenstein, Y.
(Journal of Leukocyte Biology. 2003;74:1083-1093.)
© 2003 by Society for Leukocyte Biology

T cell aggregation induced through CD43: intracellular signals and inhibition by the immunomodulatory drug leflunomide

Esther Layseca-Espinosa*,{dagger}, Gustavo Pedraza-Alva*, José Luis Montiel*, Roxana del Río*, Nora A. Fierro*, Roberto González-Amaro{dagger} and Yvonne Rosenstein*,1

* Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos; and
{dagger} Department of Immunology, Facultad de Medicina, Universidad Autónoma de San Luis Potosí, México

1 Correspondence: Instituto de Biotecnología, UNAM, Apartado Postal 510-3, Cuernavaca, Morelos 62250, Mexico. E-mail: yvonne{at}ibt.unam.mx

The CD43 coreceptor molecule has been shown to participate in lymphocyte adhesion and activation. Leukocyte homotypic aggregation results from a cascade of intracellular signals delivered to the cells upon engagement of different cell-surface molecules with their natural ligands. This phenomenon requires an active metabolism, reorganization of the cytoskeleton, and relocalization of cell-surface molecules. The aim of this study was to identify some of the key members of the signaling cascade leading to T lymphocyte homotypic aggregation following CD43 engagement. CD43-mediated homotypic aggregation of T lymphocytes required the participation of Src kinases, phospholipase C-{gamma}2, protein kinase C, phosphatidylinositol-3 kinase, as well as extracellular-regulated kinase 1/2 and p38. Data shown here suggest that these signaling molecules play a central role in regulating actin cytoskeleton remodeling after CD43 ligation. We also evaluated the ability of immunomodulatory drugs such as leflunomide to block the CD43-mediated homotypic aggregation. Leflunomide blocked the recruitment of targets of the Src family kinases as well as actin polymerization, diminishing the ability of T lymphocytes to aggregate in response to CD43-specific signals, suggesting that this drug might control the migration and recruitment of lymphoid cells to inflamed tissues.

Key Words: adhesion • leukosialin • cytoskeleton • lymphocyte • signaling pathways




This article has been cited by other articles:


Home page
 BloodHome page
I. Mattioli, O. Dittrich-Breiholz, M. Livingstone, M. Kracht, and M. L. Schmitz
Comparative analysis of T-cell costimulation and CD43 activation reveals novel signaling pathways and target genes
Blood, November 15, 2004; 104(10): 3302 - 3304.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
T. Korn, T. Magnus, K. Toyka, and S. Jung
Modulation of effector cell functions in experimental autoimmune encephalomyelitis by leflunomide-- mechanisms independent of pyrimidine depletion
J. Leukoc. Biol., November 1, 2004; 76(5): 950 - 960.
[Abstract] [Full Text] [PDF]