RT info:eu-repo/semantics/article
T1 Secreted phospholipase A2 type IIA as a mediator connecting innate and adaptive immunity: new role in atherosclerosis
A1 Ibeas, Elvira
A1 Fuentes, Lucía
A1 Martín Martín, Rubén
A1 Hernández Garrido, Marita
A1 Nieto Callejo, María Luisa
K1 Atherosclerosis
K1 Aterosclerosis
K1 Dendritic cells
K1 Células dendríticas
K1 Macrophages
K1 Macrófagos
AB Aims: Human atherosclerotic plaques express markers of macrophage/dendritic cells as well as high levels of inflammatory proteins such as secreted phospholipase A2 type IIA (sPLA2-IIA). To understand the cellular changes associated with the progress of atherosclerosis, we evaluated the role of sPLA2-IIA in mediating monocyte recruitment and differentiation into antigen-presenting cells. Methods and results:The effect of sPLA2-IIA on monocyte differentiation was evaluated in human THP-1 cells, a cellular line widely used as a model for monocyte–macrophage differentiation. Changes in functional processes, morphology and expression of antigens, characteristic of differentiated cells, were monitored over a 1–3 day period. sPLA2-IIA inhibited CD14 expression in a time- and concentration-dependent manner and upregulated dendritic cell-specific ICAM-3 grabbing non-integrin levels at the cell surface, findings that were the same for human monocytes. In addition, sPLA2-IIA-differentiated cells showed a dendritic cell phenotype characterized by the generation of fine dendritic protrusions and an increase in surface markers such as CD40, CD83, CD54, CD61, and CD62L. Furthermore, cell adhesion, migration, endocytic activity, and allogeneic T cell proliferation capacity were markedly increased after sPLA2-IIA treatment. Conclusion: sPLA2-IIA induces the differentiation of mononuclear cells and increases their adhesive and migratory capabilities, which suggests a novel function for sPLA2-IIA as a mediator connecting innate and adaptive immunity. These findings may provide insight into the immuno-inflammatory processes occurring in atherosclerosis, helping us to understand the cellular changes associated with the development of atherosclerosis.
PB Oxford University Press
SN 1755-3245
YR 2009
FD 2009
LK https://uvadoc.uva.es/handle/10324/47006
UL https://uvadoc.uva.es/handle/10324/47006
LA eng
NO Cardiovascular Research, 2009, vol. 81, n. 1. p. 54-63
NO Producción Científica
DS UVaDOC
RD 22-nov-2024