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Fuentes, Lucía Hernández Garrido, Marita Fernández Avilés, Francisco Jesús Sánchez Crespo, Mariano Nieto Callejo, María Luisa Producción Científica Atherogenesis is the consequence of a variety of effector mechanisms rather than the result of a single functional molecule. In this connection, type IIA secretory phospholipase A2 (sPLA2) is an acute-phase reactant, which accumulates in atherosclerotic arterial walls, elicits several effects on monocytes, and has been related to the development of atherosclerosis. CD40/CD40 ligand pair is also a strong proatherogenic system. sPLA2 produced an increase of the surface expression of CD40 in THP-1 monocytes and enhanced the effect of CD40 ligation on the expression of both Fas and FasL, thus indicating the existence of a positive cooperation between sPLA2 and different elements of the TNF-receptor superfamily. Activation of the CD40/CD40L dyad with anti-CD40 antibody produced a small release of arachidonic acid and lacked any significant effect on the induction of cyclooxygenase-2, whereas the secretion of the chemokine MCP-1 and the surface display of CD11b, the α chain of the integrin Mac-1, were upregulated. Engagement of CD40 did not influence the survival of THP-1 monocytes, but coincubation of THP-1 monocytes pretreated with anti-CD40 antibody and Jurkat cells induced a significant increase of the number of Jurkat cells showing binding of annexin-V, and nuclear condensation and fragmentation, thus indicating that this treatment might trigger a juxtacrine/paracrine mechanism of apoptotic death in sensitive cell types. This data indicates the existence of overlapping routes for the response to CD40, TNF-α, and sPLA2, thus allowing the development of distinct patterns of response in monocytic cells. 2021-06-22 2021-06-22 2002 info:eu-repo/semantics/article Circulation Research, 2002, vol. 91, n. 8. p. 681-688 0009-7330 https://uvadoc.uva.es/handle/10324/47010 10.1161/01.RES.0000038341.34243.64 eng https://www.ahajournals.org/doi/10.1161/01.RES.0000038341.34243.64 info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/4.0/ © 2002 American Heart Association Attribution-NonCommercial-NoDerivatives 4.0 Internacional American Heart Association