Visit our Expo - Redox and Inflammation signaling 2012

VIII. Inflammation specific signaling Poster VIII, 36
T cell aggregation induced through CD43: Intracellular signals and inhibition by the
immunomodulatory drug leflunomide.
Esther Layseca-Espinosa1,2, Gustavo Pedraza-Alva1, José Luis Montiel1, Roxana del
Río1, Nora A. Fierro1, Roberto González-Amaro2, and Yvonne Rosenstein1.
1Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca,
Mor., and 2Department of Immunology, Facultad de Medicina, Universidad Autónoma
de San Luis Potosí, San Luis Potosí, S.L.P., México
The CD43 co-receptor 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 following 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, PLC-$2, PKC, PI3-K as well as
ERK1/2 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.
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