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Título: | CD5 provides viability signals to B cells from a subset of B-CLL patients by a mechanism that involves PKC |
Autor: | Pérez-Chacón, Gema CSIC ORCID; Vargas, Juan A.; Jordá, Julia; Morado, Marta; Rosado, Silvia; Martín-Donaire, Trinidad; Losada-Fernández, Ignacio; Rebolleda, Nerea CSIC; Pérez-Aciego, Paloma | Palabras clave: | Signal transduction Kinases/Phosphatases B-CLL Apoptosis B cells |
Fecha de publicación: | feb-2007 | Editor: | Elsevier | Citación: | Leukemia Research 31(2): 183-193 (2007) | Resumen: | B-chronic lymphocytic leukaemia (B-CLL) is a heterogeneous disease characterized by an accumulation of B lymphocytes expressing CD5. To date, the biological significance of this molecule in B-CLL B cells remains to be elucidated. In this study, we have analysed the functional consequences of the binding of an anti-CD5 antibody on B-CLL B cells. To this purpose, we have measured the percentage of viability of B-CLL B cells in the presence or in the absence of anti-CD5 antibodies and also examined some of the biochemical events downstream the CD5-signalling. We demonstrate that anti-CD5 induces phosphorylation of protein tyrosine kinases and protein kinase C (PKC), while no activation of Akt/PKB and MAPKs is detected. This signalling cascade results in viability in a group of patients in which we observe an increase of Mcl-1 levels, whereas the levels of bcl-2, bcl-xL and XIAP do not change. We also report that this pathway leads to IL-10 production, an immunoregulatory cytokine that might act as an autocrine growth factor for leukaemic B cells. Inhibition of PKC prevents the induction of Mcl-1 and IL-10, suggesting that the activation of PKC plays an important role in the CD5-mediated survival signals in B cells from a subset of B-CLL patients. | Versión del editor: | https://doi.org/10.1016/j.leukres.2006.03.021 | URI: | http://hdl.handle.net/10261/342826 | DOI: | 10.1016/j.leukres.2006.03.021 | ISSN: | 0145-2126 | E-ISSN: | 1873-5835 |
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